Thyroid Status in Anemic Pregnant Women Under Conditions of Endemic Goiter

[Thyroid status in anemic pregnant women under conditions of endemic goiter]. [Article in Russian] Zel'tser ME, Mezinova NN, Kobzar' NN, Bazarbekova RB, Nazyrov AT, Kim GG, Nurbekova AA, Nugmanova MI. Abstract Anemia is a highly prevalent condition among pregnant women in the Republic of Kazakhstan. The causes of this anemia are not quite clear, as is the problem of resistance of this type of anemia to therapy with iron preparations. The authors propose that this may be explained by the fact that many regions of the Republic are foci of endemic goiter, because tentative studies indicate a relationship between endemic goiter and hypothyrosis. The present study was aimed at examination of the thyroid status in pregnant women suffering from anemia in the town of Alma-Ata, a region endemic for goiter. Altogether 120 anemic pregnant women were examined, 60 of these with goiter and 60 without it. Control group consisted of 20 healthy pregnant women. Clinical and ultrasonic examinations, puncture biopsy of the thyroid, measurements of blood levels of TTH, total and free triiodothyronine and thyroxin, thyroxin-binding globulin, as well as of peripheral blood red cell counts, levels of hemoglobin, serum iron, assessment of total iron-binding capacity of the serum and saturation coefficient, were carried out. Healthy pregnant women from a focus of endemic goiter were found to represent a group at risk of anemia in the third pregnancy trimester. In anemic pregnant women endemic goiter aggravated anemia. Chronic iodine deficiency is conductive to formation in pregnant women of subclinical hypothyrosis whose severity increased in the presence of anemia, more so if anemia is paralleled by goiter. PMID: 7899433 [PubMed - indexed for MEDLINE]

Hypothyroidism and Iron: Anemia and Hemochromatosis The relationship between hypothyroidism and iron levels By Mary Shomon, About.com Guide Updated July 03, 2008 About.com Health's Disease and Condition content is reviewed by our Medical Review Board See More About:

 fatigue  anemia  hypothyroidism symptoms  hemachromatosis  hemochromatosis

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 Thyroid Disease Symptoms  Thyroid Symptoms  Low Thyroid Symptoms  Iron Rich Foods Anemia  Symptoms of Thyroid Disease Conditions related to iron levels in the blood are more common with hypothyroidism than in the average population, according to researchers.

Iron-deficiency anemia (insufficient iron) is more common in people with hypothyroidism. Symptoms or signs of anemia include:  Feeling tired or weak  Pale appearance to the lining of lower eyelids  palpitations, fast or irregular heart beat.  faintness and breathlessness.  hair loss.  bruising that occurs without reason  dizziness  long or unusually heavy menstrual periods Anemia is diagnosed using a comprehensive iron panel blood test.

In addition to your doctor's recommendations regarding treatment for anemia and any suggested iron supplementation, you can also consider the following recommendations  Eat more foods that are good sources of iron.  Help your body absorb iron better by eating foods high in vitamin C.  Red meat can supply iron, but also helps your body absorb iron from other foods.  Limit your use of tea, except herbal teas.  Increase dietary fiber to prevent constipation. Hemochromatosis is less common, but more frequently seen in people with hypothyroidism Symptoms of hemochromatosis include:  chronic fatigue  arthritis-like pain in joints, in particular, the middle two fingers  loss of libido (sex drive), impotence  early absence of menstrual periods  changes in skin color, yellowish, bronze, grey, olive  redness in the palms  abdominal pain  shortness of breath  heart arrhythmia  depression  elevated blood sugar Hemochromatosis is not easy to diagnose, as it is not revealed in routine blood work so doctors need to request specific tests to diagnose it.

Treatment for hemochromatosis is a doctor-supervised program of giving blood, known as phlebotomy.

A detailed article on Hypothyroidism and Iron Levels is featured online.

CHAPTER 34 ANEMIA OF ENDOCRINE DISORDERS Posted by medtextfree on December 27, 2011 in Hematology

CHAPTER 34 ANEMIA OF ENDOCRINE DISORDERS Williams Hematology CHAPTER 34 ANEMIA OF ENDOCRINE DISORDERS ALLAN J. ERSLEV Anemia of Pituitary Deficiency Anemia of Thyroid Dysfunction Anemia of Adrenal Dysfunction Anemia of Gonadal Dysfunction Anemia of Pregnancy Anemia of Parathyroid Dysfunction Anemia of Pancreatic Dysfunction Chapter References The hormones released by specific endocrine organs all play a role in modulating the rate of red cell production. The mechanisms involved vary greatly, and current interest in unraveling single actions have been replaced by attempts to integrate the actions of multiple hormonal- like growth factors and cytokines on the sequential proliferation and differentiation of red cell precursors. Consequently, the discussion in this chapter of anemias caused by a deficiency of a single traditional hormone is by necessity more historic than current. Acronyms and abbreviations that appear in this chapter include: ACTH, adrenocorticotrophic hormone; 2,3-BPG, 2,3-bisphosphoglycerate; TSH, thyroid-stimulating hormone. Numerous growth factors and cytokines are involved in the regulation and function of the erythropoietic tissue (see Chap. 14). Some are autocrine and released by the same cells on which they are acting, some are paracrine and released by neighboring cells, and some are endocrine and released from distant tissue and carried by blood to their target cells. The latter are traditionally designated hormones, and the effect on red cell production of altered hormone levels in blood due to endocrine tissue dysfunction is described here.1,2 The effect of the renal hormone erythropoietin is covered in Chap. 33. ANEMIA OF PITUITARY DEFICIENCY Hypophysectomy in the experimental animal is regularly followed by the development of moderately severe erythroid hypoplasia and anemia.3,4 In rats, the selective removal of the posterior or intermediate lobe does not cause anemia,5 and it is generally assumed that the pathogenesis of the anemia is related to the absence of anterior lobe hormones, which in turn modulate renal erythropoietin production.6 Of these, TSH is probably of most importance, since the anemia of hypophysectomy is very similar to the anemia of thyroidectomy.7 Nevertheless, it is claimed that the rate of red cell production in hypophysectomized animals is restored to normal only if the administration of TSH is supplemented by ACTH8 or if the administration of thyroid hormone is supplemented by both glucocorticoids and androgens.3 It has been proposed repeatedly that the pituitary gland produces a specific erythropoietic hormone,9,10 but the therapeutic effectiveness of target organ hormones alone is not in accord with such a possibility. Growth hormone has been shown to be capable of stimulating red cell production in vitro,11 an effect possibly mediated by insulin-like growth factor,12 but whether this effect is of physiologic significance remains unclear.13 The same holds true for the hypothetical effect of the hypothalamus on red cell production. It has been claimed that hypothalamic injury may affect erythropoietin release,14 the rate of red cell production,15 or both,16 and it has been proposed that these effects are mediated via the hypophysis. However, the experimental data provided in support of this hypothesis are unimpressive.15,16 In human subjects, hypophyseal dysfunction or hypophyseal ablation is often associated with leukopenia and is regularly accompanied by a normochromic and normocytic anemia. The red cell life span is normal, but marrow examination and ferrokinetic studies disclose moderate hypoplasia and relative marrow failure.17,18 Replacement therapy with a combination of thyroid, adrenal, and gonadal hormones usually corrects the anemia.19,20 It is probable that treatment with recombinant human erythropoietin would also do so. ANEMIA OF THYROID DYSFUNCTION In 1881, Charcot21 first recognized that cretins and patients with myxedema were anemic. At about the same time, the great Swiss surgeon Kocher22 reported that thyroidectomy also is followed by a reduction in the red cell count. The character of this type of anemia has been a source of debate ever since, and it has been variously described as normocytic, microcytic, or macrocytic.23 Studies have clarified the pathogenesis by separating the component caused by a lack of thyroid hormone from the components caused by complicating deficiencies of iron, vitamin B12, or folic acid.24,25,26 The rate of red cell production in experimental animals increases after the administration of thyroxin, triiodothyronine, or desiccated thyroid27,28 and decreases after thyroidectomy.29,30 These erythropoietic responses appear to be quite appropriate, since the need for circulating red cells depends on the cellular requirements for oxygen, which in turn are influenced by thyroid hormones.23,31,32 Nevertheless, it has also been proposed that the thyroid hormones have a noncalorigenic effect on red cell production.33 Studies of the influence of thyroid hormones on in vitro erythropoiesis have shown that both calorigenic T3 and T4 and noncalorigenic rT3 potentiate the effect of erythropoietin on the formation of erythroid colonies34,35 or increasing hypoxia-induced production of erythropoietin.36 This effect appears to be mediated by burst-promoting factors released by activated lymphocytes37 and/or by receptors with b2-adrenergic properties.37 Anemia observed in thyroidectomized animals conforms to both mechanisms by being normochromic and normocytic and associated with reticulocytopenia and hypoplasia of the erythropoietic tissue in the marrow. The red cell life span is normal, and ferrokinetic studies indicate the existence of a hypofunctioning but effective marrow.38 Anemia observed in human subjects with myxedema or other hypothyroid conditions is not always this clear-cut, since the condition may be complicated by nutritional deficiencies. However, many hypothyroid patients have a hypoplastic anemia that is unresponsive to therapy with iron, vitamin B12, or folic acid and is very similar to the form of anemia observed in thyroidectomized animals.23,24,39 The degree of anemia is mild to moderate, with a hemoglobin concentration rarely less than 8 to 9 g/dl. The corresponding decrease in erythroid marrow activity is frequently too small to be morphologically demonstrable.40 Ferrokinetic studies show a decrease in the turnover of plasma and red cell iron, a decrease that also may be so small that it is first recognized when compared with values obtained after thyroid replacement therapy.41,42 As in hypothyroid animals, the red cell life span and the rate of red cell utilization of iron are normal. The degree of anemia does not always reflect the reduction in marrow activity and the size of the red cell volume, since the plasma volume is decreased in hypothyroid patients.43 This may result in a temporary aggravation of apparent anemia after thyroid replacement therapy, since the plasma volume will be restored to normal before the red cell volume. Although normochromic and normocytic anemia must be considered the characteristic form of anemia of hypothyroidism, the most frequent type of anemia observed is a microcytic, hypochromic anemia caused by iron deficiency.23,44 In hypothyroid women, menorrhagia is a frequent complication and may explain adequately the lack of iron. However, even in men, iron is in short supply either because of the histamine- refractory achlorhydria, which is present in about 50 percent of anemic patients,45 or possibly because of intestinal malabsorption of iron.46,47 Macrocytosis is frequently identified with anemia of hypothyroidism.23,39 However, when a substantial increase in the mean corpuscular volume occurs, it is usually caused by a megaloblastic erythropoiesis owing to vitamin B12 or folic acid deficiency.24 In hypothyroid patients, the incidence of true pernicious anemia with gastric atrophy and intrinsic factor deficiency appears to be unusually high.48,49,50 This has led to interesting but still inconclusive speculations on the effect of cross-reacting autoantibodies against thyroglobulins and intrinsic factor or gastric parietal cells.51,52,53 This may be of special etiologic importance for Graves’ disease and Hashimoto’s thyroiditis, both autoimmune disorders. However, in a study of eight patients with coexisting megaloblastic anemia and hypothyroidism, it was concluded that all eight, rather than having vitamin B12 deficiency, had folic acid deficiency from either poor dietary intake of folic acid or intestinal malabsorption.26 Despite the direct and indirect erythropoietic effect of thyroid hormones, patients with hyperthyroidism or thyrotoxicosis rarely have elevated hemoglobin concentrations or hematocrit percentages43,54 and may even be moderately anemic.55,56 This absence of an expected secondary polycythemia has been explained by assuming that an increased cardiac output and rate of tissue perfusion meet the increased tissue requirements for oxygen. Conflicting data have been presented as to the effect of thyroid hormone in vitro on the intracellular concentration of 2,3-BPG and, in turn, the oxygen affinity of hemoglobin.57 So far, however, direct studies of hyperthyroid patients do not suggest the presence of enhanced oxygen transport to the tissues.58 It actually seems more likely that the absence of an overt secondary polycythemia is due to hemodilution. Direct measurements of the size of the red cell volume,43 the erythroid activity of the marrow,40 and the turnover of plasma and red cell iron54 show them to be above normal. If it were not for the concomitant increase in plasma volume, these patients would have elevated hemoglobin and hematocrit levels. Studies of the red cell life span in patients with thyrotoxicosis suggest a moderate shortening in red cell survival,59 possibly reflecting an autoimmune etiology with the production of anti–red-cell antibodies.60 In a few cases, severe hyperthyroidism has been found to be associated with anemia and abnormal iron utilization, apparently reflecting ineffective red cell production,44 or the production of erythropoietin-directed antibodies.61 The institution of radioiodine therapy results in a reduction in the size of the red cell volume to normal but only a slight change in the hematocrit. ANEMIA OF ADRENAL DYSFUNCTION Adrenalectomy in experimental animals causes a mild anemia responsive to therapy with adrenal glucocorticoids or erythropoietin.17,29,62 A similar type of normochromic, normocytic anemia has been observed in Addison’s disease,17,63 but because of the concomitant reduction in plasma volume, the hemoglobin concentration and the hematocrit percentage do not reflect the true decrease in red cell volume. The character of this type of anemia and the erythropoietic effect of physiologic amounts of ACTH or adrenal cortical hormones are still unclear, possibly because the changes involved are too small for adequate study. When administered in pharmacologic amounts, these hormones appear to cause mild erythrocytosis64 of about the same magnitude as that observed in Cushing’s disease65,66 and occasionally in Bartter’s syndrome67 and pheochromocytoma.68 However, whether this is mediated via release of renal erythropoietin or by direct action on the erythropoietic cells in the marrow is unknown.69 ANEMIA OF GONADAL DYSFUNCTION The erythropoietic effect of androgens in both physiologic and pharmacologic dosages is well recognized and extensively utilized in the treatment of patients with various types of refractory anemia. Castration of the male experimental animal causes a decrease in the rate of red cell production until the hemoglobin concentration and the red cell volume become stabilized at levels approximately the same as those of the normal female.70,71 In sexually mature human males, the hemoglobin level is 1 to 2 g/dl higher than the level observed in males during childhood, advanced age, orchiectomy, or gonadal hypofunction. Under those circumstances, the hemoglobin level is similar to that of the normal human female.72,73,74 In pharmacologic doses androgens have been shown to stimulate red cell production75,76 by increasing the production of erythropoietin77 and by enhancing the effect of erythropoietin on the marrow.78 These actions have been attributed to two isomeric metabolites formed by the reduction of a 4-5 double bond. The 5a-H isomer is androgenic and believed to cause a release of erythropoietin from the kidney.79 The 5b-H isomer is not androgenic or erythropoietinogenic but is believed to cause inactive marrow stem cells to enter an erythropoietin-responsive phase.80 Before being replaced by recombinant human erythropoietin in the treatment of anemia of renal failure, androgens were used extensively.81,82 Even now, androgens may enhance the effect of erythropoietin and reduce the cost of such therapy.83 Studies on the effect of physiologic doses of estrogens suggest that these hormones cause a slight suppression of red cell production.83 In large doses, estrogens have been shown to cause the development of moderately severe anemia,84,85 but it has not been resolved whether this is caused by suppressed erythropoietin production85 or by inhibition of the progenitor cell action of erythropoietin.86 Inhibin and activin, two glycoprotein hormones released by gonadal cells in both male and female, have been shown in vitro to have an effect on human erythroid progenitor cells.87,88,89 The physiologic significance of these observations is still unknown. Human placental lactogen and sheep prolactin have been shown to have erythropoietic activity in the mouse.90 It has been proposed that human placental lactogen is in part responsible for the stimulation of red cell production in pregnancy.91 ANEMIA OF PREGNANCY Although pregnancy is not an endocrine disorder, it is associated with a mild anemia, presumably caused by changes in the hormonal environment.92 Studies of pregnant mice have shown that, despite a progressive decrease in the hematocrit, the red cell volume, erythropoietin secretion, and rate of red cell production increase during pregnancy.90 Placental lactogen, which is erythropoietically active in the mouse,92 may in part be responsible for the erythropoietic stimulation, but the hormonal mechanisms underlying both the increase in red cell volume and the even more pronounced increase in plasma volume are not precisely known. In humans, anemia in pregnancy is most often aggravated by dietary restrictions93 and a concomitant iron deficiency.94,95 In a smaller number of cases, folic acid deficiency may also play a pathogenetic role,96 and it seems appropriate to give every pregnant woman preventive iron and folic acid supplements. However, even in the well-cared-for pregnant woman, anemia becomes manifest at about the eighth week of pregnancy, progresses slowly until the thirty-second to thirty-fourth week, and is then stable until it rather suddenly improves just before delivery.97,98 It is moderate in severity, with hemoglobin concentrations rarely below 10 g/dl, and studies of the red cell volume have shown it to be a dilution anemia.97,98 There has been an obvious reluctance to use radioactive tracers to measure red cell and plasma volume in early pregnancy. However, using a nonradioactive biotin technique,99 it has been shown that there is a gradual increase in red cell volume beginning before the twelfth week of pregnancy. This early increase is not associated with measurable changes in the concentration of serum transferrin receptors, reticulocyte counts, or erythropoietin titers.99,100 However, in the second and third trimester, erythrokinetic studies using both radioactive iron101 and serum transferrin receptor concentrations100 have shown an increased erythropoietic activity. The associated changes in reticulocyte counts, serum ferritin concentrations, and erythropoietin titers are small and difficult to detect102 but in some studies quite significant.103,104 Despite the increase in red cell volume, the hemoglobin concentration falls as a consequence of an even greater increase in plasma volume. The total increase in red cell volume during pregnancy is about 20 percent, while the increase in plasma volume is about 30 percent. The increase in plasma volume can probably be explained on the basis of an increase in the size of the uterine vascular bed, with a shift of fluid from extravascular to vascular space. The induction of this hypervolemia creates a low-viscosity erythrocytosis, which promotes oxygen transport to the tissues. Although the hemoglobin concentration is decreased, the hypervolemic state ensures the pregnant uterus of an excellent blood perfusion and oxygen supply. ANEMIA OF PARATHYROID DYSFUNCTION Primary hyperparathyroidism is occasionally105,106 associated with anemia that disappears after parathyroidectomy.107,108 Similarly, it has been reported that parathyroidectomy in chronic renal disease often results in some improvement in the anemia,109,110 and it has been suggested that the parathyroid hormone may be a toxin that can suppress normal red cell production.111,112 However, other studies have not supported this suggestion.112,113,114,115 These suggest that primary or secondary hyperparathyroidism, when associated with suppressed red cell production, acts by causing either renal calcification with reduction in erythropoietin formation or marrow sclerosis with reduction in erythroid proliferation.116 ANEMIA OF PANCREATIC DYSFUNCTION Although insulin and the insulin-like growth factors I and II appear to be involved in expanding the red cell mass after treatment with growth hormones, there is little evidence for the notion that insulin is an erythropoietic agent.119,120 CHAPTER REFERENCES 1. Adamson JW, Popovic WJ, Brown JE: Hormonal control of erythropoiesis, in Hematologic Cell Differentiation, edited by DW Golde, MJ Cline, D Metcalf, pp 53–67. Academic, New York, 1978. 2. Orwoll FS, Orwoll RL: Hematologic abnormalities in patients with endocrine and metabolic disorders. Hematol Oncol Clin North Am 1:261, 1987. 3. Crafts RC, Meineke HA: The anemia of hypophysectomized animals. Ann NY Acad Sci 77:501, 1959. 4. Gordon AS: Endocrine influences upon the formed elements of blood and blood forming organs. Prog Hormone Res 10:339, 1954. 5. Van Dyke DC, Garcia JF, Simpson ME, et al: Maintenance of circulating red cell volume in rats after removal of the posterior and intermediate lobes of the pituitary. Blood 7:1017, 1952. 6. Peschle C, Rappaport IA, Magli MC, et al: Role of hypophysis in erythropoietin production during hypoxia. Blood 5:1117, 1978. 7. Crafts RC: The similarity between anemia induced by hypophysectomy and that induced by a combined thyroidectomy and adrenalectomy in adult female rats. Endocrinology 53:465, 1953. 8. Fisher JW, Crook JJ: Influence of several hormones on erythropoiesis and oxygen consumption in the hypophysectomized rat. Blood 19:557, 1962. 9. Contopoulos AN, Simpson ME, Van Dyke DC, et al: The pituitary erythropoietic factor. Anat Rec 118:290, 1954. 10. Lindeman R, Trygstad O, Halvorsen S: Pituitary control of erythropoiesis. Scand J Haematol 6:77, 1969. 11. Golde DW, Bersch N, Li CH: Growth hormone: Species specific stimulation of erythropoiesis in vitro. Science 196:1112, 1977. 12. Merchav S, Tatarsky I, Hochberg Z: Enhancement of erythropoiesis in vitro by human growth hormone is mediated by insulin-like growth factor I. Br J Haematol 70:267, 1988. 13. Jepson JH, McGarry EE: Hemopoiesis in pituitary dwarfs treated with human growth hormone and testosterone. Blood 39:238, 1972. 14. 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Ardeman S, Chanarin I, Krafchik B, Singer W: Addisonian pernicious anemia and intrinsic factor antibodies in thyroid disorders. Q J Med 35:421, 1966. 54. Donati RM, Warnecke MA, Gallagher NJ: Ferrokinetics in hyperthyroidism. Ann Intern Med 63:945, 1963. 55. Rivlin RS, Wagner HN: Anemia in hyperthyroidism. Ann Intern Med 70:507, 1969. 56. Perlman JA, Sternthal PM: Effect of 131I on the anemia of hyperthyroidism. J Chron Dis 36:405, 1983. 57. Miller WW, Delivoria-Papadopoulos M, Miller LD, Oski FA: Oxygen releasing factor in hypothyroidism. JAMA 211:1824, 1970. 58. Zaroulis CG, Kourides JA, Valeri CR: Red cell 2,3-diphosphoglycerate and oxygen affinity of hemoglobin in patients with thyroid disorders. Blood 52:181, 1978. 59. McClellan JE, Donegan C, Thorup OA, Leavell BS: Survival time of the erythrocyte in myxedema and hyperthyroidism. J Lab Clin Med 51:91, 1958. 60. Bouchou K, Andre M, Cathebras P, et al: Pathologie thyroidienne et syndromes auto-immuns multiples: Aspects clinique et immunogenetique aá-propos de 11 observations. Rev Med Interne 16:283, 1995. 61. Jyo-Oshiro Y, Nomura S, Fukushima T, Tamai H, Fueki H, Osawa G: Primary hyperthyroidism induced erythropoietin-resistant anemia? Intern Med 36:903, 1997. 62. Van Dyke DC, Contopoulos AN, Williams BS, et al: Hormonal factors influencing erythropoiesis. Acta Haematol (Basel) 11:203, 1954. 63. Baez-Villasenor J, Rath CE, Finch CA: The blood picture in Addison’s disease. Blood 3:769, 1948. 64. Fisher JW: Increase in circulating red cell volume of normal rats after treatment with hydrocortisone or cortico-sterone. Proc Soc Exp Biol Med 97:502, 1958. 65. Platz CM, Knowlton AJ, Ragan C: The natural history of Cushing’s syndrome. Am J Med 13:597, 1952. 66. Ross EJ, Marshall-Jones P, Friedman M: Cushing’s syndrome: Diagnostic criteria. Q J Med 35:149, 1966. 67. Erkelens DW, Statius van Eps LWS: Bartter’s syndrome and erythrocytosis. Am J Med 55:711, 1973. 68. Shulkin BL, Shapiro B, Sisson JC: Pheochromocytoma, polycythemia and venous thrombosis. Am J Med 83:773, 1987. 69. Golde DW, Bersch N, Cline MJ: Potentiation of erythropoiesis in vitro by dexamethasone. J Clin Invest 57:57 1976. 70. Steinglass P, Gordon AS, Charipper HA: Effect of castration and sex hormones on blood of the rat. Proc Soc Exp Biol Med 48:169, 1941. 71. Crafts RC: Effect of hypophysectomy, castration and testosterone propionate on hemopoiesis in the adult male rat. Endocrinology 39:401, 1946. 72. Hawkins WW, Speck E, Leonard VG: Variation of the hemoglobin level with age and sex. Blood 9:999, 1954. 73. Fonseca R, Rajkumar SV, White WL, Tefferi A, Hoaglund HC: Anemia after orchiectomy. Am J Hem 59:230, 1998. 74. Matsumoto AM, Bremner WJ: Hypogonadism: Androgen therapy, in Current Therapy in Endocrinology and Metabolism, edited by DT Krieger, CW Bardin, pp 145–149. Dekker, Toronto, 1986. 75. Kennedy BJ, Gilbertsen AS: Increased erythropoiesis induced by androgenic-hormone therapy. N Engl J Med 256:719, 1957. 76. Shahidi NT: Androgens and erythropoiesis. N Engl J Med 289:72, 1973. 77. Alexanian R: Erythropoietin and erythropoiesis in anemic man following androgens. Blood 33:564, 1969. 78. Singer JW, Samuels AJ, Adamson JW: The effect of steroids on in vitro erythroid colony growth: Structure/activity relationships. J Cell Physiol 88:127, 1976. 79. Paulo LG, Fink GD, Roh BL, Fisher JW: Effects of several androgens and steroid metabolites on erythropoietin production in the isolated perfused dog kidney. Blood 43:39, 1974. 80. Gorshein D, Hait WN, Besa EC, et al: Rapid stem cell differentiation induced by 19- nortestosterone decanoate. Br J Haematol 26:215, 1974. 81. Eschbach JW, Adamson JW: Improvement in the anemia of chronic failure with fluoxymesterone. Ann Intern Med 78:527, 1973. 82. 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Broxmeyer HE, Lu L, Coopers S, et al: Selective and indirect modulation of human multipotential and erythroid hematopoietic progenitor cell proliferation by recombinant human activin and inhibin. Proc Natl Acad Sci USA 85:9062, 1988. 89. Yu J, Shao A, Vaughan J, et al: Characterization of the potentiation effect of activin on human erythroid colony formation in vitro. Blood 73:952, 1989. 90. Jepson JH, Lowenstein L: Hormonal control of erythropoiesis during pregnancy in the mouse. Br J Haematol 14:555, 1968. 91. Berczi I, Wage E: Placental lactogen is a haemopoietic hormone. Br J Haematol 79:355, 1991. 92. Letsky EA: Erythropoiesis in pregnancy. J Perinatal Med 23:39, 1995. 93. Simmons WK, Simeon DT, Bramble D, Buffonge C, Gallagher P: Marked reduction of anemia during pregnancy over a 10-year period in Montserrat. Bull Pan Am Health Organ 30:18, 1996. 94. Benjamin F, Bassen FA, Meyer LM: Serum levels of folic acid, vitamin B12 and iron in anemia of pregnancy. 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Pritchard JA, Adams RH: Erythrocyte production and destruction during pregnancy. Am J Obstet Gynecol 79:750, 1960. 102. Harstad TW, Mason RA, Cox SM: Serum erythropoietin quantitation in pregnancy using an enzyme-linked immunoassay. Am J Perinatol 9:233, 1992. 103. Howells MR, Jones SE, Napier JA, et al: Erythropoiesis in pregnancy. Br J Haematol 64:595, 1986. 104. Cotes PM, Canning CE, Lind T: Changes in immunoreactive erythropoietin during the menstrual cycle and normal pregnancy. Br J Obstet Gynaecol 90:304, 1983. 105. Malette LE, Bilezikian JP, Heath DA, Aurbach GD: Primary hyperparathyroidism: Clinical and biochemical features. Medicine (Baltimore) 53:127, 1974. 106. Abarca J, Trisonis C, Hamberser B, Granbers PO: Anaemia in primary hyperparathyroidism: Fantasy or reality? Ann Chir Gynaecol 74:74, 1985. 107. Boxer M, Ellman L, Geller R, Wang CA: Anemia in primary hyperparathyroidism. Arch Intern Med 13:588, 1977. 108. Falco JM, Guy JT, Smith RE, Mazzaferri EL: Primary hyperthyroidism and anemia. Arch Intern Med 136:887, 1976. 109. Zingraff J, Drueke T, Marie P, et al: Anemia and secondary hyperparathyroidism. Arch Intern Med 138:1650, 1978. 110. Kotzmann H, Abela C, Heindl J, et al: Effect of successful parathyroidectomy on hematopoietic progenitor cells and parameters of red blood cells in patients with primary hyperparathyroidism. Horm Metab Res 29:387, 1997. 111. Massry SG: Is parathyroid hormone a uremic toxin? Nephron 19:125, 1977. 112. Fujita Y, Inoue S, Horiguchi S, Kuki A: Excessive level of parathyroid hormone may induce the reduction of recombinant human erythropoietin effect on renal anemia. Miner Electrolyte Metab 21:50, 1995. 113. Delwiche F, Garrity MJ, Powell JS, et al: High levels of the circulating form of parathyroid hormone do not inhibit in vitro erythropoiesis. J Lab Clin Med 102:613, 1983. 114. Lutton JD, Solangi KB, Ibraham NG, et al: Inhibition of erythropoiesis in chronic renal failure: The role of parathyroid hormone. Am J Kidney Dis 3:380, 1984. 115. McGonigle RJS, Wallin JD, Husserl F, et al: Potential role of parathyroid hormone as an inhibitor of erythropoiesis in the anemia of renal failure. J Lab Clin Med 104:1016, 1984. 116. Slackman N, Green AA, Naiman JL: Myelofibrosis in children with chronic renal insufficiency. J Pediatr 87:720, 1975. 117. Ishimura E, Nishizawa Y, Okuno S, et al: Diabetes mellitus increases the severity of anemia in non-dialyzed patients with renal failure. J Nephrol 11:83, 1998. 118. James SH, Meyers AM: Microangiopathic hemolytic anemia as a complication of diabetes mellitus. Am J Med Sci 315:211, 1998. 119. Sawada K, Krantz SB, Dessypris EN, et al: Human colony-forming-units-erythroid do not require accessory cells but do require direct interaction with insulin-like growth factor I and/or insulin for erythroid development. J Clin Invest 83:1701, 1989. 120. Ten Have SM, van der Lely AJ, Lamberts SW: Increase in haemoglobin concentrations in growth hormone deficient adults during human recombinant growth hormone replacement therapy. Clin Endocrinol 47:565, 1997. Books@Ovid Copyright © 2001 McGraw-Hill Ernest Beutler, Marshall A. Lichtman, Barry S. Coller, Thomas J. Kipps, and Uri Seligsohn Williams Hematology Like

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Casey L. Holley, Yahoo! Contributor Network Sep 1, 2010 "Share your voice on Yahoo! websites. Start Here."  More:  Thyroid  Pregnancy Brain   tweet  Print Flag During pregnancy, estrogen and human chorionic gonadotropin (hCG) are produced. These increase the thyroid hormones in the blood. When the mother's thyroid function is abnormal, there is a chance that the baby will get too much or not enough of the thyroid hormone. This affects the way the baby's brain and nervous system develop. The baby needs thyroid hormone so its nervous system and brain develop properly. Up until the 10th to 12th week of pregnancy, the baby gets all of the thyroid hormone it needs from the mother. After that time, the baby's own thyroid begins to function, but the baby still needs the mother to get enough iodine to support proper thyroid function. Possible Complications Congestive heart failure, low birth weight, developmental disabilities, premature birth, miscarriage and still birth are all possible during a pregnancy when the mother's thyroid function is abnormal. Preeclampsia, or high blood pressure during pregnancy, and anemia, or low levels of iron in the blood that affect the way oxygen is carried to the organs, are both possible. Delivery complications, such as stalled labor or prolonged labor are also possible. Some women may experience thyroid storms, or worsened thyroid function and symptoms, during the first trimester when the baby relies on her thyroid hormones. During the second and third trimesters, however, the woman may experience a period of remission because of the body's natural immune system suppression that occurs during that period. The remission phase usually ends at delivery, when the thyroid storms begin again. These storms usually last two to three months and begin to stabilize as the mother's hormones return to normal. Postpartum Thyroiditis Approximately 8 percent of women who have delivered a baby will suffer from an inflammation of the thyroid called postpartum thyroiditis. This condition may go undiagnosed because the symptoms often mimic postpartum blues. These symptoms include lethargy, exhaustion, fatigue and moodiness. Sources: http://www.endo-society.org/guidelines/final/upload/Clinical-Guideline-Management-of- Thyroid-Dysfunction-during-Pregnancy-Postpartum.pdf http://www.guidelines.gov/content.aspx?id=11283 A woman who is suffering from postpartum thyroiditis will go through a cycle of symptoms. One to eight months after delivery, the woman will go through a mild phase of hyperthyroidism lasting one to two months. From there, a period of approximately six months to a year, the woman will suffer from hypothyroidism. In most cases, after the period of hyperthyroidism, the thyroid will begin to function properly. However, in a small number of women, the thyroid is severely damaged by the inflammation and function never returns to normal. In that case, the woman will have to take synthetic hormones. Conclusion Because of the effects of thyroid dysfunction on the baby and the mother, it is necessary for a obstetrician to treat the mother, sometimes with synthetic hormones, during pregnancy and in the postpartum period. Published by Casey L. Holley Casey Holley is a freelance writer specializing in Christian content and medical content. She has more than a decade of experience. She also enjoys writing about animals, beauty, fitness, weight loss, travel... View profile  Vegetables that Cause Decreased Thyroid FunctionOf course vegetables are healthy, but too many of certain types could be a problem if you have an underactive thyroid. Here's why.  Understanding Pregnancy-Induced HypothyroidismIf you are pregnant and experiencing fatigue, here is what you need to know about pregnancy induced hypothyroidism.  Common Thyroid ProblemsTwo common problems of the thyroid are hyperthyroidism and hypothyroidism. Learn about the causes and symptoms of these two most common thyroid problems.  How Does a Doctor Diagnose Thyroid Disease?In the front of your neck, just about at the level of your voice box, is a the thyroid gland. This little organ is responsible for making hormones that can have dramatic effects on the metabolic functions of the body.  Reasons to Double Dose T3 Thyroid MedicationsIf your doctor has prescribed T3 thyroid medication, such as Cytomel, it is important to become familiar with the reasoning behind a double, or even triple, dosing per day.

 Learn About Thyroid Hormones

 How to Balance Thyroid Levels

 Treatment Plan for Pregnant Woma...  Thyroid Problems and Their Affect on Fertility  Fetal Thyroid Development and Congenital Abnormality Risks  How Thyroid Problems Affect Fertility and Pregnancy  Thyroid Disorder or Postpartum Depression?  Medical Emergency: Thyroid Storm  The Relationship Between Hypothyroidism and Pregnancy  Illnesses and Infections During Pregnancy To comment, please sign in to your Yahoo! account, or sign up for a new account.

THYROID AUTOIMMUNITY AND PREGNANCY OUTCOME Alex F. Muller Department of Internal Medicine, Diakonessenhuis Utrecht, Bosboomstraat 1 ,3582 KE, Utrecht ,The Netherlands , email: [email protected]

Arie Berghout Department of Internal Medicine, Medical Center Rijnmond Zuid - Zuiderziekenhuis, Groene Hilledijk 315 ,3075 EA, Rotterdam ,The Netherlands.

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Introduction Several, disorders that are historically associated with pregnancy loss - such as collagen vascular diseases (most notably systemic lupus erythematosus), chronic active hepatitis, inflammatory bowel disease, diabetes mellitus and thyroid disease - are autoimmune disorders (1). A number of studies have specifically addressed the relationship between thyroid autoimmunity and spontaneous pregnancy loss. Autoimmune hypo- and hyperthyroidism also increase the risk for obstetrical complications. It appears that low birth weight; prematurity and eclampsia are associated with the severity of the thyroid dysfunction (2-5). Thyroid failure (6) - and even low normal free thyroxine (fT4) levels! (7) - in early pregnancy are associated with impaired neuropsychological development. Considering the fact that thyroid autoimmunity often leads to the gradual development of permanent thyroid failure it becomes clear that the presence of thyroid autoimmunity has important repercussions on clinical practice in women of childbearing age (8). In conclusion, there is accumulating evidence that thyroid autoimmunity is associated - causally or as an epiphenomenon - with adverse pregnancy outcomes. In this comment we will discuss some aspects of thyroid autoimmunity and pregnancy outcome. For an oversight of the factors that are involved in the pathogenesis of autoimmune thyroiditis, especially in relation to pregnancy the reader is referred a recent review (9). Thyroid autoimmunity and pregnancy loss Spontaneous pregnancy loss is common. It has been shown that the total rate of spontaneous pregnancy loss is 31% (10). An increasingly recognized factor in the aetiology of pregnancy loss is the presence of autoantibodies (11). How might autoimmunity influence miscarriage? An extensive discussion of this issue is beyond the scope of this comment, for this the reader is referred to some excellent reviews (12;13). However, several points are worth mentioning at this point. Since the fetus expresses paternal MHC molecules adaptation of the maternal immune system is essential for a successful pregnancy. Such adaptation is accomplished through an increased production of cytokines that have immunosuppressive capacities. These cytokines are produced by so-called (CD4+) T-helper 2 (TH2) lymphocytes. Another subset of T cells exists that is also CD4+, these so-called T-helper 1 (TH1) lymphocytes are - unlike TH2 cells - well equipped to stimulate the cytotoxic and cytolytic arm of the cell mediated immune system (e.g. to activate macrophages and Natural Killer cells) via TH1 cytokines to kill target cells. During successful pregnancy there is a TH1 to TH2 shift characterized by down-regulation of the TH1 mediated effector arms of the immune system, concomitantly there is increased immunoglobulin production (9). Interestingly, experimentally induced changes in the TH1 / TH2 balance during pregnancy can induce increased rates of miscarriage (14). From these data it is clear that an adequate adaptation of the immune system is of paramount importance for a successful pregnancy to occur. Stagnaro-Green et al. studied 552 consecutive women in the first trimester of pregnancy and found that the presence of thyroid peroxidase (TPO) and/or thyroglobulin (Tg) antibodies in the first trimester of pregnancy is a risk factor for spontaneous fetal loss (17% vs. 8.4% in controls) (15). These results were confirmed by Glinoer et al. who found a higher rate of spontaneous abortion in 45 women with thyroid autoantibodies compared to 603 controls: 13.3% vs. 3.3% (16). In a prospective study of 54 women who conceived after in vitro fertilization (IVF) we were unable to find a significant association between the spontaneous abortion rate and the presence of TPO antibodies before pregnancy. Although miscarriages occurred in 33% of TPO antibody positive women and in only 19% of the TPO antibody negative women, the difference was not statistically significant (17). Our results thus contradict those of the two studies mentioned above and several biases can be proposed to explain this discrepancy (18). Firstly, the prevalence of thyroid autoimmunity was low in our pregnant women and if present the severity of the thyroid autoimmune process was mild. Secondly, we determined TPO antibodies before pregnancy, while in the other studies antibodies were determined during pregnancy. In view of the immunologic changes that occur during pregnancy (see ref. 7 for review) these differences in study design have probably led to inclusion of women with less severe forms of thyroid autoimmunity which might - at least in part - explain the discrepancy. In women with a history of habitual abortion the presence of non-organ specific autoantibodies, notably of antiphospholipid and anticardiolipin antibodies, has been associated with fetal loss (19). Data on the relationship between thyroid autoantibodies and habitual abortion are conflicting. Several studies found an association between TPO antibodies and recurrent first- trimester fetal loss (20-24). However, others could not confirm this observation (25;26). Interestingly, Vaquero et al. have recently investigated the role of mild thyroid abnormalities in women with thyroid antibodies and recurrent first trimester abortions (27). In this small study the authors showed that treatment with thyroid hormone was more effective than treatment with intravenous immunoglobulins. These data might be taken to suggest that mild degrees of thyroid insufficiency and not thyroid autoimmunity per se - is causal in the association between the presence of thyroid antibodies and recurrent abortion (27;28). In conclusion there are presently sufficient data showing an association of thyroid autoimmunity in early pregnancy and subsequent 'incidental' miscarriage. However, the data on the presence of thyroid antibodies and recurrent abortion are conflicting. Most likely, 'incidental' and recurrent abortion represent distinctive entities. Autoimmune thyroid dysfunction and obstetrical complications Despite the association between decreased fertility and hypothyroidism 2- 2.5% of pregnant women have elevated TSH levels (29-31). Hyperthyroidism in pregnancy is less often encountered: approximately only in 1 of 1000-2000 pregnancies (2;3;32) When women with hypothyroidism do become pregnant it appears that the most prevalent disorder is pregnancy induced hypertension (33-36). Other complications that have been described in some but not all studies are placenta abruptio, postpartum haemorrhage, stillbirths, low birth weight and significant anaemia (33;35;36). Considering treatment it is important to note that thyroid hormone replacement with T4 significantly improves - but not diminishes - the excess risk of obstetrical complications (33). Hyperthyroidism during gestation is also associated with obstetrical complications such as low birth weight, prematurity and eclampsia (2). It is outside the scope of this editorial to discuss the treatment of hyperthyroidism during pregnancy, for this purpose the reader is referred to some excellent recent overviews (2;33). Thyroid autoimmunity and offspring Several studies have shown that the presence of thyroid antibodies is a powerful risk marker for the transition from subclinical to overt hypothyroidism (8;37). Indeed, women with thyroid antibodies are at risk of becoming hypothyroid during pregnancy with its increased demand for thyroid hormones (34). In a recent study by Pop et al. it has been shown that children born to women with maternal serum fT4 levels below the 10th percentile at 12 weeks gestation (irrespective of elevation of TSH and/or presence of TPO antibodies), had significantly lower neurodevelopmental scores compared to children of mothers with higher fT4 values. It is important to note that women with low fT4 levels at 12 weeks gestation were largely affected by autoimmune thyroiditis. However, there was no correlation between neurodevelopmental scores of the infants and maternal fT4 at 32 weeks gestation which is a puzzling finding in view of the expected deterioration in thyroid function during pregnancy in women with autoimmune thyroiditis (7;34). Whatever the explanation for this unexpected finding the fact remains that after appropriate statistical analysis fT4 levels below the 10th percentile at 12 weeks gestation represented a significant risk factor for impaired psychomotor development. Haddow et al. have extended the findings of Pop et al. by (6). These investigators provided evidence that children born to mothers with hypothyroidism during the second trimester of pregnancy, as determined by an elevated TSH, have lower IQ-scores and more educational difficulties at age 7-9 than children born to mothers with normal TSH levels during pregnancy. In their study 25,216 serum samples were prospectively collected and 47 women with TSH-levels at or above the 99th percentile of the values for all pregnant women were identified. Additionally 15 women with TSH values between the 98th and 99.6th percentiles, and low thyroxine levels were also included, as were 124 matched controls. The children of the 62 women with elevated TSH levels during pregnancy performed less well on all 15 neuropsychological tests carried out (in 2 of these the difference was significant), and children had more school difficulties and learning problems (p=0.06). In this study 77% of the women with hypothyroidism had high titres of TPO antibodies (6). These data further underline the notion that chronic autoimmune thyroiditis is the most frequent cause of low normal fT4 levels and raised TSH levels in these women. Taken together, the studies by Pop et al. and Haddow et al. provide evidence that not only overt but also relatively mild and hitherto unrecognised states of thyroid failure are associated with persistent and significant impairment in neuropsychological performance of the offspring. Concluding remarks and consequences for clinical practice Thyroid autoimmunity with its impaired thyroid reserve has important consequences on pregnancy outcome (table 1). Table: key messages Thyroid autoimmunity and recurrent pregnancy loss --> consider treatment with L-thyroxine Thyroid autoimmune dysfunction during pregnancy --> hypothyroidism should be treated with full replacement dose immediately --> hyperthyroidism should be treated according to fT4 levels Thyroid autoimmunity and offspring --> check for overt hypothyroidism and act accordingly. No data are available on the effects of LT4 in cases of mild/subclinical thyroid failure. Thyroid autoimmunity and pregnancy loss: As there are now data to suggest that recurrent miscarriage in women with thyroid antibodies can be prevented by thyroxine administration (27), we are of the opinion that in women with recurrent miscarriage and thyroid antibodies treatment with L-thyroxine should be considered, though further controlled studies are essential. Autoimmune thyroid dysfunction and obstetrical complications: As the risk to mother and child seems to be correlated with the severity of the thyroid dysfunction it is clear that - depending on the fT4 level at presentation - treatment should be instituted immediately. Thus, when a woman is diagnosed with hypothyroidism during pregnancy full replacement with thyroxine (1.6µg/kg ideal body weight) should be started immediately. In view of the expected increase in thyroxine requirement during gestation regular clinical and laboratory follow-up is essential, with periodic determinations of TSH and free T4 concentrations (30). Women diagnosed with hyperthyroidism during pregnancy should be treated with antithyroid drugs exclusively, aiming at a fT4 at - or slightly above - the upper limit of normal (33) Thyroid autoimmunity and offspring: In a recent publication Morreale de Escobar et al. have summarized and discussed epidemiological and experimental evidence and - convincingly - argued that conditions resulting in first trimester hypothyroxinaemia (defined as a low for gestational age circulating maternal free T4, whether or not TSH is increased) pose an increased risk for poor neuropsychological development of the fetus (38). It is at present unknown if thyroxine replacement therapy will effectively prevent detrimental effects on the offspring in these cases. Clearly, double blind randomised trails are needed to clarify this issue (39).

Reference List (1) Gleicher N. Autoantibodies and pregnancy loss. Lancet 1994; 343(8900):747-748. (2) Mandel SJ, Cooper DS. The use of antithyroid drugs in pregnancy and lactation. J Clin Endocrinol Metab 2001; 86(6):2354-2359. (3) Millar LK, Wing DA, Leung AS, Koonings PP, Montoro MN, Mestman JH. Low birth weight and preeclampsia in pregnancies complicated by hyperthyroidism. Obstet Gynecol 1994; 84(6):946-949. (4) Davis LE, Leveno KJ, Cunningham FG. Hypothyroidism complicating pregnancy. Obstet Gynecol 1988; 72(1):108-112. (5) Leung AS, Millar LK, Koonings PP, Montoro M, Mestman JH. Perinatal outcome in hypothyroid pregnancies. Obstet Gynecol 1993; 81(3):349-353. (6) Haddow JE, Palomaki GE, Allan WC, Williams JR, Knight GJ, Gagnon J et al. Maternal thyroid deficiency during pregnancy and subsequent neuropsychological development of the child. N Engl J Med 1999; 341(8):549-555. (7) Pop VJ, Kuijpens JL, van Baar AL, Verkerk G, van Son MM, de Vijlder JJ et al. Low maternal free thyroxine concentrations during early pregnancy are associated with impaired psychomotor development in infancy. Clin Endocrinol (Oxf) 1999; 50(2):149-155. (8) Vanderpump MP, Tunbridge WM, French JM, Appleton D, Bates D, Clark F et al. The incidence of thyroid disorders in the community: a twenty- year follow-up of the Whickham Survey. Clin Endocrinol (Oxf) 1995; 43(1):55-68. (9) Muller AF, Drexhage HA, Berghout A. Postpartum thyroiditis and autoimmune thyroiditis in women of childbearing age: recent insights and consequences for antenatal and postnatal care. Endocr Rev 2001; 22(5):605- 630. (10) Wilcox AJ, Weinberg CR, O'Connor JF, Baird DD, Schlatterer JP, Canfield RE et al. Incidence of early loss of pregnancy. N Engl J Med 1988; 319(4):189-194. (11) Gleicher N, Pratt D, Dudkiewicz A. What do we really know about autoantibody abnormalities and reproductive infertility? A critical review. Contracept Fertil Sex 1995; 23(4):239-254. (12) Formby B. Immunologic response in pregnancy. Its role in endocrine disorders of pregnancy and influence on the course of maternal autoimmune diseases. Endocrinol Metab Clin North Am 1995; 24(1):187-205. (13) Wegmann TG, Lin H, Guilbert L, Mosmann TR. Bidirectional cytokine interactions in the maternal-fetal relationship: is successful pregnancy a TH2 phenomenon?. Immunol Today 1993; 14(7):353-356. (14) Szekeres-Bartho J, Par G, Szereday L, Smart CY, Achatz I. Progesterone and non-specific immunologic mechanisms in pregnancy. Am J Reprod Immunol 1997; 38(3):176-182. (15) Stagnaro-Green A, Roman SH, Cobin RH, el Harazy E, Alvarez- Marfany M, Davies TF. Detection of at-risk pregnancy by means of highly sensitive assays for thyroid autoantibodies. JAMA 1990; 264(11):1422-1425. (16) Glinoer D, Soto MF, Bourdoux P, Lejeune B, Delange F, Lemone M et al. Pregnancy in patients with mild thyroid abnormalities: maternal and neonatal repercussions. J Clin Endocrinol Metab 1991; 73(2):421-427. (17) Muller AF, Verhoeff A, Mantel MJ, Berghout A. Thyroid autoimmunity and abortion: a prospective study in women undergoing in vitro fertilization. Fertil Steril 1999; 71(1):30-34. (18) Glinoer D. Thyroid autoimmunity and spontaneous abortion [letter]. Fertil Steril 1999; 72(2):373-374. (19) Cowchock S, Smith JB, Gocial B. Antibodies to phospholipids and nuclear antigens in patients with repeated abortions. Am J Obstet Gynecol 1986; 155(5):1002-1010. (20) Roberts J, Jenkins C, Wilson R, Pearson C, Franklin IA, MacLean MA et al. Recurrent miscarriage is associated with increased numbers of CD5/20 positive lymphocytes and an increased incidence of thyroid antibodies. Eur J Endocrinol 1996; 134(1):84-86. (21) Pratt DE, Kaberlein G, Dudkiewicz A, Karande V, Gleicher N. The association of antithyroid antibodies in euthyroid nonpregnant women with recurrent first trimester abortions in the next pregnancy. Fertil Steril 1993; 60(6):1001-1005. (22) Kutteh WH, Yetman DL, Carr AC, Beck LA, Scott RT, Jr. Increased prevalence of antithyroid antibodies identified in women with recurrent pregnancy loss but not in women undergoing assisted reproduction. Fertil Steril 1999; 71(5):843-848. (23) Mecacci F, Parretti E, Cioni R, Lucchetti R, Magrini A, La Torre P et al. Thyroid autoimmunity and its association with non-organ-specific antibodies and subclinical alterations of thyroid function in women with a history of pregnancy loss or preeclampsia. J Reprod Immunol 2000; 46(1):39-50. (24) Bussen SS, Steck T. Thyroid antibodies and their relation to antithrombin antibodies, anticardiolipin antibodies and lupus anticoagulant in women with recurrent spontaneous abortions (antithyroid, anticardiolipin and antithrombin autoantibodies and lupus anticoagulant in habitual aborters). Eur J Obstet Gynecol Reprod Biol 1997; 74(2):139-143. (25) Esplin MS, Branch DW, Silver R, Stagnaro-Green A. Thyroid autoantibodies are not associated with recurrent pregnancy loss. Am J Obstet Gynecol 1998; 179(6):1583-1586. (26) Rushworth FH, Backos M, Rai R, Chilcott IT, Baxter N, Regan L. Prospective pregnancy outcome in untreated recurrent miscarriers with thyroid autoantibodies. Hum Reprod 2000; 15(7):1637-1639. (27) Vaquero E, Lazzarin N, De Carolis C, Valensise H, Moretti C, Ramanini C. Mild thyroid abnormalities and recurrent spontaneous abortion: diagnostic and therapeutical approach. Am J Reprod Immunol 2000; 43(4):204-208. (28) Glinoer D. Thyroid immunity, thyroid dysfunction, and the risk of miscarriage: a propos article by Vaquero et al. Mild thyroid abnormalities and recurrent spontaneous abortion: diagnostic and therapeutical approach. Am J Reprod Immunol 2000; 43(4):202-203. (29) Glinoer D, Riahi M, Grun JP, Kinthaert J. Risk of subclinical hypothyroidism in pregnant women with asymptomatic autoimmune thyroid disorders. J Clin Endocrinol Metab 1994; 79(1):197-204. (30) Glinoer D. Potential repercussions for the progeny of maternal hypothyroxinemia during pregnancy. Thyroid 2000; 10(1):59-62. (31) Klein RZ, Haddow JE, Faix JD, Brown RS, Hermos RJ, Pulkkinen A et al. Prevalence of thyroid deficiency in pregnant women. Clin Endocrinol (Oxf) 1991; 35(1):41-46. (32) Davis LE, Lucas MJ, Hankins GD, Roark ML, Cunningham FG. Thyrotoxicosis complicating pregnancy. Am J Obstet Gynecol 1989; 160(1):63-70. (33) Glinoer D. The regulation of thyroid function in pregnancy: pathways of endocrine adaptation from physiology to pathology. Endocr Rev 1997; 18(3):404-433. (34) Glinoer D, Delange F. The potential repercussions of maternal, fetal, and neonatal hypothyroxinemia on the progeny. Thyroid 2000; 10(10):871-887. (35) Mestman JH, Goodwin TM, Montoro MM. Thyroid disorders of pregnancy. Endocrinol Metab Clin North Am 1995; 24(1):41-71. (36) Brent GA. Maternal hypothyroidism: recognition and management. Thyroid 1999; 9(7):661-665. (37) Geul KW, van Sluisveld IL, Grobbee DE, Docter R, de Bruyn AM, Hooykaas H et al. The importance of thyroid microsomal antibodies in the development of elevated serum TSH in middle-aged women: associations with serum lipids. Clin Endocrinol (Oxf) 1993; 39(3):275-280. (38) Morreale dE, Obregon MJ, Escobar dR. Is neuropsychological development related to maternal hypothyroidism or to maternal hypothyroxinemia?. J Clin Endocrinol Metab 2000; 85(11):3975-3987. (39) Smallridge RC, Ladenson PW. Hypothyroidism in pregnancy: consequences to neonatal health. J Clin Endocrinol Metab 2001; 86(6):2349- 2353.

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THYROID AUTOIMMUNITY AND PREGNANCY OUTCOME

Hypothyroidism In-Depth Report Background The thyroid is a small, butterfly-shaped gland located in the front of the neck that produces hormones, notably thyroxine (T4) and triiodothyronine (T3), which stimulate vital processes in every part of the body. These thyroid hormones have a major impact on the following functions:  Growth  Use of energy and oxygen  Heat production  Fertility  The use of vitamins, proteins, carbohydrates, fats, electrolytes, and water  Immune regulation in the intestine These hormones can also alter the actions of other hormones and drugs.

The thyroid gland, a part of the endocrine (hormone) system, plays a major role in regulating the body's metabolism. Iodide and Thyroid Hormone Production Regulating thyroid function is a complex and important process that involves several factors, including iodide and four thyroid hormones. Any abnormality in this intricate system of hormone synthesis and production can have far-reaching consequences on health. Iodide. An understanding of the multi-step thyroid hormone process begins with iodide, a salt that is extracted from the blood and trapped by the thyroid gland. Iodide is converted to iodine in the thyroid gland. (Eighty percent of the body's iodine supply is stored here.) Iodine is the material used to make the hormone thyroxine (T4). Thyroid Hormones. Four hormones are critical in the regulation of thyroid function:  Thyroxine (T4) and Triiodothyronine (T3). Thyroxine (T4) is the key hormone produced in the thyroid gland. Low levels of T4 produce hypothyroidism, and high levels produce hyperthyroidism. Thyroxine converts to triiodothyronine (T3), which is a more biologically active hormone. Only about 20% of triiodothyronine is actually formed in the thyroid gland. The rest is manufactured from circulating thyroxine in tissues outside the thyroid, such as those in the liver and kidney. Once T4 and T3 are in circulation, they typically bind to substances called thyroid hormone transport proteins, after which they become inactive.  Thyrotropin. Thyrotropin (also called thyroid-stimulating hormone or TSH) is another very important hormone in the process. Secreted by the pituitary gland, this hormone directly influences the process of iodine trapping and thyroid hormone production. When thyroxine levels drop even slightly, the pituitary gland goes into action to pump up secretion of thyrotropin so that it can stimulate thyroxine production. So, when T4 levels fall, TSH levels increase.  Thyrotropin-releasing hormone (TRH), the final critical thyroid hormone, is produced in a region in the brain called the hypothalamus, which monitors thyrotropin levels. Hypothyroidism Hypothyroidism occurs when thyroxine (T4) levels drop so low that body processes begin to slow down. Hypothyroidism was first diagnosed in the late nineteenth century when doctors observed that surgical removal of the thyroid resulted in the swelling of the hands, face, feet, and tissues around the eyes. They named this syndrome myxedema and correctly concluded that it was the outcome of the absence of substances, thyroid hormones, normally produced by the thyroid gland. Hypothyroidism is usually progressive and irreversible. Treatment, however, is nearly always completely successful and allows a patient to live a fully normal life. Hypothyroidism is separated into either overt or subclinical disease. That diagnosis is determined on the basis of the TSH laboratory blood tests. The normal range of TSH concentration falls between 0.45 - 4.5 mU/L.  Patients with mildly underactive (subclinical) thyroid have TSH levels of 4.5 - 10mU/L.  Patients with levels greater than 10mU/L are considered to have overt hypothyroidism and should be treated with medication. Subclinical, or mild, hypothyroidism (mildly underactive thyroid), also called early-stage hypothyroidism, is a condition in which thyrotropin (TSH) levels have started to increase in response to an early decline in T4 levels in the thyroid. However, blood tests for T4 are still normal. The patient may have mild symptoms (usually slight fatigue) or none at all. Mildly underactive thyroid is very common (affecting about 10 million Americans) and is a topic of considerable debate among professionals because it is not clear how to manage this condition. Mildly underactive thyroid does not progress to the full-blown disorder in most people. Each year, about 2 - 5% of people with subclinical thyroid go on to develop overt hypothyroidism. Other factors associated with a higher risk of developing clinical hypothyroidism include being an older woman (up to 20% of women over age 60 have subclinical hypothyroidism), having a goiter (enlarged thyroid gland) or thyroid antibodies, or harboring immune factors that suggest an autoimmune condition. Causes Many permanent or temporary conditions can reduce thyroid hormone secretion and cause hypothyroidism. About 95% of hypothyroidism cases occur from problems that start in the thyroid gland. In such cases, the disorder is called primary hypothyroidism. (Secondary hypothyroidism is caused by disorders of the pituitary gland. Tertiary hypothyroidism is caused by disorders of the hypothalamus.) The two most common causes of primary hypothyroidism are:  Hashimoto's thyroiditis. This is an autoimmune condition in which the body's immune system attacks its own cells.  Overtreatment of hyperthyroidism (an overactive thyroid). Autoimmune Diseases of the Thyroid Hashimoto's thyroiditis, atrophic thyroiditis, and postpartum thyroiditis are all autoimmune diseases of the thyroid. An autoimmune disease occurs when the immune system mistakenly attacks the body's own healthy cells. In the case of autoimmune thyroiditis, a common form of primary hypothyroid disease, the cells under attack are in the thyroid gland. All forms of thyroid autoimmunity typically start with T and B cells:  Important immune factors called T and B cells infiltrate the thyroid gland in equal numbers. These white blood cells are the primary infection-fighting immune cells. T cells identify invasive molecules, such as viral proteins, and help B cells to produce antibodies that are designed specifically to attack these invaders.  In cases of autoimmunity, T cells are tricked into classifying molecules on the body's own cells as invaders. In such cases, B cells then produce antibodies, called autoantibodies, which attack those cells.  In most cases of thyroid autoimmunity, the autoantibodies launch an attack on a thyroid protein called thyroid peroxidase; this attack appears to destroy thyroid cells. Hashimoto's Thyroiditis. The most common form of hypothyroidism in the U.S. is Hashimoto's thyroiditis, a genetic disease named after the Japanese doctor who first described thyroid inflammation. It occurs in about 0.3 - 5 people per 1,000 per year, and women are 15 - 20 times more likely than men to develop this disease. An enlargement of the thyroid gland, called a goiter, is almost always present and may appear as a cyst-like or fibrous growth in the neck. Hashimoto's thyroiditis is permanent and requires lifelong treatment. Both genetic and environmental factors appear to play a role in its development. One theory proposes that Hashimoto's thyroiditis and Graves' disease (a form of hyperthyroidism) are caused by a similar immunologic dysfunction. Similar immune system substances called antibodies are present in both diseases, and some researchers believe that the predominance of one or another antibody determines which of the diseases become manifest. The two diseases, then, are essentially two sides of a single coin. Atrophic Thyroiditis. Atrophic thyroiditis is similar to Hashimoto's thyroiditis, except a goiter is not present. Riedel's Thyroiditis. Riedel's thyroiditis is a rare autoimmune disorder, in which scar tissue progresses in the thyroid until it produces a hard stony mass that suggests cancer. Hypothyroidism develops as the scar tissue replaces healthy tissue. Surgery is usually required, although early stages may be treated with corticosteroids or other immunosuppressive drugs. Autoimmune Thyroiditis Due to Pregnancy. Hypothyroidism may also occur in women who develop antibodies to their own thyroid during pregnancy, causing an inflammation of the thyroid after delivery. Subacute Thyroiditis Subacute thyroiditis is a temporary condition that passes through three phases: hyperthyroidism, hypothyroidism, and a return to normal thyroid levels. Patients may have symptoms of both hyperthyroidism and hypothyroidism (such as rapid heartbeat, nervousness, and weight loss), and they can feel extremely sick. Symptoms last about 6 - 8 weeks and then resolve in most patients, although each form carries some risk for becoming chronic. Subacute thyroiditis appears to be responsible for about 10% of all cases of hypothyroidism. The three forms of subacute thyroiditis follow a similar course: Painless Postpartum Subacute Thyroiditis. Postpartum thyroiditis is an autoimmune condition that occurs in up to 10% of pregnant women and tends to develop between 4 - 12 months after delivery. In most cases, a woman develops a small, painless goiter. It is generally self-limiting and requires no therapy unless the hypothyroid phase is prolonged. If so, therapy may be thyroxine replacement for a few months. A doctor will prescribe beta- blockers if the hyperthyroid phase needs treatment. Some evidence suggests that half of women with this condition develop permanent hypothyroidism within 7 years. Women who have had recurrent episodes after previous pregnancies and women who have other autoimmune disorders are at higher risk for this form of subacute thyroiditis. Painless Sporadic, or Silent, Thyroiditis. This painless condition is very similar to postpartum thyroiditis except it can occur in both men and women and at any age. About 20% of patients with silent thyroiditis may develop chronic hypothyroidism. Treatment considerations are the same as for postpartum subacute thyroiditis. Painful, or Granulomatous, Thyroiditis. This condition comes on suddenly with flu-like symptoms and severe neck pain and swelling. It generally occurs in the summer and is five times more common in women. It recurs in about 2% of patients. Hypothyroidism persists in about 5%. Treatments typically include pain relievers and, in severe cases, corticosteroids. Post-Treatment of Hyperthyroidism Up to half or more of patients who receive radioactive iodine treatments for an overactive thyroid develop permanent hypothyroidism within a year of therapy. This is the standard treatment for Graves' disease, which is the most common form of hyperthyroidism, a condition caused by excessive secretion of thyroid hormones. By the end of 5 years, about 65% of treated patients have developed hypothyroidism, after which the rate of this condition levels off to about 1% a year. Such patients need to take thyroid hormones for the rest of their lives. Other forms of treatment for overactive thyroid glands using either antithyroid drugs or surgery may also result in hypothyroidism. Iodide Abnormalities Too much or too little iodide can cause hypothyroidism. If there is a deficiency of iodide, the body cannot manufacture thyroxine. About 200 million people around the world have hypothyroidism because of insufficient iodine in their diets. Too much iodide is a signal to inhibit the conversion process of thyroxine to T3. The end result in both cases is inadequate production of thyroid hormones. Some evidence suggests that excess iodine triggers the process leading to Hashimoto's thyroiditis. Thyroid Surgery Patients who have complete removal (total thyroidectomy) of the thyroid to treat thyroid cancer need lifetime treatment with thyroid hormone. Removing one of the two lobes of the thyroid gland (hemithyroidectomy), usually because of benign growths on the thyroid gland, rarely produces hypothyroidism. The remaining thyroid lobe will generally grow so that it can produce sufficient amounts of thyroid hormone for normal function. Many doctors recommend thyroid hormone treatment, however, to prevent the formation of additional nodules. Patients with Graves' disease who have surgery to remove most of both thyroid lobes (subtotal thyroidectomy) may develop hypothyroidism. It is important to find an experienced surgeon for this procedure and to have the thyroid checked at 6- or 12-month intervals. Thyroid Dysfunction Syndromes Researchers have identified several additional syndromes that also cause hypothyroidism. These generally involve abnormalities in thyroid hormone itself or genetic deficiencies in certain proteins that impair thyroid hormone conversion processes or responses. Drugs and Medical Treatments that Reduce Thyroid Levels Lithium. Lithium, a drug widely used to treat psychiatric disorders, has multiple effects on thyroid hormone synthesis and secretion. Up to 50% of patients who take lithium develop a goiter, with 20% developing symptomatic hypothyroidism, and another 20 - 30% developing hypothyroidism without symptoms. Amiodarone. The drug amiodarone (Cordarone), which is used to treat abnormal heart rhythms, contains high levels of iodine and can induce hyper- or hypothyroidism, particularly in patients with existing thyroid problems. Hypothyroidism occurs in 20% of patients and is the more common effect in the U.S. and other countries where dietary iodine is abundant. Hyperthyroidism is a less common effect in these regions. Other Drugs. Drugs used for treating epilepsy, such as phenytoin and carbamazepine, can reduce thyroid levels. Certain antidepressants may cause hypothyroidism, although this is rare. Interferons and interleukins are used for treating hepatitis, multiple sclerosis, and other conditions. Evidence suggests that these drugs increase antibodies that put patients at risk for hypo- or hyperthyroidism. Some drugs used in cancer chemotherapy, such as sunitinib (Sunent) or imatinib (Gleevec), can also cause or worsen hypothyroidism. Radiation Therapy. High-dose radiation for cancers of the head or neck and for Hodgkin's disease can also cause hypothyroidism in up to 65% of patients within 10 years after treatment. Other Medical Conditions A number of medical conditions can involve the thyroid and change the normal gland tissue so that it no longer produces enough thyroid hormone. Examples include hemochromatosis, scleroderma, and amyloidosis. Causes of Secondary and Tertiary Hypothyroidism In rare instances, usually due to a tumor, the pituitary gland will fail to produce thyrotropin (TSH), the hormone that stimulates the thyroid to produce its hormones. In such cases, the thyroid gland withers. When this happens, secondary hypothyroidism occurs. Causes of Hypothyroidism in Infants Hypothyroidism in newborns (known as congenital hypothyroidism) occurs in one in every 3,000 - 4,000 births, making it the most common hormonal disorder in infants. In 90% of these cases, it persists throughout life. Permanent Congenital Hypothyroidism. In up to 85% of permanent congenital hypothyroidism cases, the thyroid gland is missing, underdeveloped, or not properly located. In most cases the cause or causes of these conditions are unknown. In about 10 - 15% of cases, processes involved in hormone production are impaired, most likely because of genetic abnormalities. In less than 5% of cases, the pituitary or hypothalamus function abnormally. Temporary Hypothyroidism in Infants. Temporary hypothyroidism can also occur in infants. In about 20% of cases, the cause remains unknown. The known causes stem from various immunologic, environmental, and genetic factors, including those in the mother:  Women who have an underactive (“low”) thyroid, including those who develop the problem during pregnancy, are at increased risk for delivering babies with congenital (newborn) hypothyroidism. Maternal hypothyroidism can also cause premature delivery and low-birth weight.  Some of the drugs used to treat hyperthyroidism (overactive thyroid) block the production of thyroid hormone. These same drugs can also cross the placenta and cause hypothyroidism in the infant.  If a pregnant woman has untreated hyperthyroidism, her newborn infant may be hypothyroid for a short period of time. This is because the excess thyroid hormone in the women's blood crosses the placenta and signals the fetus not to produce as much of its own thyroid hormone.  Iodine deficiency. This may cause temporary hypothyroidism. (Exposure to too much iodine immediately after birth, for example, from iodine-containing disinfectants or medicines, can also cause thyroid dysfunction.)  Premature birth. Temporary hypothyroidism in infants can occur in premature babies.  The central nervous system connections between the hypothalamus and pituitary gland may mature late; this condition generally resolves 4 - 16 weeks after birth. Children with temporary congenital hypothyroidism should be followed-up regularly during adolescence and adulthood for possible thyroid problems. The risk for further thyroid problems is highest in these adult women during pregnancy. Newborn siblings of these children should also be screened for possible thyroid defects. Risk Factors About 15 million Americans have unrecognized thyroid disease, mostly subclinical hypothyroidism (mildly underactive thyroid). Less than 2% of the U.S. population has full- blown hypothyroidism. Women. Women have 10 times the risk of hypothyroidism as men, with the difference being significant after age 34. Because the symptoms of hypothyroidism and menopause are so similar, hypothyroidism may easily be missed. Pregnancy is a major factor in the higher risk in women. It affects the thyroid in a number of ways and poses a high risk for hypothyroidism, both during pregnancy and afterward. For one, iodine requirements are high in both the mother and the fetus. Changes in reproductive hormones also cause changes in thyroid hormone levels. In addition, some women develop antibodies to their own thyroid during pregnancy, causing a condition known as postpartum autoimmune, or subacute, thyroiditis. This occurs in up to 10% of pregnant women and tends to develop 4 - 12 months after delivery. It is a limited condition and nearly always clears up. However, it does pose a risk for the development of permanent hypothyroidism later on. Age. The risk for hypothyroidism is greatest after age 50 and increases with age. However, hypothyroidism can affect people of all ages. Genetic Defects Genetics plays a role in many cases of underactive and overactive thyroid. The genetics involved with hypothyroidism are complicated, however. Certain genetic features, for example, appear to play a role in Hashimoto's thyroiditis and postpartum thyroiditis in Caucasians, but others affect different ethnic groups. Thyroid disease will often skip generations. For example, someone with an underactive thyroid may have healthy parents but have grandparents who had thyroid troubles. Some people inherit a tendency for thyroid problems but never become ill, while others become very sick. Smoking Smoking significantly increases risk for thyroid disease, particularly autoimmune Hashimoto's thyroiditis and postpartum thyroiditis. Smoking also increases the negative effects of hypothyroidism, notably on the arteries and heart. Medical Conditions Associated with Hypothyroidism People with certain medical conditions have a higher risk for hypothyroidism. These conditions include:  Autoimmune diseases. People with many autoimmune diseases have a higher risk for hypothyroidism. Type 1 (insulin-dependent) diabetes poses a higher risk and is a special problem since hypothyroidism can affect insulin requirements. Women with other autoimmune diseases, including systemic lupus erythematosus, pernicious anemia, and rheumatoid arthritis, are also at higher risk for hypothyroidism. Pregnant women with autoimmune conditions have a 25% risk for hypothyroidism during gestation.  Gout. Hypothyroidism and gout often coexist and may have biologic mechanisms in common.  Addison's disease.  Myasthenia gravis.  Polycystic ovarian syndrome.  Anorexia or bulimia. People with eating disorders are at risk for hypothyroidism. In these patients, however, reduced thyroid function may be an adaptation to malnutrition and, therefore, some experts think that only the eating disorder should be treated, not hypothyroidism.  Turner syndrome. As many as half of patients with Turner syndrome have hypothyroidism, usually in the form of Hashimoto's thyroiditis. This inherited condition is one of the most common genetic diseases in women. Many drugs affect the thyroid, so anyone being treated for a chronic disease, taking thyroid medication, and those at risk for a thyroid disorder should discuss the impact these drugs may have on their thyroid. Symptoms Early Symptoms. Early symptoms of hypothyroidism are subtle and, in older people, can be easily mistaken for symptoms of stress or aging. They include:  Chronic fatigue  Difficulty concentrating  Sensitivity to cold  Headache  Muscle and joint aches  Weight gain, despite diminished appetite  Constipation  Dry skin  Early puberty  Menstrual irregularities (either heavier-than-normal or lighter-than-normal bleeding)  Milky discharge from the breasts (galactorrhea) Later Symptoms. As free thyroxine levels fall over the following months, other symptoms may develop:  Impaired mental activity, including problems with concentration and memory, particularly in the elderly.  Depression. Some doctors believe that even mild thyroid failure may increase susceptibility to major depression.  Muscle weakness, numbness, pain, and cramps. This can cause an unsteady gait. Muscle cramps are common, and carpal tunnel syndrome or symptoms similar to arthritis sometimes develop. In some cases, the arms and legs may feel numb.  Numbness in the fingers.  Hearing loss.  Husky voice.  Continuing weight gain and possible obesity, in spite of low appetite.  Some people experience less sweating, and their skin becomes pale.  Skin and hair changes. Skin becomes pale, rough, and dry. Patients may sweat less. Hair coarsens and even falls out. Nails become brittle.  Snoring and obstructive sleep apnea (a condition in which in the soft palate in the throat collapses at intervals during sleep, thereby blocking the passage of air). Symptoms in Infants and Children All babies are now screened for hypothyroidism in order to prevent retardation that can occur if treatment is delayed. Symptoms of hypothyroidism in children vary depending on when the problem first develops.  Most children who are born with a defect that causes congenital hypothyroidism have no obvious symptoms. Symptoms that do appear in newborns may include jaundice (yellowish skin), noisy breathing, and an enlarged tongue.  Early symptoms of undetected and untreated hypothyroidism in infants include feeding problems, failure to thrive, constipation, hoarseness, and sleepiness.  Later on, symptoms in untreated children include protruding abdomens; rough, dry skin; and delayed teething. Rarely, in advanced cases, yellow raised bumps (called xanthomas) may appear under the skin, the result of cholesterol build-up.  If they do not receive proper treatment in time, children with hypothyroidism may be extremely short for their age, have a puffy, bloated appearance, and have below- normal intelligence. Any child whose growth is abnormally slow should be examined for hypothyroidism. Possible Complications All patients with hypothyroidism are at serious risk for physical and mental problems. Emergency Conditions Myxedema Coma. Myxedema coma is a rare, life-threatening complication of untreated hypothyroidism. Symptoms include a severe drop in body temperature (hypothermia), delirium, reduced lung function, slow heart rate, constipation, urine retention, seizures, stupor, fluid build-up, and finally coma. It is uncommon, but may develop in untreated patients subjected to severe stress, such as infection, surgery, or extreme cold. Certain drugs (such as sedatives, painkillers, narcotics, amiodarone, and lithium) may increase the risk. Emergency treatment is required. Mortality rates are high (30 - 60%) with the highest risks in older patients and those with persistent hypothermia or heart problems. Suppurative Thyroiditis. Suppurative thyroiditis is a life-threatening infection of the thyroid gland. It is very rare, since the thyroid is normally resistant to infection. People with pre- existing thyroid diseases, such as Hashimoto's thyroiditis, however, may be at higher than average risk for suppurative thyroiditis. It often begins with an upper respiratory infection. Symptoms include fever, neck pain, rash, and trouble swallowing and speaking. Immediate treatment is critical. Effects of Hypothyroidism and Subclinical Hypothyroidism on the Heart Thyroid hormones, notably triiodothyronine (T3), affect the heart directly and indirectly. They are closely linked with heart rate and heart output. T3 provides particular benefits by relaxing the smooth muscles of blood vessels. This helps keep the blood vessels open so that blood flows smoothly through them. Hypothyroidism is associated with:  Unhealthy cholesterol levels . Hypothyroidism raises levels of total cholesterol, LDL (the so-called bad cholesterol), triglycerides, and other lipids (fat molecules) associated with heart disease. Treating the thyroid condition with thyroid replacement therapy can significantly reduce these levels.  Mild high blood pressure . Hypothyroidism may slow the heart rate to less than 60 beats per minute, reduce the heart's pumping capacity, and increase the stiffness of blood vessel walls. All of these effects may lead to high blood pressure. Indeed, patients with hypothyroidism have triple the risk of developing hypertension. All patients with chronic hypothyroidism, especially pregnant women, should have their blood pressure checked regularly.  Heart failure . Hypothyroidism can affect the heart muscle’s contraction and increase the risk of heart failure in people with heart disease. The evidence for subclinical hypothyroidism and heart disease is mixed. Some studies suggest that subclinical hypothyroidism increases the risks for coronary artery disease and heart failure. The only randomized controlled trial dealing with subclinical hypothyroidism and heart disease evaluated only the thickness of atherosclerosis in the blood vessels and not whether patients actually had clinical heart disease. Many doctors believe that treatment of subclinical hypothyroidism will not help prevent or improve heart problems. More research is underway. Effects of Hypothyroidism and Subclinical Hypothyroidism on the Mind Depression. Depression is common in hypothyroidism and can be severe. Hypothyroidism should be considered as a possible cause of any chronic depression, particularly in older women. Mental and Behavioral Impairment. Untreated hypothyroidism can, over time, cause mental and behavioral impairment and, eventually, even dementia. Whether treatment can completely reverse problems in memory and concentration is uncertain, although many doctors believe that only mental impairment in hypothyroidism that occurs at birth is permanent. Other Health Effects of Hypothyroidism The following medical conditions have been associated with hypothyroidism. Often the causal relationship is not clear in such cases:  Iron deficiency anemia.  Respiratory problems.  Kidney function.  Glaucoma. (Some research has associated hypothyroidism with an increased risk for glaucoma.)  Headache. (Hypothyroidism may worsen headaches in people predisposed to them.)  Thyroid lymphoma. (Patients with Hashimoto's thyroiditis are at higher risk for this rare form of cancer.)  Joint stiffness. (Women with hypothyroidism may actually have fewer problems with joint stiffness than women with normal thyroid.) Effects of Hypothyroidism on Infertility and Pregnancy In premenopausal women, early symptoms of hypothyroidism can interfere with fertility. A history of miscarriage may be a sign of impending hypothyroidism. (A pregnant woman with hypothyroidism has a fourfold risk for miscarriage.) Studies suggest that even if thyroid levels are normal, women who have a history of miscarriages often have antithyroid antibodies during early pregnancy and are at risk for developing autoimmune thyroiditis over time. Most women with overt hypothyroidism have menstrual cycle abnormalities and often fail to ovulate. Overt hypothyroidism in a pregnant woman can affect normal fetal development. Women who have hypothyroidism near the time of delivery are in danger of developing high blood pressure and premature delivery. They are also prone to postpartum thyroiditis, which may be a contributor to postpartum depression. Effects of Hypothyroidism on Infants and Children Children of Untreated Mothers. Children born to untreated pregnant women with hypothyroidism are at risk for impaired mental performance, including attention problems and verbal impairment. Studies of children of women with subclinical hypothyroidism are less clear, with some reporting lower IQs in such children and others reporting no significant problems. Effects of Hypothyroidism During Infancy. Transient hypothyroidism is common among premature infants. Although temporary, severe cases can cause difficulties in neurologic and mental development. Infants born with permanent congenital (inborn) hypothyroidism need to receive treatment as soon as possible after birth to prevent mental retardation, stunted growth, and other aspects of abnormal development (a syndrome referred to as cretinism). Untreated infants can lose up to three to five IQ points per month during the first year. An early start of lifelong treatment avoids or minimizes this damage. Even with early treatment, however, mild problems in memory, attention, and mental processing may persist into adolescence and adulthood. Effects of Childhood-Onset Hypothyroidism. If hypothyroidism develops in children older than 2 years, mental retardation is not a danger, but physical growth may be slowed and new teeth delayed. If treatment is delayed, adult growth could be affected. Even with treatment, some children with severe hypothyroidism may have attention problems and hyperactivity. Effects of Hypothyroidism and Childhood X-Ray Treatments Two million Americans, mostly children, received x-ray treatments to the head or neck between 1920 - 1960 for acne, enlarged thymus gland, recurrent tonsillitis, or chronic ear infections. The risk of developing thyroid nodules and thyroid cancers is increased in these individuals, especially if they have hypothyroidism. Cancer can develop as late as 40 years after the original treatment. Everyone who has had head and neck radiation should have their thyroid glands examined regularly. Diagnosis Doctors diagnose hypothyroidism after completing a history and physical exam of the patient and performing sensitive laboratory tests on the patient's blood. Because symptoms of hypothyroidism can mimic those of many other conditions, blood tests for measuring levels of thyroid stimulating hormone (TSH) and free thyroxine (T4) are the only definitive way to diagnose hypothyroidism. However, the results of these blood tests can be affected by illnesses that are not thyroid related. Physical Examination The doctor will check the heart, eyes, hair, skin, and reflexes for signs of hypothyroidism. Goiter. The presence of a goiter (an enlarged thyroid), especially a rubbery, painless one, may be an indication of Hashimoto's disease. If the thyroid is tender and enlarged but not necessarily symmetrical, the doctor may suspect subacute thyroiditis. A diffusely enlarged gland may occur in hereditary hypothyroidism, in postpartum patients, or from use of iodides or lithium. Goiters may also develop in people with iodide deficiency. Thyroid Hormone and Antibody Tests In diagnosing hypothyroidism, blood tests measuring hormone levels are needed to make a correct diagnosis. In some cases, antibody tests are also helpful. Thyroxine (T4). Hypothyroidism is a condition marked by low thyroxine (T4) hormone levels, and a test can measure levels of this hormone in the blood. However, this test is usually inadequate for the following reasons:  T4 levels can be normal early in the disease process leading to hypothyroidism. If hypothyroidism is suspected, other tests are needed.  T4 levels can be low in patients who do not have hypothyroidism. For instance, thyroxine can be extremely variable in very elderly or seriously ill patients and during pregnancy. Measuring thyroxine is usually performed using a process called a T3 resin uptake to correct for the presence of medications (such as birth control pills, aspirin, and others) that could distort the results. Other tests are needed to confirm a diagnosis of hypothyroidism. Thyrotropin (Thyroid-Stimulating Hormone or TSH). Measuring TSH is the most sensitive indicator of hypothyroidism. (As with thyroxine levels, however, TSH levels can vary in pregnant women and patients who are ill with other conditions.) In general, results indicate the following:  TSH levels over 10mU/L. This is a clear indicator of hypothyroidism if T4 levels are low -- and, in most cases, even if they are normal. Patients usually need thyroxine (T4) replacement therapy. They should also be tested for high cholesterol levels and antithyroid antibodies.  Levels between 4.5 - 10 mU/L. Patients with signs and symptoms of hypothyroidism usually need thyroxine replacement therapy. Patients without symptoms have subclinical hypothyroidism and should be rechecked every 6 - 12 months. Antibody tests may also be performed.  TSH levels between 0.45 - 4.5 mU/L. These indicate normal thyroid function. (Abnormally low levels suggest hyperthyroidism, which is overactive thyroid.)  Specific TSH measurement -- even if it is significantly higher than 10 mU/L -- is not associated with the severity of the condition. This can be determined only by measuring thyroxine levels and evaluating the patient's symptoms. Antithyroid Antibodies. If TSH levels suggest hypothyroidism or subclinical hypothyroidism, the doctor may choose to perform a blood test for specific antithyroid antibodies that act against a factor called thyroperoxidase (TPO). Tests can also check for antibodies to thyroglobulin. Results are particularly helpful in deciding how to treat someone with subclinical hypothyroidism. About 10% of the American population and 25% of women over 60 years old carry these antibodies, the majority of these women having no thyroid problems. Only about 0.5% have full-blown hypothyroidism, and 10% have subclinical hypothyroidism. Other Hormone Tests Used for Thyroid Function. Other hormone tests are done if hyperthyroidism is suspected. They include tests for triiodothyronine (T3) and thyroglobulin (also called thyroid binding globulin). Such measurements, however, may also be helpful in detecting sudden temporary increases in thyroid hormone (thyrotoxicosis) that can precede certain forms of autoimmune thyroiditis. Imaging Tests Thyroid Scintigraphy. Thyroid scintigraphy, or scan, can be used to determine which areas of the thyroid are producing normal amounts of hormone. The patient drinks a small amount of radioactive iodine or technetium and waits until the substance has passed through the thyroid. Images of a properly functioning thyroid show uniform levels of absorption throughout the gland. Overactive areas show up white, and underactive areas appear dark. Thyroid scans are more likely to be done to evaluate a goiter (swollen thyroid) or thyroid nodules. They can help identify areas of the gland that may have cancer. Ultrasound. Ultrasound has limited value, but it can visualize the thyroid and specific abnormalities, such as nodules. (It cannot measure the thyroid gland's function, however.) More Advanced Imaging Tests. If laboratory tests suggest that a pituitary or hypothalamus problem is causing hypothyroidism, the doctor will usually order brain imaging procedures using computed tomography (CT) scans or magnetic resonance imaging (MRI). MRIs may also be used for determining the extent of thyroid cancers and of goiters. MRIs are also being used for investigating hypothyroidism in infants and for determining widespread effects of autoimmune thyroiditis (such as Hashimoto's hypothyroidism). Needle Aspiration Biopsy Needle aspiration biopsy is used to obtain thyroid cells for microscopic evaluation. It may be useful to rule out thyroid cancer in patients with thyroid nodules, abnormal findings on a thyroid scan or ultrasound, or those who have a goiter that is large or feels unusual on physical exam. Much like drawing blood, the doctor injects a small needle into the thyroid gland and draws cells from the gland into a syringe. The cells are put onto a slide, stained, and examined under a microscope. Other Blood Tests Cholesterol levels need to be checked. Other blood tests may be performed to detect levels of calcitonin, calcium, prolactin, and thyroglobulin and to check for anemia and liver function, all of which may be affected by hypothyroidism. Screening Recommendations for Hypothyroidism Screening in Older Adults. Some doctors believe that because thyroid problems are so common in the elderly and thyroid hormone tests are so inexpensive, blood tests for thyroid function should be routine. Undiagnosed hypothyroidism in elderly patients can develop into a serious and even life-threatening situation. Hyperthyroidism also poses many health risks. In fact, during the period around menopause, the symptoms of menopause and hypothyroidism are similar and can easily be confused with each other. Professional organizations differ widely on screening recommendations. Most do not recommend widespread screening for healthy adults:  The American College of Physicians recommends that women over 50 years old be screened for thyroid disorders every 5 years. The American Academy of Family Physicians believes that adults do not have to be screened until they are over 60.  The American Thyroid Association, however, recommends that all adults, both men and women, begin their screening at age 35 and every 5 years thereafter. Experts in this organization argue that such early screening is inexpensive and would prevent progression to hypothyroidism, and therefore possibly heart disease, in people with subclinical hypothyroidism.  The U.S. Preventive Task Force recommends against routine screening for thyroid disease in adults. Screening in Pregnant Women. Untreated overt hypothyroidism in a pregnant woman, particularly in the first trimester, may cause premature delivery and birth defects. Birth defects can affect a baby’s intelligence, mental development, and motor skills. Subclinical hypothyroidism also may increase the risk for premature delivery but does not seem to be associated with neurologic or developmental outcomes in children. Current guidelines recommend targeting screening of women before or during pregnancy based on symptoms or history. Factors that suggest screening is indicated include: History of thyroid disease, goiter, type 1 diabetes or other autoimmune illnesses, history of miscarriages, and history of head and neck radiation or surgery. Women with these factors should have their thyroid checked before pregnancy, or within the first weeks of pregnancy, and should be retested during each trimester. Screening in Infants. It is very difficult to diagnose hypothyroidism in newborns by symptoms alone. Fortunately, almost all newborns with hypothyroidism are identified shortly after birth through an effective national screening program using a thyroid blood test. Ruling out Other Disorders Because the symptoms of hypothyroidism are so similar to common conditions, including aging, diagnosis can be difficult. Aging-Related Disorders. Some symptoms of hypothyroidism and aging are very similar. Menopausal symptoms often resemble hypothyroidism. Many other problems related to aging -- such as vitamin deficiencies, Parkinson's and Alzheimer's diseases, and arthritis -- also have characteristics that can mimic hypothyroidism. Depression. A lack of interest in personal relationships, drowsiness, an increase in sleep, slowing of speech, and general apathy are signs of clinical depression as well as hypothyroidism. The two disorders often coexist, particularly in older women, so diagnosing one does not rule out the presence of the other. Diseases of Muscles and Joints. Joint and muscle aches may be the first symptoms of hypothyroidism. Most likely, however, such pain is not caused by hypothyroidism if other thyroid symptoms remain absent. Numerous conditions can cause muscle and joint pain, and if thyroid levels are normal the doctor should look for other causes. Treatment A variety of factors affect the decision of whether to treat a patient for hypothyroidism, which dosage to begin with, and how rapidly treatment should be started or increased:  First, an elevated TSH (thyrotropin) level should be confirmed and thyroxine (T4) level determined. Other thyroid tests may also be helpful.  Measuring cholesterol levels is also important. Doctors should also consider:  Age of the patient  Presence of other medical problems that may benefit from thyroid replacement treatment (such as heart failure or depression)  Presence of other medical problems that thyroid replacement therapy may worsen (such as osteoporosis) Treating Overt Hypothyroidism. Patients with overt hypothyroidism, indicated by clear symptoms and blood tests that show high TSH (generally 10 mU/L and above) and low thyroxine (T4) levels, must have thyroid replacement therapy. Treating Subclinical or Mild Hypothyroidism. Considerable debate exists about whether to treat patients with subclinical hypothyroidism (slightly higher than normal TSH levels, normal thyroxine levels, and no obvious symptoms). Some doctors opt for treatment and others opt for simply monitoring patients. It is not clear if the benefits of treating subclinical hypothyroidism outweigh the risks and potential complications. Doctors who do not advocate treatment argue that thyroid levels can vary widely, and subclinical hypothyroidism may not persist. In such cases, overtreatment leading to hyperthyroidism is a real risk. There is reasonable evidence and consensus to recommend treatment for subclinical hypothyroidism in the presence of other factors, including:  High total or LDL cholesterol levels  Blood tests that show autoantibodies indicating a future risk for Hashimoto's thyroiditis or other forms of other autoimmune hypothyroidism  Blood tests that show TSH levels greater than 10 mU/L  Goiter  Pregnancy  Female infertility associated with subclinical hypothyroidism Treatment is optional in patients with subclinical hypothyroidism who have no obvious symptoms and normal cholesterol levels. Some doctors feel that treating this group of patients will prevent progression to overt hypothyroidism and future heart disease, as well as increase a patient's sense of well-being. However, the evidence to support treatment of this patient group is not nearly as strong. Many doctors recommend against treatment and suggest that these patients should simply have lab tests every 6 - 12 months. Suppressive Thyroid Therapy. Suppressive thyroid therapy involves taking levothyroxine in doses that are high enough to block the production of natural TSH but too low to cause hyperthyroid symptoms. It may be used for patients with large goiters or thyroid cancer. Suppressive thyroid therapy places patients, particularly postmenopausal women, at risk for accelerated osteoporosis, a disease that reduces bone mass and increases risk of fractures. Some researchers suggest, however, that such bone loss is too slight to pose any significant risk for fracture. Furthermore, the cholesterol-lowering benefits of suppressive therapy outweigh this small risk. Bone density loss can be reduced or avoided by taking no higher a dose of thyroxine than necessary to restore normal thyroid function. In any case, doses of T4 must be continuously and carefully tailored in all patients to avoid adverse effects on the heart. Treatment of Special Cases Treating the Elderly and Patients with Heart Disease. Thyroid dysfunction is common in elderly patients, with most having subclinical hypothyroidism. There is no evidence that this condition poses any great harm in this population, and most doctors recommend treating only high-risk patients. Elderly patients, particularly people with heart conditions, usually start with very low doses of thyroid replacement, since thyroid hormone may cause angina or even a heart attack. Patients who have heart disease must take lower-than-average maintenance doses. Doctors do not recommend treatment for subclinical hypothyroidism in most elderly patients with heart disease. Such patients should be closely monitored, however. Treating Newborns and Infants with Hypothyroidism. Babies born with hypothyroidism (congenital hypothyroidism) should be treated with levothyroxine (T4) as soon as possible to prevent complications. Early treatment can help improve IQ and other developmental factors. However, even with early treatment, mild problems in mental functioning may last into adulthood. In general, children born with milder forms of hypothyroidism will fare better than those who have more severe forms. Oral levothyroxine (T4) can usually restore normal thyroid hormone levels within 1 - 2 weeks. It is critical that normal levels are achieved within a 2-week period. If thyroid function is not normalized within 2 weeks, it can pose greater risks for developmental problems. Infants should continue to be monitored closely to be sure that thyroxine levels remain as consistently close to normal as possible. These children need to continue lifelong thyroid hormone treatments. Treatment During Pregnancy and for Postpartum Thyroiditis. Women who have hypothyroidism before becoming pregnant may need to increase their dose of levothyroxine during pregnancy. Women who are first diagnosed with overt hypothyroidism during pregnancy should be treated immediately, with quick acceleration to therapeutic levels. Although not well proven, doctors often recommend treating patients diagnosed with subclinical hypothyroidism while pregnant. There are no risks to the developing baby when the pregnant woman takes appropriate doses of thyroid hormones. The pregnant woman with hypothyroidism should be monitored regularly and doses adjusted as necessary. If postpartum thyroiditis develops after delivery, any thyroid medication should be reduced or temporarily stopped during this period. Treatment of Hypothyroidism and Iodide Deficiency. People who are iodide deficient may be able to be treated for hypothyroidism simply by using iodized salt. In addition to iodized salt, seafood is a good source. Except for plants grown in iodine-rich soil, most other foods do not contain iodine. The current RDA for iodide is 150 micrograms for both men and women, with an upper limit of 1,100 micrograms to avoid thyroid injury. Medications Thyroid Hormone Replacement The goal of thyroid drug therapy is to provide the body with replacement thyroid hormone when the gland is not able to produce enough itself. A synthetic thyroid hormone called levothyroxine is the treatment of choice for hypothyroidism. This drug is a synthetic derivative of T4 (thyroxine), and it normalizes blood levels of TSH, T4, and T3. Brand Names . A number of levothyroxine brands are available. Synthroid is the oldest brand and has been used for over 40 years. In the past, manufacturers of levothyroxine did not need to meet as strict standards as in the production of other drugs. This resulted in thyroid products with varying quality. The FDA has issued stronger requirements that have largely corrected this problem. Generics versus Brand-Name Products. Generic brands are available and are subject to the same FDA guidelines as brand-name products. There is still debate over whether generic thyroid preparations are as effective as brand products. Any change, such as being switched between brand-name and generic or between two different generics, requires additional testing of thyroid hormone levels. Many doctors still prefer to use brand-name products, noting that the cost difference between brand and generic thyroid drugs is not substantial. Regardless of which type is used, once a patient is stable, doctors generally recommend sticking with one type or brand since potency often varies from one drug to the next. Natural Thyroid Hormone. Dried powdered thyroid hormone (such as Armour Thyroid, S-P- T, Thyrar, and Thyroid Strong) is made from animal glands. It was once the most common form of thyroid therapy, but it is no longer generally recommended because potency varies. Some people argue that with stricter FDA regulations, this natural form is better controlled and may even reduce the risk of developing autoimmunity factors. Dried thyroid also contains both T3 and T4 and is favored as a natural treatment by many alternative practitioners. However, studies need to be conducted to evaluate its benefits. T3 and T4 Combinations. Triiodothyronine (T3), the other important thyroid hormone, is not ordinarily prescribed except under special circumstances. Most patients respond well to thyroxine (T4) alone, which is converted in the body into T3. In addition, the use of T3 may cause disturbances in heart rhythms. Some patients treated only with thyroxine continue to have mood and memory problems or other symptoms. Combination products containing T4 and T3, such as liotrix (Thyrolar), are available, but there is some controversy concerning their benefits. Several recent studies have indicated that although some patients may prefer combination therapy, T3 and T4 together do not work better than T4 alone. Patients might like the combined drugs because they cause more weight loss, or a placebo effect may be involved. It does not appear that combination products offer any advantage for normalizing TSH levels. Levothyroxine Regimens Levothyroxine needs to be taken only once a day. It is slowly assimilated by body organs, so it usually takes up to 6 weeks before symptoms improve in adults. Nevertheless, many patients feel better after 2 - 3 weeks of treatment. The speed at which specific symptoms improve varies:  Weight loss, less puffiness, and improved pulse usually occur early in the treatment.  Improvements in anemia and skin, hair, and voice tone may take a few months.  High LDL ("bad cholesterol") levels decline very gradually. HDL ("good cholesterol") levels are not affected by treatment.  Goiter size declines very slowly, and some patients may need high-dose thyroid hormone (called suppressive thyroid therapy) for a short period. Levothyroxine reduces blood pressure in about half of hypothyroid patients with hypertension, although blood pressure medications may still be needed. Appropriate Dosage Levels. Initial dosage levels are determined on an individual basis and can vary widely, depending on a person's age, medication condition, other drugs they are taking, and, in women, whether or not they are pregnant. For example, pregnant women with hypothyroidism may need higher than normal doses.  Starting out. Most people need to build up gradually until they reach a maintenance dose. In uncomplicated cases, the dose typically starts at 50 micrograms per day, which then increases in 3- to 4-week intervals until thyroid hormone levels are normal. Seniors and those with heart disease may start at 12.5 - 25 micrograms per day. On the other hand, young adults with a short history of hypothyroidism might be able to tolerate a full maintenance dosage right away.  Maintenance dose. Maintenance dose for most patients averages 112 micrograms, but it can vary between 75 - 260 micrograms. If conditions such as pregnancy, surgery, or other drugs alter hormone levels, the patient's thyroid needs will have to be reassessed. Daily Regimen. Because thyroid replacement is usually lifelong, setting up a regular daily routine is helpful. Here are some tips to remember:  Establish a habit of taking the medication at the same time each day. This may help prevent missed doses.  If you miss a dose of your medicine, use it as soon as you can. If it is almost time for your next dose, take your medicine then and skip the missed dose. Do not use extra medicine to make up for a missed dose.  Fiber and common daily supplements, such as calcium, may interfere with thyroxine absorption. Although levothyroxine can be taken at any time of day, either with or without food, some doctors recommend taking thyroid hormone upon awakening and at least 30 minutes before eating anything, including breakfast or supplements. Annual Evaluation. Thyroid failure is an ongoing process and so is its treatment. Many factors can cause changes that require modifying the thyroxine dosages. A dose that is appropriate for one year may be too low the next. To maintain normal thyroid levels, some patients may need to take gradually increasing doses of thyroid hormone every year or two. Doctors recommend that patients be reevaluated 6 months after normal TSH levels have been reached and then once a year thereafter. Specific factors, such as changes in health or diet, new medications for other conditions, or simply switching brands, can also cause changes in thyroid hormone levels that require different doses. If patients change dose levels or thyroxine brands, they should be checked again at least 6 weeks later. Problems Encountered with Levothyroxine Treatment Because levothyroxine is identical to the thyroxine the body manufactures, side effects are rare. Over- or under-dosing, however, is fairly common, although rarely serious in the short term. Symptoms of Under- and Over-Dosing of Levothyroxine

Under-Dosing Over-Dosing

Sluggishness Heart symptoms (rapid heart beat, palpitations, and wide variations in pulse; possible angina or heart failure)

Mental Agitation (tremor, nervousness, insomnia, excessive sweating) dullness

Feeling cold Pain (headache and muscle pain)

Muscle crampsIntestinal and metabolic symptoms (change in appetite, diarrhea, weight loss)

Fever and intolerance to heat

No Symptom Improvement When Normal Thyroid Levels Are Reached. Some patients fail to feel significantly better even when their thyroid levels become normal after taking thyroid replacement. Some patients with persistent symptoms may benefit from triiodothyronine (T3), the other important thyroid hormone. In such cases, either a combination of a lower-dose of thyroxine with a small amount of T3 or natural dried thyroid hormone, which contains T3, may be helpful. Side Effects of Overdosing. Overdosing can cause symptoms of hyperthyroidism. A patient with too much thyroid hormone in the blood is at an increased risk for abnormal heart rhythms, rapid heartbeat, heart failure, and possibly a heart attack if the patient has underlying heart disease. Excess thyroid hormone is particularly dangerous in newborns, and their drug levels must be carefully monitored to avoid brain damage. Side Effects of Long-Term Treatment. Patients with hypothyroidism usually receive lifelong levothyroxine therapy. There has been some concern that long-term use will increase the risk of osteoporosis, as suppression therapy does. Studies indicate that postmenopausal women who are taking long-term replacement thyroxine at the appropriate dosage have no significantly increased risk for osteoporosis. Drug Interactions with Levothyroxine. Many drugs interact with levothyroxine and may either enhance or interfere with its absorption. These drugs include:  Amphetamines  Anticoagulants (blood thinners)  Tricyclic antidepressants  Anti-anxiety drugs  Arthritis medications  Aspirin  Beta blockers  Insulin  Oral contraceptives  Digoxin  Certain cancer drugs  Iron replacement therapy (ferrous sulfate)  Calcium carbonate and aluminum hydroxide  Anticonvulsants (phenytoin, phenobarbital, carbamazepine)  Rifampin (antibiotic used to treat or prevent tuberculosis) Large amounts of dietary fiber may also reduce the drug’s effectiveness. People whose diets are consistently high in fiber may need larger doses of the drug. Since thyroid hormones regulate the metabolism and can affect the actions of a number of medications, dosages may also need to be adjusted if a patient is being treated for other conditions. Even changing thyroxine brands can have a different effect. Inappropriate Use of Thyroid Hormone Thyroid replacement hormone is sometimes prescribed inappropriately. It should only be used to treat diagnosed low thyroid. In some cases of infertility, women with menstrual problems and repeated miscarriages and men with low sperm counts have been treated with thyroid hormones even when there was no evidence of thyroid abnormalities. Other inappropriate uses for thyroid hormones are for weight loss and to reduce high cholesterol levels. Thyroid hormones have also been given to treat so-called metabolic insufficiency. Vague symptoms suggesting low metabolism, such as dry skin, fatigue, slight anemia, constipation, depression, and apathy, should not be treated indiscriminately with thyroid hormone. No evidence exists that thyroid therapy is beneficial unless the patient has proven hypothyroidism. Indiscriminate use of thyroid hormones can weaken muscles and, over the long term, even the heart. One exception is the use of thyroxine to enhance drugs used for the treatment of severe depression. Resources  www.aace.com -- American Association of Clinical Endocrinologists  www.thyroid.org -- American Thyroid Association  www.hormone.org -- Hormone Foundation  www.endo-society.org -- Endocrine Society References Abalovich M, Amino N, Barbour LA, Cobin RH, De Groot LJ, Glinoer D, et al. Management of thyroid dysfunction during pregnancy and postpartum: an Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2007 Aug;92(8 Suppl):S1-47. Allahabadia A, Razvi S, Abraham P, Franklyn J. Diagnosis and treatment of primary hypothyroidism. BMJ. 2009 Mar 26;338:b725. doi: 10.1136/bmj.b725. American Academy of Pediatrics, Rose SR; Section on Endocrinology and Committee on Genetics, American Thyroid Association, Brown RS; Public Health Committee, et al. Update of newborn screening and therapy for congenital hypothyroidism. Pediatrics. 2006 Jun;117(6):2290-303. Brent GA, Larsen PR, Davies TF. Hypothyroidism and thyroiditis. In: Kronenberg: HM, Shlomo M, Polonsky KR, Larsen PR, eds. Williams Textbook of Endocrinology. 11th ed. Philadelphia, Pa: Saunders Elsevier; 2008:chap 12. Fatourechi V. Subclinical hypothyroidism: an update for primary care physicians. Mayo Clin Proc. 2009;84(1):65-71. Gyamfi C, Wapner RJ, D'Alton ME. Thyroid dysfunction in pregnancy: the basic science and clinical evidence surrounding the controversy in management. Obstet Gynecol. 2009 Mar;113(3):702-7. Kliegman RM. Hypothyroidism. In: Kliegman RM, Behrman RE, Jenson HB, Stanton BF, eds. Nelson Textbook of Pediatrics. 18th ed. Philadelphia, Pa: Saunders Elsevier; 2007:chap 566. Mestman JH. Thyroid and parathyroid diseases in pregnancy. In: Gabbe SG, Niebyl JR, Simpson JL, eds. Obstetrics: Normal and Problem Pregnancies. 5th ed.Philadelphia, Pa: Elsevier Churchill Livingstone; 2007:chap 38. Ochs N, Auer R, Bauer DC, Nanchen D, Gussekloo J, Cornuz J, Rodondi N. Meta-analysis: subclinical thyroid dysfunction and the risk for coronary heart disease and mortality. Ann Intern Med. 2008 Jun 3;148(11):832-45. Epub 2008 May 19. Roberts LM, Pattison H, Roalfe A, Franklyn J, Wilson S, Hobbs FD, et al. Is subclinical thyroid dysfunction in the elderly associated with depression or cognitive dysfunction? Ann Intern Med. 2006 Oct 17;145(8):573-81. Rodondi N, Aujesky D, Vittinghoff E, Cornuz J, Bauer DC. Subclinical hypothyroidism and the risk of coronary heart disease: a meta-analysis. Am J Med. 2006 Jul;119(7):541-51. Stagnaro-Green A. Maternal thyroid disease and preterm delivery. J Clin Endocrinol Metab. 2009 Jan;94(1):21-5. Epub 2008 Nov 4. Vaidya B, Pearce SH. Management of hypothyroidism in adults. BMJ. 2008 Jul 28;337:a801. doi: 10.1136/bmj.a801. Villar HC, Saconato H, Valente O, Atallah AN. Thyroid hormone replacement for subclinical hypothyroidism. Cochrane Database Syst Rev. 2007 Jul 18;(3):CD003419. 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 Home Well Women Guide to Pregnancy and the Thyroid  Sitemap  About Me  Contact Me  Latest News  Well Women Blog  Support Group  Paul Robinson CT3M  Womens Stories  Articles By During pregnancy a great deal of hormonal and other changes occur Others and these in turn alter thyroid function. Thyroid function tests need to  Scoliosis be interpreted with care as during this time they will be very different.  Bipins Spine The two hormones responsible for altering thyroid function are Surgery Oestrogen and hCG, (human chorionic gonadotrophin) This is the  Thyroid Guide hormone that is measured in a pregnancy test and raised levels are what show as a positive result in the test.  Pregnancy and Thyroid The volumes of hCG circulating in early pregnancy can cause TSH levels to be low. Oestrogen, however, increases the amount of thyroid  Thyroid binding proteins in the serum and this increases thyroid hormone levels treatment as most thyroid hormones in the blood are bound to these proteins.  Treatment Measurements of “free” hormone usually remain unchanged. Problems The size of the thyroid can increase and this is usually only minimal  Armour and not detectable under medical examination, however should there Thyroid be a significant increase or unusual discomfort in the neck or when  The Endocrine swallowing, then this should be reported and thyroid function tests System performed.  Lyme Disease During the first trimester, the baby is totally dependant upon its mother  The Immune for thyroid hormone. After this time, the baby’s thyroid starts System producing its own thyroid hormones. It must be mentioned though, that  Hashimoto's since the baby is dependant on its mother for nutritional intake, that Disease iodine intake, being an important nutritional requirement to proper thyroid function, should be carefully maintained. The World Health  Autoimmune Page Organisation recommends 200 mcg per day during pregnancy. This would be applicable for mothers who otherwise have a normal  Adrenals thyroid  Cushings What complications can occur during pregnancy? (Please bear in Syndrome mind that complications generally apply to untreated Thyroid  Fibromyalgia conditions or where the mother is unaware that she has a thyroid  CFS condition)  Candida Hyperthyroidism (overactive thyroid)  The Most cases of hyperthyroidism in pregnancy are caused by Graves Menopause disease, although very high levels of hCG (also associated with morning sickness) can cause transient hyperthyroidism. Severe  Progesterone morning sickness is called Hyperemesis Gravidarum and in some  Depression cases, mothers need to be hospitalised.  Migraine Since scanning for hyperthyroidism in pregnancy is not recommended,  Panic Attacks diagnosis will come from laboratory testing and family history  Stress Relief Those with pre existing Graves disease will require monitoring and symptoms are often aggravated during pregnancy. Poorly monitored  Other Health Hyperthyroidism in pregnancy can lead to pre eclampsia and mothers Problems are also susceptible to very severe hyperthyroidism known as Thyroid  Healthy Life storm  Healthy Diet Ironically, Graves disease can improve during the third trimester but  Raw Food can also get worse after the birth of the baby.  Vitamin Guide Can Hyperthyroidism and Graves Disease affect my baby?  Colloidals, Uncontrolled hyperthyroidism can cause fast heart beat (tachycardia) in minerals the baby, babies that are small for gestational age, premature birth, stillbirth and sometimes congenital abnormalities.  Natural Anti- ageing This can be due to the following:  Essential Fatty Uncontrolled Maternal Hyperthyroidism Acids High levels of TSI (thyroid stimulating immunoglobulins)  Superfoods Graves disease is an autoimmune disease and caused by the production  Maca of anti-bodies that stimulate the thyroid gland and known as thyroid  Magnesium stimulating immunoglobulins. These anti-bodies are able to cross the placenta and affect the baby’s thyroid gland. Although it is rare and  MSM only seen in around 2 per cent of Graves disease related pregnancies,  Rosa high levels of TSI’s have been known to cause either foetal or neonatal Mosqueta hyperthyroidism. However, this is generally only seen where TSI’s are  Water source very high in the mother. Mothers with existing Graves disease of life generally have their TSI levels checked in the third trimester.  Beauty It is very important to tell you doctor if you have or have ever had Graves disease and whether you are taking antithyroid drugs as  Aromatherapy these can cross the placenta. It is also important to tell the doctor if  Books you have ever had radioactive iodine or surgery Your baby will need careful monitoring during your pregnancy to ensure foetal health  E-Books is not affected.  FAQs Antithyroid drug therapy (ATD) can impair the baby’s thyroid and  Archived Info cause foetal goitre so minimal doses should be used to ensure foetal  Working from thyroid health. However, the benefits to the bay of treating a mother Home with Hyperthyroidism far outweighs the risks providing drug therapy is carefully monitored.  Advice Should the hyperthyroidism be mild, then drug therapy will be avoided  Links and just careful monitoring used provided mother and baby are well. [?]Subscribe To This When treatment is needed the object is to keep free T3 and free T4 Site levels on the high side or normal and on the lowest dose of ATD as possible (with Propylthiouracil PTU generally being the chosen drug), and is the preferable range to avoid the baby developing  hypothyroidism or goitre and monitoring will be by monthly thyroid function tests. Mothers who can not tolerate ATD will sometimes have  their thyroid removed by surgery and this is very rare due to the risks of surgery and anaesthesia to the mother and baby and is only used if  no other alternative. Radioactive iodine treatment will not be used due to its ability to cross  the placenta and have a direct affect on the baby’s thyroid gland, thus destroying it and causing hypothyroidism.  Mothers on anti thyroid drugs (PTU) can also breastfeed but the baby will require careful monitoring. Beta blockers can also be used to treat the symptoms of hyperthyroidism in pregnancy but are generally used sparingly as they can affect the growth of the baby and are not recommended long term during the pregnancy and are preferable only for significant symptoms of tremors and severe palpitations whilst anti-thyroid medication is being evaluated and until sufficiently controlled by it, so only in the short term should beta blockers be used. Graves disease usually worsens after delivery especially in the first three months and higher doses of ATD’s will be required and close monitoring of thyroid function during this time. Hypothyroidism (Underactive thyroid) As we already know, the autoimmune condition, Hashimoto's Disease is the most common cause of hypothyroidism. Other causes are over treatment of an overactive condition. Please Click HERE to go to the Thyoid page to read about all the various causes and symptoms of both hyper and Hypo thyroid There are various conditions associated with hypothyroidism in pregnancy, one of which is anaemia. Muscle pain and weakness, (myopathy), pre-eclamsia, placenta abnormalities and post partumn haemorrhage being the others, but usually only presenting a problem in those women with severe hypothyroidism. Of course, severe untreated hypothyroidism in the mother could lead to congenital hypothyroidism in the infant which can cause brain development problems. Women should ask for their TSH, T3 and T4 levels to be checked whether they have a thyroid condition or not and when planning a pregnancy, this may be something that should be considered before becoming pregnant. Women with a family history of hypothyroidism should ensure these tests are performed as a matter of course, even though they themselves may not be presenting any symptoms. It is important to get your TSH levels checked as early as possible in the pregnancy due to TSH levels rising. Women who already have a thyroid condition should ensure their TSH, T3 and T4 levels are monitored during pregnancy, and as soon as pregnancy is confirmed, a visit to the GP to put plans in place for monitoring. Levothyroxine medication may have to be adjusted throughout the course of the pregnancy due to fluctuating levels and often this can mean an increase in dose by as much as 50 per cent. Levels should be checked every 6 weeks or every 4 weeks when dosage needs adjustment. Your baby's only source of thyroid hormone is your thyroid medication so you must ensure that you take it daily and preferably at the same time every day. (In the morning on waking is a good time) The only treatment required for hypothyroidism in pregnancy is medication in the form of thyroxine. However, since anaemia is commonplace is hypothyroid women, iron levels require careful monitoring in order to avoid severe anaemia. Another point worth noting and of utmost importance is that supplements containing iron will impair the absorbtion of thyroid medication, so a large gap between dosage should be observed. E.g If you take your thyroid medication in the moring, leave at least 6 hours before taking an iron or multivitamin supplement containing iron. After delivery, mothers can return to their normal dose of thyroxine but should be monitored for a while to ensure normal levels return. Points to note Women with an existing treated hypothyroid condition have no more chance of birth defects in their baby than anyone else. So, if you have been reading about things like low birth weight, low IQ, miscarriage, birth defects, still birth etc, it should be noted that this is only in women with untreated hypothyroidism who are unaware that they have the condition and where TSH tests have not been performed to identify this. I had a miscarriage in June 1997 and my thyroid condition had not then been identified. I also suffered with gestational diabetes, high blood pressure and anaemia during my pregnancy in 1998 when the condition was still unidentified and therefore untreated. My daughter Niamh displays no signs of problems (thank God) and is as bright as a button. Women with Hashimoto's disease are much more likely to suffer from gestational diabetes during their pregnancy or have blood sugar problems. Gestational Diabetes This is a condition diagnosed in pregnancy when blood or urine is taken for testing. Since urine is regularly assessed in pregnancy, the repeated presence of sugar may indicate gestational diabetes. A blood test will confirm this. High blood sugar levels are a sign of this condition. What causes it? Impaired glucose intolerance is something that many pregnant women experience during pregnancy due to the high level of hormones and hormonal changes. It is in the third trimester that the hormonal changes can cause a pregnant woman to become at risk. Due to increased levels of various hormones a strain is put on the pancreas which needs to produce three times the normal amount of insulin in pregnancy to counteract the increasing blood sugar levels due to pregnancy hormones. However the pancreas may not be able to produce sufficient levels of insulin to counteract this rise and then blood sugar will continue to rise and Gestational diabetes will result. Since diabetes can affect the developing baby by possibly causing birth defects and also contributing to increased growth of the baby in the womb due to a higher level of nutrition, the baby may be larger than normal at delivery which can cause problems to both mother and baby and more risks at delivery. Also after the birth the baby will no longer be receiving nourishment from it's mother so the sudden drop in blood sugar can cause some problems for the baby. Who is a risk of getting Gestational Diabetes? Sufferers of Hashimoto's Disease and other Autoimmune Diseases Constantly having the presence of glucose in your urine Being overweight prior to pregnancy Impaired glucose tolerance or fasting glucose Family history of diabetes Having given birth to previous large babies Previous gestational diabetes Polyhydramnios. A condition where the mother has too much amniotic fluid. How will I know? Women are now screened at 24+ weeks. High risk women will be screened earlier. This involves a glucose tolerance test where a sweet drink is consumed and about an hour later, a blood sample is taken. This checks as to how the glucose was metabolised by the body. Can it be treated? You will monitor your blood sugar yourself throughout the remaining weeks of your pregnancy. You will be given a blood glucose meter by your hospital or doctor and asked to test your blood several times a day by pricking your finger with a special lancet and putting a small drop of blood on a test strip which is then put into the meter. The meter then reads the results which should be written in a specially provided book for inspection at anti natal and/or doctors visits. You may be referred to a special clinic who can monitor your diet and advise of what you can and can't eat to keep blood sugar as normal as possible. The midwife will also test your urine at each visit to check for ketones which is an acid indicating that your diabetes is not being properly controlled. It may be the case that diet alone will not be enogh to control it and insulin may be needed by injection. You will be shown how to do this yourself and will be closely monitored and advised regarding this procedure in case of hypoglycemia. Symptoms of this include dizziness and fainting, feeling shaky, weakness, headaches, excessive sweating etc. Should you feel like this, test your blood and drink some fruit juice or a soft drink and then after about 15 minutes, check your blood again. If it is still low, take some more fruit juice or eat in advance of your next meal if it is some way off. This should all be carefully recorded in your book. I myself had gestational diabetes with my fourth pregnancy which was controlled with diet and I went on to have an 8 pound 1 oz baby, although my birth was medically managed due to the diabetes and high blood pressure. I also had an epidural as the stress of the delivery was pushing my blood pressure to an all time high. One week before she was due, they asked me to come in early and I refused. Fortunately, I went into labour that night. Your blood pressure and any resulting rise will also need to be carefully monitored. Persistant high blood pressure may indicate that your baby may need to be delivered early and you may be asked to come in to hospital for bed rest. Foetal monitoring will also be a matter of course and expect to sit on a monitor for up to an hour while your babies heart is recorded. What happens afer the birth? Your baby's blood glucose will be tested at birth. With gestational diabetes there is an increased risk of jaundice in the baby. Treatment includes either feeding the baby regularly or light treatment where the baby is put under special lights that remove the pigment resposible for jaundice called bilirubin. Jaundice goes away quickly when these treatments are carried out. My son, Sean had jaundice after he was born and this was eliminated with lots of feeding. I had to stay in hospital for 5 days during this time so that the staff could monitor him. I particularly remember my father saying "God, what a great sun tan he has!" and he nicknamed him "Golden Child" Will the diabetes remain after my baby is born? Normally your blood glucose levels will return to normal within 6 weeks post natal because the placenta is no longer present and producing hormones responsible for the disruption. Your blood sugar will once again be checked at the hospital in the form of a glucose tolerance test around 6 weeks after delivery to ensure things have returned to normal. However women who have had gestational diabetes have an increased risk of going on to develope type 2 diabetes in later life. You also have a much greater risk of devloping gestational diabetes with further pregnancies. In these cases it would be a good idea to keep to a healthy diet reducing sugar in your diet, stopping smoking and maintaining a healthy body weight in order to reduce your risk in the future. Never stop taking your thyroid medication as the baby needs thyroid hormone and it's only source of this is you. This also applies to breatfeeding. It is completely safe to breastfeed your baby when taking levothyroxine Can my child develope Hashimoto's Disease? Hashimoto's disease has been said to be hereditary but this is often not the case. It would not appear until the teenage years if this is the case. It is rare in newborn babies but occasionally this can happen and thyroid treatment will be required. My cousin's baby was born without a thyroid gland and takes thyroid hormone for life. He is fine and developing well. Thyroid and fertility The thyroid has a big impact on fertility. It interferes with everything including your ability to become pregnant, maintain the pregnancy to full term, your health after delivery and of course the health of your baby. It is not surprising that in view of this, I wonder how many miscarriages are due to undiagnosed thyroid conditions? Also, how many women who are unable to get pregnant and go through years of expensive fertility treatments really have an undiagnosed thyroid condition that could be remedied with thyroxine medication?. Please click here to go the Fertility page. What about complications during pregnancy itself? Throid conditions can worsen pregnancy complications and morning sickness can be much more severe. Hair loss can be greater, tiredness and fatigue whilst considered normal in pregnancy, can be amplified to quite an extent.Thyroid conditions can cause foetal growth problems, anaemia during pregnancy and afterwards, pre-eclampsia, gestational diabetes, premature labour, still birth and development and retardation problems in the baby after delivery. I had an undiagnosed Hashimoto's disease during my 4th pregnancy with my daughter, Niamh in June 1998. I was ill throughout the entire pregnancy from conception to delivery and afterwards. I had extreme fatigue, severe muscle pain (myopathy) accelerated hair loss, high blood pressure, gestational diabetes, anaemia just to name a few. I had to be closely monitored during the third trimester and constant foestal monitoring in the final weeks. Needless to say, my labour was managed and I was unable to have much choice regarding a birth plan. My labour was long and drawn out, some 22 hours in duration culminating in the need for an epidural and foetal distress as well as my own high stress levels. Also, whether this is relevent, a week prior to my miscarriage in June 1997, I suffered an extremely sore throat. Sore to the point where I could not swallow at all due to the pain. I developed a very high temperature which lasted a few days. Could this have been Thyroid storm? A week later I miscarried. After the miscarriage I was very ill and so fatigued I could not stand up or walk for months. No interest was taken by the medical profession and it was deemed normal in the circumstances. Not at any time was a thyroid condition thought of. What about after the birth? Symptoms such as tiredness hairloss and depression are ignored as doctors put it down to normal feelings after birth and the strain of being a new mother. Given this, how many cases of "post natal depression" are actually undiagnosed thyroid conditions? Last but not least and no less important, thyroid conditions can cause breast feeding difficulties and poor milk supply. There are many books covering this subject and one of the best is Mary Shomons "Thyroid Hormone Breakthrough" Please click here to see Mary Shomons Book about successful pregnancy with a thyroid condition This book will help you understand the important information you need to become pregnant, have a healthy baby, stay healthy yourself, and breastfeed your baby successfully. Most of all, when planning a pregnancy, make sure you get your TSH, T3 and T4 levels checked as part of the planning process, whether you have a thyroid condition or not and eliminate the worry at the start either by early diagnosis or confirmation so that you can enjoy a happy worry free pregnancy.

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Anemia and Hypothyroidism So, at the same appointment where I learned that my TSH was up but my access to Armour thyroid meds was gone, I also learned that I'm borderline anemic again. In particular, I'm very iron-deficient. My ferritin levels are down the tubes.

Ferritin is a protein that binds with iron and keeps it available for use, if I understand it correctly. It's one measure of stored iron in your body, basically.

Online, ferritin levels considered "normal" vary from source to source. The lab I used listed 11-307 as "normal." Medline Plus lists normal ferritin levels as:

Male: 12-300 ng/mL Female: 12-150 ng/mL

"The lower the ferritin level, even within the "normal" range, the more likely it is that the patient does not have enough iron."

Most online sources I've read state that while "normal" may be as low as 12, people should start getting concerned with levels below about 50.

Guess what my level was? 7.2. Definitely below any measure of "normal" and basically in the toilet. Great.

Now, my hemoglobin and hematocrit are in the "normal" range.....but only just barely. My hemoglobin was 11.6 and the cutoff is 11.5; my hematocrit was 35.4 and the cutoff is 34.7 at my lab. So not "officially" anemic, but barely above the cutoffs. And the ferritin is definitely abnormally low (7.2 when it should be at least 11).

The good news is that we had other levels tested last year to figure out which kind of anemia I had. My folate levels are good (I have aggressively supplemented these over the years because of pregnancy and breastfeeding) and my B12 levels are also good. So with the really low ferritin levels, it looks like it's iron deficiency anemia.

I've been struggling with this for a while. I've often been a bit borderline anemic over the years, but not enough to cause big problems. In pregnancy, I used "Floradix" - an herbal over-the-counter preparation - and that helped immensely without causing constipation, the way that iron pills can. It's great stuff, much better than OTC iron. It's what got my hemotocrit and hemoglobin levels up this past year.....but apparently it doesn't have as much effect on ferritin levels. Bummer.

As I've gotten older, I've had more issues with anemia, enough so that I was no longer able to donate blood to the Red Cross anymore. I'm a fairly rare blood type so they love me, but I haven't been able to donate now in several years because of the anemia. In fact, my donations probably exacerbated my low iron issues.....but I haven't donated in several years now, and my ferritin levels are still down to 7.2, so obviously it's much more than just blood donation going on.

Part of the problem is being perimenopausal. One symptom of impending menopause you don't hear a lot about is extremely heavy periods, called "menorrhagia." Colloquially, it's called the "blood flood" and sadly, it's very aptly named.

My periods were always reasonably normal, not usually too heavy or too painful. I skipped months periodically because of the PCOS, but once my hypothyroidism was finally diagnosed and treated, I never skipped a period again. (Still have other PCOS symptoms but as long as they hypothyroidism is treated, they stay relatively mild. Now, with my TSH going up, they're starting to act up more again. Ugh.)

As I've become perimenopausal, the periods became heavier and heavier. So this is quite likely a big cause of the low ferritin levels too. But I'm happy to report that as I move closer to menopause (and with the help of acupuncture), the heavy periods have eased up, thank goodness! And yet, despite this, my ferritin levels are still at an all-time low. So obviously, menorrhagia is not the only cause for my low ferritin levels.

I eat plenty of iron foods, I cook in iron skillets, I regularly take vitamin C with my iron, I avoid calcium etc. with the iron, I eat plenty of red meat (a more easily absorbed source of iron), and basically do all the things that are supposed to "fix" this problem. And none of them are working.

What I learned recently, though, is that hypothyroidism and anemia tend to go hand in hand. When you have one, you often have the other, especially if there are any other challenges to your system (like pregnancy, birth, blood donation, heavy periods, etc.). And apparently, undertreated hypothyroidism in particular tends to result in low ferritin levels.

So it will be interesting to see whether getting my TSH levels back to where they feel better to me will also coincide with an improvement in my ferritin levels. I am also taking supplemental iron and Floradix. Hopefully all of that will be enough to get things back to normal. Keep your fingers crossed!

[Anyone else with hypothyroidism had problems with anemia and low ferritin in particular? I'd love to hear about other people's experiences and what helped you.]

Posted by Well-Rounded Mama at 11:46 AM

Labels: anemia, menopause, thyroid

16 comments:

Bonnie said...

Here is a link to the site where I get my natural thyroid. Hope it helps.

http://www.nutri- meds.com/Nutri_Meds_Desiccated_Porcine_Thyroid_Capsules_p/nm-g-ptc.htm January 22, 2010 1:30 PM

Cya said...

I am also hypothyroid with low ferrtin. I started feeling better once my ferritin hit 20, which I suspect also got my thyroid levels to shape up. I have now reached a ferritin of 45, but since I started to exercise my levels have not increased (rather decreased somewhat).

Last week I found out my DD 9 was also hypothyroid with low ferritin.

After letting the news sink in, I convinced my very reluctant DD 12 to go for a test.

Yesterday we received the news, hypo and low ferritin.

Our doctor liked to call them subclinical, but no way did I agree! With THS for both at about 20 (0.35 - 6.0) and Free T4 at 11 and 8.5 (8.0 - 22.0), I requested to see a pediatric endo.

My youngest has started on medication, and I am sure my eldest will as soon as she get to see the endo.

I will give them both liquid iron for 2 - 3 months, hopefully it will make them perk up. I curse myself for not catching on to it sooner, but it never occured to me until my youngest displayed a goiter.

Do keep an eye on your children, and have them tested if you suspect something.

All the best,

Cya January 22, 2010 6:38 PM

kathmandu said...

On the subject of iron supplements, for people who don't have ferritin problems and just need more iron: the constipation is caused by ferrous sulphate. That's the cheapest and commonest form of iron in supplements. But if you can find supplements containing ferrous gluconate or ferrous fumerate, those won't cause constipation. January 24, 2010 5:08 PM

Anonymous said...

I have two more weeks left in a 6-week course of Ferlicet (I think that's the spelling) to get my iron levels up. My ferritin was at a 4. Yikes! No hypothyroidism for me, however. I've also had weight loss surgery (the duodenal switch) and gave birth via C- section to twin boys this summer. My iron levels, already low, but a stable low, crashed immediately thereafter. When you're that low, no amount of supplementing is going to get you up when you add in a malabsorption factor. So, it was infusion city for me.

In addition, I'm also choking down a tablespoon of blackstrap molasses every day. You get 40% of your RDA of iron from that. Utterly incredible, if you can stand getting it down.

If all else fails, go with the infusions. They're the quickest way to resolve at least part of your problem. Good luck!

Sarah January 24, 2010 8:21 PM

Well-Rounded Mama said...

Thanks for the comments folks. The type of iron I am taking is mostly ferrous gluconate so it's easier on my system. And of course, Floradix, which is really helpful too overall, just not as helpful with the ferritin.

Cya, thanks for the heads-up on watching the kids' levels. I did start having my teenage daughter tested for hypothyroidism recently because mine first presented in my late teens and I wanted a baseline for her. So far so good...but we'll watch the ferritin too.

Sarah, the combo of WLS and the blood loss you can have with childbirth (esp c/s) is a tough combo. I'm sorry you had to go through that. I know that nearly all the WLSers I have known have ended up on IV iron sooner or later. It's just too hard to keep those levels up without it because of the malabsorption.

Interesting how you ended up with a level of 4 with the WLS, and I'm at 7----without WLS. Yipes. Scary what it might be with WLS!! Well, hopefully I can start getting it back up again pronto! If not, thanks for the hint about the IV iron protocol. Here's hoping I won't need it....but thanks for sharing.

Congrats on your twins, btw! January 24, 2010 10:46 PM

Anonymous said...

http://www.latimes.com/features/health/la-he-capsule25-2010jan25,0,3227448.story

Just read that, and ran right over here to share it.

BBBW (big beautiful breastfeeding woman) right here. Nursed my 4yo til she was 3. January 25, 2010 3:20 PM

Anonymous said...

I used a product called Ferrasorb when my iron levels were low. January 26, 2010 9:10 AM

Hazelnut said...

Do you know what your red cells actually look like? I'm a veterinarian, not a doctor, and employed in a research lab rather than in practice, but what I was taught is that true iron deficiency anemia will typically cause a hypochromic microcytic anemia (cells are pale and smaller than normal). I never hear about this in human medicine, and I always wonder. January 27, 2010 8:53 AM

Anonymous said...

Glad to see this post. I too have been dealing with low ferritin and life without a thyroid. Ferrous Gluconate is also my choice of supplement. I take synthroid.

So what have I learned? Low ferritin, hypothyroidism and perimenopause symptoms mimic one another. I feel best when my ferritin is over 70. As I approach menopause and my ferritin levels come up, I became hyperthyroid and need less synthroid. I feel best when my TSH is between 1-2.

Oh yes, iron supplements and calcium interfere with synthroid (and each other) - give them a 4 hour window from each other.

Thanks for the opportunity to share! April 22, 2010 11:30 AM

Sick of being tired! said...

Hey! Who stole my body? We share so many common symptoms it was kinda weird reading your comment!-Perimenopause, Hypothyroid, Low iron, & Low Vit D!?! I just found out about the last 2 this week. The way the symptoms mimic each other is crazy and confusing at times- I wonder if it amplifies the symptoms? I appreciate the comments from everyone and look forward to walking down the road to health because I have too many things to do in life beginning with keeping up with and enjoying my 3 teenagers! I am looking for a healthy way to jumpstart my health in addition to my supplements. If anyone has advice..."sick of being tired" June 12, 2010 4:27 PM

Anonymous said...

Skin Bright says I am also hypothyroid with low ferrtin. I started feeling better after I got my ferritin into the mid twenties. Through exercise I have now been able to get my ferrtin level up into the forties. June 19, 2010 5:40 AM

Home Remedies said... There are also different types of anemia: iron deficiency anemia, vitamin deficiency anemia, and anemia of chronic disease, as well as aplastic anemia, anemia associated with bone marrow disease, hemplytic anemia and sickle cell anemia. September 3, 2010 4:57 AM

Anonymous said...

I'm 4 years post-menopausal, and the blood lab turned me away in April after 30 loyal years of donating due to low iron -- turned out I was anemic, leading to thyroid check, and Hashimoto's diagnosis... Also low in calcium, Vit. D, globulin, etc. Like "sick of being tired," I wonder whether all these conditions' symptoms amplify one another, and what more is recommended aside from religiously taking iron supps, thyroid meds, and the low-dose anti-depressants the docs have prescribed. It's tough enough keeping up with teenagers, work, and home, without all this... September 5, 2010 8:54 AM

Anonymous said...

Joe said,,, I have got rock bottom ferritin levels. Below 4 at its lowest & I felt wrecked. Even managed to crash the car I was so spaced out! Fortuneately no serious injuries but I blame my low ferritin for that. I am also hypothyroid. Spent most of last year on iron supplements & my ferritin was hardly raised off the floor. I got it up to about 20. I was sent for various investigations including an upper & lower endoscopy to no avail. Just found this website & feel some hope. I am off to my gp with a print out ASAP. Thanks to the well rounded mama. March 20, 2011 4:31 PM

Anonymous said...

Iam recenlty diagnosed with hypothyroidism and anemia.. Im afraid that i might pregnant this month as we did not use any protective measures and i also assume Im ovulating as i have lots of discharge..Should i use any contraceptive pills or is it okay if im pregnant?.. I wanted to have a baby but before that i wanted to get back to normal.. But Im worried that if i get preg this month what will happen to the baby..

Please advise. October 18, 2011 6:36 AM Well-Rounded Mama said...

Anonymous, I'm not a health care provider and I don't give medical advice. Besides, there is no way for me to know what your iron and thyroid levels are, which is important. My suggestion is to consult a midwife or your GP as soon as you can.

To answer on a basic level, I think a lot depends on how bad your anemia and hypothyroidism is and whether you are on meds. People do have generally healthy pregnancies with mild hypothyroidism and mild anemia; if you were pregnant and your condition was mild, you could start getting those labs improved via meds and diet and go from there. It doesn't have to be a disaster. But more severe deficiencies might mean more problems.

Really, you need to see a healthcare professional who is familiar with your details and ask them these questions. Sorry I can't help you more. October 18, 2011 10:52 AM