DOCSLIB.ORG

Silent Thyroiditis

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Silent Thyroiditis CLINICAL REVIEW Silent Thyroiditis Roland Sakiyama, MD Los Angeles, California Silent thyroiditis is an increasingly recognized cause of transient thyrotoxicosis. Inflammatory destruction of thyroid follicles results in release of preformed thyroxine and triiodothyronine. Patients present with symptoms of thyrotoxicosis, but unlike subacute thyroiditis, lack thyroid pain or ten­ derness. The thyrotoxic state spontaneously resolves in 2 to 12 weeks at which time the patient either returns to a euthyroid state or passes through a transient hypothyroid phase. Diagnostic laboratory findings include eleva­ tions of thyroxine and triiodothyronine and a markedly depressed radioactive iodine uptake. It is imperative for the primary care physician to distinguish silent thyroiditis from chronic causes of hyperthyroidism, eg, Graves' dis­ ease, since treatment must be palliative rather than definitive. Long-term prognosis is usually excellent. ver the past decade a newly recognized subacute majority of cases of hyperthyroidism. Silent thyroiditis O thyroid disorder has emerged as an important now accounts for upwards of 20 to 30 percent of newly cause of thyrotoxicosis. First described in 1975 by diagnosed cases of thyrotoxicosis.2'6 While growing Gluck et al,1 this disease, like classical subacute physician awareness may account for part of the in­ thyroiditis, is characterized by inflammation and dis­ creased incidence, this silent form of subacute thy­ ruption of normal thyroid architecture resulting in the roiditis appears to be occurring with increased fre­ release of preformed stores of thyroid hormone. Un­ quency.2 like subacute thyroiditis, however, patients lack Silent thyroiditis afflicts women more commonly thyroid pain or tenderness. This subacute form of than men in an approximately 2:1 to 3:1 ratio. The thyroid disease has been referred to by a variety of majority of patients are between 20 and 40 years of terms. Although lymphocytic thyroiditis with spontane­ age, although the range is from the first to the ninth ously resolving hyperthyroidism remains the most decade.2 The clinician needs to be aware of the fre­ accurate descriptive term, “silent” and “painless” quent occurrence of silent thyroiditis during the thyroiditis reflect the absence of thyroid pain and sub­ postpartum period. Thyroid dysfunction has been sequently have gained popularity. Recognition and found in 5.5 percent of postpartum women.6 Of those proper management of this newly described disorder are affected, transient thyrotoxicosis alone was found in critical, since its transient nature renders traditional 50 percent. The remaining patients were equally di­ means of treatment ineffective and potentially harm­ vided into having transient thyrotoxicosis followed by ful. transient hypothyroidism and transient hypothyroid­ ism alone. Of those patients found to have silent thyroiditis, 10 percent are postpartum women.7 INCIDENCE Until a decade ago chronic thyroid disease, such as PATHOGENESIS Graves’ disease (toxic diffuse goiter), toxic multinodu­ lar goiter, and toxic adenoma, accounted for the vast Fundamental to the pathogenesis of the thyrotoxic state in both silent and subacute thyroiditis is destruc­ tion of follicular epithelium and loss of integrity of the storage follicle. In this first phase of silent thyroiditis, Submitted, revised, June 27, 1986. free triiodothyronine (T3) and free thyroxine (T4) are From the Department of Medicine, School of Medicine, University of Cali­ released, producing the clinical manifestations of fornia, Los Angeles, Los Angeles, California. Requests for reprints should thyrotoxicosis (Figure 1). Suppressed thyroid-stimu­ f>o addressed to Dr. Roland Sakiyama, Department of Medicine, Division of Family Medicine, UCLA School of Medicine, CHS, BH-134, Los lating hormone (TSH) secretion from high levels of cir­ Angeles, CA 90024. culating T4 and T:i and destruction of follicular epithe- ® 1986 Appleton-Century-Crofts THE JOURNAL OF FAMILY PRACTICE, VOL. 23, NO. 4: 367-369, 1986 367 SILENT THYROIDITIS I n in m TABLE 1. DIFFERENTIAL DIAGNOSIS OF i i THYROTOXICOSIS ACCORDING TO RADIOACTIVE I IODINE UPTAKE (RAIU) \ 1 1 H yperthyroid \ I \ j fO 1 ' 1 - N 1 1 Low RAIU "D i i l ! / 1 1. Silent thyroiditis sr N 1 I 2. Subacute thyroiditis I ___ / | 3. Graves’ disease with iodine excess I l i H y p o t h y r o i d 4. Iodine-induced hyperthyroidism I 1 1 __|_ 1 1 (Jod-Basedow) T i m e — > 5. Factitious hyperthyroidism 6. Struma ovarii PHASE I II I I I IV 7. Metastatic thyroid cancer T4 a n d T 3 H ig h N o rm a l Low N o rm a l High RAIU R A IU Low Low Normal-high Normal-high 1. Graves' disease TSH Low Low Normal-high Normal-high 2. Toxic multinodular goiter 3. Toxic adenoma Figure 1. Four phases of silent thyroiditis 4. Pituitary tumor secreting thyroid-stimulating hormone 5. Trophoblastic tumor lium lead to suppression of iodine uptake, that is, low radioactive iodine uptake. As follicular stores of pre­ formed hormone are depleted, serum levels of T4 and symptoms typically seen in chronic thyroid diseases T3 normalize (phase 2), although 25 to 40 percent of such as Graves’ disease, onset of symptoms in silent patients transiently fall into a hypothyroid range thyroiditis is often sudden and can be pinpointed in (phase 3).8 During this stage, suppression of TSH secre­ time by the patient. The hallmark finding of pain or tion is released, with serum TSH rising often to ele­ tenderness of the thyroid seen in subacute thyroiditis vated levels. Radioactive iodine uptake returns to is absent in silent thyroiditis. Furthermore, patients normal or supranormal values. Thyroid hormone syn­ with silent thyroiditis lack associated symptoms of thesis is now stimulated by TSH and the increased malaise, myalgia, fatigue, and fever commonly seen in iodine uptake, returning the patient to a euthyroid subacute thyroiditis. Patients may present with the state (phase 4). typical eye stare and lid lag indicative of increased While both silent and subacute thyroiditis are man­ sympathetic tone from any cause of hyperthyroidism; ifest by similar alterations in thyroid hormone concen­ however, signs of infiltrative opthalmopathy (limita­ tration, they differ in a number of important ways. tion of extraocular movements and proptosis) and pre- Subacute thyroiditis is thought to have a viral origin tibial myxedema characteristic of Graves’ disease are and is associated with prodromal symptoms of myal­ rarely seen in silent thyroiditis. Examination may re­ gia, malaise, and fatigue. Histologically, subacute thy­ veal signs of thyrotoxicosis including a resting roiditis is found to have acute inflammatory changes tachycardia, warm, moist skin, fine tremor, and a with polymorphonuclear leukocytes, giant cells, and quickened Achilles-tendon relaxation time. In approx­ granulomas. The thyroid gland of patients with silent imately one half the patients, the thyroid is enlarged thyroiditis demonstrates distinctly different histologic and often firm, while the remainder lack a goiter.2’8'10 features characterized by diffuse or focal lymphocytic There are no historical or physical findings that are infiltration, scant fibrosis, and absence of giant cells diagnostic of silent thyroiditis. In the absence of infil­ and granulomas.2'7-9 Histologically, this state is remin­ trative opthalmopathy, it is virtually impossible to dis­ iscent of chronic lymphocytic (Hashimoto’s) thyroid­ tinguish between thyrotoxicosis caused by silent itis, an autoimmune disease of the thyroid. Whether thyroiditis and Graves’ disease. Proper diagnosis re­ silent thyroiditis is a variant of subacute thyroiditis quires appropriate use of laboratory aids. based on a parallel clinical presentation, a variant of Hashimoto’s thyroiditis based on its histologic find­ ings, or a newly recognized disease is still debated. LABORATORY EVALUATION The clinical suspicion of hyperthyroidism can be CLINICAL PRESENTATION readily confirmed by measurements of serum concen­ trations of T4 and T;,. A T /F, ratio of less than 20:1 Patients typically present during the initial stage of suggests the diagnosis of silent thyroiditis rather than thyroiditis with overt symptoms of thyrotoxicosis— uncomplicated Graves’ disease.11 The critical diag­ nervousness, palpitations, tremor, heat intolerance, nostic study is measurement of radioactive iodine up­ and weight loss. Contrary to the insidious onset of take (RAIU). During the initial thyrotoxic stage of si- 368 THE JOURNAL OF FAMILY PRACTICE, VOL. 23, NO. 4, 1986 SILENT THYROIDITIS lent thyroiditis, the RAIU is suppressed to values of PROGNOSIS less than 3 percent. The causes of thyrotoxicosis can be separated into two groups based on either a low or As previously stated, recurrent episodes of silent high RAIU reading (Table 1). Other causes of thyro­ thyroiditis occur in approximately 10 percent of pa­ toxicosis associated with suppressed RAIU can usu­ tients. In contrast, recurrent episodes of subacute thy­ ally be distinguished from silent thyroiditis based on roiditis are rare. Additionally, patients with silent thy­ historical or physical findings. Patients with thyrotoxi­ roiditis often have a persistent goiter and a positive cosis factitia often present a difficult diagnostic chal­ titer of antithyroid antibodies.15 Permanent hypothy­ lenge. Presence of a low level of serum thyroglobulin is roidism is a definite although uncommon sequela of an important diagnostic clue.12 silent thyroiditis. Subclinical hypothyroidism, how­ Additional laboratory studies
Load more

Recommended publications
  • Thyroid Hormone Misuse and Abuse
    Endocrine (2019) 66:79–86 https://doi.org/10.1007/s12020-019-02045-1 REVIEW Thyroid hormone misuse and abuse Victor J. Bernet 1,2 Received: 11 June 2019 / Accepted: 2 August 2019 © Springer Science+Business Media, LLC, part of Springer Nature 2019 Abstract Thyroid hormone (TH) plays an essential role in human physiology and maintenance of appropriate levels is important for good health. Unfortunately, there are instances in which TH is misused or abused. Such misuse may be intentional such as when individuals take thyroid hormone for unapproved indications like stimulation of weight loss or improved energy. There are instances where healthcare providers prescribe thyroid hormone for controversial or out of date uses and sometimes in supraphysiologic doses. Othertimes, unintentional exposure may occur through supplements or food that unknowingly contain TH. No matter the reason, exposure to exogenous forms of TH places the public at risk for potential adverse side effects. Keywords Thyrotoxicosis ● Thyroid hormone abuse ● Thyroid hormone misuse ● Factitious thyrotoxicosis ● Supplements ● 1234567890();,: 1234567890();,: Analogs Overdose Thyroid hormone misuse and abuse secondary to exogenous TH ingestion that may be unin- tentional or purposeful such as in some cases of Munch- Almost any substance that impacts body physiology and ausen syndrome. Instances of TH misuse can be associated function is at risk for misuse or frank abuse, usually in the with the development of significant side effects. There are misgiven belief that the particular agent whether it be a other instances of chronic, low-grade over treatment with herb, supplement, medication, or hormone has healing TH, which occur for various misreasoning such as weight properties beyond that of which it actually possesses.
    [Show full text]
  • Subacute Thyroiditis with Non-Toxic Hyperfunctioning Thyroid Nodules
    Open Access Austin Endocrinology and Diabetes Case Reports Clinical Image Subacute Thyroiditis with Non-Toxic Hyperfunctioning Thyroid Nodules Samer El-Kaissi*, Christine Hughes and Hussein Saadi Department of Endocrinology, Cleveland Clinic Abu Dhabi, UAE *Corresponding author: Samer El-Kaissi, Cleveland Clinic Abu Dhabi, Medical Subspecialties Institute, Department of Endocrinology, PO Box 112412, Al Maryah Island, Abu Dhabi, UAE Received: August 15, 2016; Accepted: August 22, 2016; Published: August 23, 2016 Keywords Thyroiditis; Thyroid nodule; Multinodular goitre; Hyperthyroidism Clinical Image A 46-year old woman presented with a 4-week history of subacute Thyroiditis following an upper respiratory tract infection. She had thyroid gland tenderness, symptoms of thyrotoxicosis, increased erythrocyte sedimentation rate [45mm/hr], raised free-T4 [29pmol/L] Panel B: Thyroid 99mTc pertechnetate scan after resolution of hyperthyroidism with thyrotropin suppression [0.005mIU/L] and normal free-T3 and discontinuation of all medications, approximately 10-weeks after the [5.64pmol/L]. Thyroid ultrasound revealed six small-moderate size initial scan in Panel A. This scan shows improved tracer uptake in the thyroid nodules. Thyroid 99mTc pertechnetate scan during the thyrotoxic at 0.6% (normal range 0.2-3%) but the foci of increased uptake in the right phase (Panel A) showed two foci of increased uptake with little midzone and left lower zone are still apparent (white arrows). activity in the rest of the gland raising the possibility of coexistent Autonomously Functioning Thyroid Nodules [AFTN] [1]. Treatment consisted of oral prednisolone and a β-blocker and in light of the thyroid scintigraphy findings, low-dose carbimazole was added. Repeat nuclear scanning after resolution of thyrotoxicosis and discontinuation of all medications (Panel B) showed persistently increased uptake in the two foci with improved uptake in the rest of the gland.
    [Show full text]
  • A Case of Thyrotoxic Paralysis Caused by Consumption of Iodocaseine
    Journal of Health and Social Sciences 2019; 4,2:277-282 CASE REPORT IN EMERGENCY MEDICINE A case of thyrotoxic paralysis caused by consumption of iodocaseine Antonio Villa1, Gabriella Nucera2 Affiliations: 1 M.D., Department of Emergency, ASST Monza, PO Desio, Monza, Italy 2 M.D., Department of Emergency Medicine, ASST Fatebenefratelli-Sacco, PO Fatebenefratelli, Milano, Italy Corresponding author: Dr Antonio Villa, ASST Monza, PO Desio. Via Fiuggi, 56 20159 Milan, Italy. E-mail: [email protected] Abstract Acute hypokalaemic paralysis is a rare but treatable cause of acute limb weakness. Thyrotoxic paralysis is an uncommon, potentially life-threatening endocrine emergency and it is a rare complication of hyperthyroidism. The most common causes of hyperthyroidism include Graves’ disease, multinodular goiters or solitary thyroid nodule, and iodine-induced thyrotoxicosis ( Jod-Basedow syndrome). Thyreotoxicosis factitia, which is caused by the excessive ingestion of exogenous thyroid hormone or iodine derivatives administration, has been rarely reported as a cause of thyrotoxic paralysis. We describe the case of a young Caucasian male with flaccid paralysis of all four limbs and severe hypokalaemia after inappropriate iodine derivatives (iodocasein) intake to show, in conclusion, how critical care physicians need to be aware of this rare but curable condition. KEY WORDS: Iodocaseine; hypokalaemia; thyrotoxic paralysis. 277 Journal of Health and Social Sciences 2019; 4,2:277-282 Riassunto La paralisi acuta ipokaliemica è una causa rara ma curabile di astenia acuta. La paralisi tireotossica è un'e- mergenza endocrina non comune e potenzialmente pericolosa per la vita ed è una rara complicanza dell'i- pertiroidismo. L'ipertiroidismo è causato prevalentemente dalla malattia di Graves, da gozzi singoli o multi- nodulari, e dalla malattia indotta da iodio ( Jod-Basedow).
    [Show full text]
  • Hyperthyroidism and Thyrotoxicosis
    Hyperthyroidism and thyrotoxicosis Assoc. prof. V. Marković, MD, PhD Assoc. prof. A. Punda, MD, PhD A. Barić, MD, nucl. med. spec. Hyperthyroidism- Thyrotoxicosis Hyperthyroidism- elevated serum levels of thyroid hormones caused by overproduction of thyroid hormones Thyrotoxicosis: elevated serum level of thyroid hormones/ excessive amount of circulating thyroid hormone Hyperthyreoidism includes thyreotoxycosis but Thyrotoxicosis is not exclusively caused by hyperthyroidism Classification of thyrotoxicosis Hyperthyroidism Thyrotoxicosis without hyperthyroidism Mb Basedow-Graves Thyrotoxicosis factitia Multinodular toxic goiter Subacute thyroiditis (painfull) Toxic adenoma Subacute thyroiditis (painless) Elevated TSH levels Ectopic thyroid tissue Trophoblastic tumors Iod-Basedow Diffuse toxic goiter (Mb Basedow, Graves) Diffuse toxic goiter Mb. Graves-Basedow Epidemiology and etiology Diffuse toxic goiter (Mb. Graves- Basedow) is an autoimune, multysistemic dissease, wich includes the thyoid gland, infiltrative ophthalmopathy, dermopathy and acropathy. World wide prevalence is about 0,4-2% in women, 0,1% in men, includes 60-90% of hyperthyroidism cases*. It is complex disease with predominant genetic component.& Sex hormones, stress. Disease is caused by TSH receptor stimulating antibodies/ TSH stimulating antibodies (TSAb), in 80-100% patients. *Taunbridge WMG, Vanderpump MPJ. Population screening for autoimmune thyroid disease. Endocriol Metab Clin North Am. 2000;29:239-253. &Brix TH, Kyvik KO, Christensen K, et al. Evdence for a major
    [Show full text]
  • Thyroid Vascularity and Blood Flow
    European Journal of Endocrinology (1999) 140 452–456 ISSN 0804-4643 Thyroid vascularity and blood flow are not dependent on serum thyroid hormone levels: studies in vivo by color flow doppler sonography Fausto Bogazzi, Luigi Bartalena, Sandra Brogioni, Alessandro Burelli, Luca Manetti, Maria Laura Tanda, Maurizio Gasperi and Enio Martino Dipartimento di Endocrinologia e Metabolismo, Ortopedia e Traumatologia, Medicina del Lavoro, University of Pisa, Pisa, Italy (Correspondence should be addressed to E Martino, Dipartimento di Endocrinologia e Metabolismo, Ortopedia e Traumatologia, Medicina del Lavoro, Universita` di Pisa, Ospedale di Cisanello, Via Paradisa, 2, 56122 Pisa, Italy) Abstract Objective: Thyroid blood flow is greatly enhanced in untreated Graves’ disease, but it is not known whether it is due to thyroid hormone excess or to thyroid hyperstimulation by TSH-receptor antibody. To address this issue in vivo patients with different thyroid disorders were submitted to color flow doppler sonography (CFDS). Subjects and methods: We investigated 24 normal subjects, and 78 patients with untreated hyperthy- roidism (49 with Graves’ hyperthyroidism, 24 with toxic adenoma, and 5 patients with TSH-secreting pituitary adenoma (TSHoma)), 19 patients with thyrotoxicosis (7 with thyrotoxicosis factitia, and 12 with subacute thyroiditis), 37 euthyroid patients with goitrous Hashimoto’s thyroiditis, and 21 untreated hypothyroid patients with Hashimoto’s thyroiditis. Results: Normal subjects had CFDS pattern 0 (absent or minimal intraparenchimal spots) and mean intraparenchimal peak systolic velocity (PSV) of 4.8 6 1.2 cm/s. Patients with spontaneous hyperthy- roidism due to Graves’ disease, TSHoma, and toxic adenoma had significantly increased PSV (P < 0.0001, P = 0.0004, P < 0.0001 respectively vs controls) and CFDS pattern.
    [Show full text]
  • SUBACUTE THYROIDITIS by SELWYN TAYLOR, M.CH., F.R.C.S
    Postgrad Med J: first published as 10.1136/pgmj.33.381.327 on 1 July 1957. Downloaded from 327 SUBACUTE THYROIDITIS By SELWYN TAYLOR, M.CH., F.R.C.S. Surgeon, King's College Hospital, Belgrave Hospitalfor Children, and Hammersmith Hospital; Lecturer in Surgery, Postgraduate Medical School of London The term ' thyroiditis ' implies inflammation of to become much more common in that particular the thyroid gland, but by long usage it has come clinic. I had never seen an example before I950, to be used for a number of conditions in which but saw six in the next three years and pro- infection or trauma play apparently no part. Sub- gressively more each year since then. The con- acute thyroiditis is the title given to a condition dition is much commoner in women than men in which was first clearly described by de Quervain the ratio of about six to one. It has not yet been in I904 and which has been rediscovered, or re- reported in a child and is commonest in the fourth described, on a number of occasions since then, and fifth decades, although I have seen it in a with the result that it now has a multiplicity of student teacher of twenty-one. In our own series different names: granulomatous thyroiditis, giant- there was a history of a pre-existing goitre in 50 cell thyroiditis, pseudotuberculous thyroiditis, per cent. of the patients. The incidence, compared creeping thyroiditis, struma granulomatosa, acute with that of Hashimoto's thyroiditis and Riedel's non-infectious thyroiditis, acute non-suppurative thyroiditis, varies widely in different clinics, but thyroiditis and de Quervain's thyroiditis.
    [Show full text]
  • Thyrotoxicosis
    THYROTOXICOSIS: A RETROSPECTIVE STUDY OF CASES SEEN AT NUCLEAR MEDICINE UNIT (NEMROCK) Thesis Submitted for the fulfillment of master degree In nuclear medicine By Amira Hodhod Elsayed M.B.B.CH Under Supervision of Professor Dr. Shawky Ibrahim El.Haddad Professor of Radiotherapy and Nuclear Medicine Faculty of medicine –Cairo University Dr. Gehan Ahmed Yuonis Lecturer of Nuclear Medicine Faculty of medicine –Cairo University Faculty of medicine Cairo University 2013 Acknowledgments First, I would like to thank all my professors who allowed me to quote their work. I particularly grateful to professor Dr/ Shawky El.hadad for his encouragement and generosity in dealing with science and Dr/ Gehan Younis, this study would be much poorer without her help. I am grateful to everyone in Nuclear Medicine department, Cairo University. A special thanks to Dr/ Ahmed Sabrey who helped me in the statistical part of the study. I am deeply indebted to my dear husband Dr/ Hisham Aboelnasr, who was encouraging and supportive throughout. This list would not be completed without mentioning the role of my great mother in supporting me. And last but not least, to my family and my friends for patiently persevering with me. Index List of figures……………………………………………….…….…………………I List of tables………………………………………………………………………….III List of abbreviations………………………………………..………………..….V Introduction and aim of the study………………………..…………….…1 Review of literature……………………………………….………..……………5 Material, methods and data collection…………………………….….49 Results………………………………………………………………………………..52
    [Show full text]
  • Endocrine Module (PYPP 5260), Thyroid Section, Spring 2002
    Endocrine Module (PYPP 5260), Thyroid Section, Spring 2002 THYROID HORMONE TUTORIAL: THYROID PATHOLOGY Jack DeRuiter I. INTRODUCTION Thyroid disorder is a general term representing several different diseases involving thyroid hormones and the thyroid gland. Thyroid disorders are commonly separated into two major categories, hyperthyroidism and hypothyroidism, depending on whether serum thyroid hormone levels (T4 and T3) are increased or decreased, respectively. Thyroid disease generally may be sub-classified based on etiologic factors, physiologic abnormalities, etc., as described in each section below. More than 13 million Americans are affected by thyroid disease, and more than half of these remain undiagnosed. The American Association of Clinical Endocrinologists (AACE) has initiated a campaign to increase public awareness of thyroid disorders and educate Americans about key periods, from birth to advanced age, when people are at increased risk for developing a thyroid disorder (see below). The diagnosis of thyroid disease can be particularly challenging. Patients often present with vague, general clinical manifestations; in particular, the elderly may not associate the signs and symptoms with a disease process and thus may not bring them to the attention of their primary care provider. The prevalence and incidence of thyroid disorders is influenced primarily by sex and age. Thyroid disorders are more common in women than men, and in older adults compared with younger age groups. The prevalence of unsuspected overt hyperthyroidism and hypothyroidism are both estimated to be 0.6% or less in women, based on several epidemiologic studies. Age is also a factor; for overt hyperthyroidism, the prevalence rate is 1.4% for women aged 60 or older and 0.45% for women aged 40 to 60.
    [Show full text]
  • Subacute Thyroiditis Christa M
    ENDOCRINECONSULT Subacute Thyroiditis Christa M. Blose, MPAS, PA-C, Holly Jodon, MPAS, PA-C erry, a 48-year-old white man, is referred to endocri- TABLE Jnology for abnormal results Lab Results for Case Patient of thyroid tests performed four Time after symptom onset weeks ago (see table for values). Two months ago, Jerry developed 1 mo 2 mo 4 mo 6 mo an upper respiratory infection TSH (0.40-4.50 mlU/mL) 0.03 0.14 8.23 3.54 (URI) with fever, odynophagia, and anterior neck discomfort. Free T4 (0.8-1.8 ng/dL) 2.58 1.74 0.72 1.66 His symptoms resolved after two weeks; however, he has since de- Free T3 (2.3-4.2 pg/mL) 4.12 1.7 3.0 veloped fatigue and nervousness. The remaining review of sys- TPO antibody (< 20) 11 tems is unremarkable. Medical ESR (0-22 mm/h) 55 history is negative. Jerry denies any factors that can affect thyroid Abbreviations: ESR, erythrocyte sedimentation rate; T3, triiodothyronine; T4, thyroxine; function: He does not take thyroid TPO, thyroid peroxidase antibody. medication, OTC thyroid supple- ments, amiodarone, lithium, or TSH, with normal free thyroxine except for a small, firm thyroid interferon-α, does not have high (T4) and free triiodothyronine gland without the tenderness iodine intake, and has not un- (T3) levels. His thyroid peroxidase elicited previously. Labwork re- dergone head/neck irradiation. antibody (Anti-TPO) is negative. veals an elevated TSH with low There is no personal or family Radioactive iodine uptake (RAIU) free T4 and free T3.
    [Show full text]
  • Thyroid Emergencies
    REVIEW ARTICLE Thyroid emergencies Dorina Ylli1, Joanna Klubo ‑Gwiezdzinska2, Leonard Wartofsky3,4 1 Endocrinology Division, University of Medicine, Tirana, Albania 2 National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, United States 3 Endocrinology Division, Department of Medicine, Georgetown University School of Medicine, Washington DC, United States 4 MedStar Health Research Institute, MedStar Washington Hospital Center, Washington DC, United states KEY WORDS ABSTRACT coma, critical care, Myxedema coma and thyroid storm are among the most common endocrine emergencies presenting to hypothermia, general hospitals. Myxedema coma represents the most extreme, life ‑threatening expression of severe hypothyroidism, hypothyroidism, with patients showing deteriorating mental status, hypothermia, and multiple organ thyrotoxicosis system abnormalities. It typically appears in patients with preexisting hypothyroidism via a common pathway of respiratory decompensation with carbon dioxide narcosis leading to coma. Without early and appropriate therapy, the outcome is often fatal. The diagnosis is based on history and physical find‑ ings at presentation and not on any objective thyroid laboratory test. Clinically based scoring systems have been proposed to aid in the diagnosis. While it is a relatively rare syndrome, the typical patient is an elderly woman (thyroid hypofunction being much more common in women) who may or may not have a history of previously diagnosed or treated thyroid dysfunction. Thyrotoxic storm or thyroid crisis is also a rare condition, established on the basis of a clinical diagnosis. The diagnosis is based on the pres‑ ence of severe hyperthyroidism accompanied by elements of systemic decompensation. Considering that mortality is high without aggressive treatment, therapy must be initiated as early as possible in a critical care setting.
    [Show full text]
  • Uncommon Causes of Thyrotoxicosis*
    CONTINUING EDUCATION Uncommon Causes of Thyrotoxicosis* Erik S. Mittra1, Ryan D. Niederkohr1, Cesar Rodriguez1, Tarek El-Maghraby2,3, and I. Ross McDougall1 1Division of Nuclear Medicine and Molecular Imaging Program at Stanford, Department of Radiology, Stanford University Hospital and Clinics, Stanford, California; 2Nuclear Medicine, Cairo University, Cairo, Egypt; and 3Nuclear Medicine, Saad Specialist Hospital, Al Khobar, Saudi Arabia Several of the conditions are self-limiting and do not need Apart from the common causes of thyrotoxicosis, such as prolonged treatment. Graves’ disease and functioning nodular goiters, there are When a patient is thought to be thyrotoxic, a convenient more than 20 less common causes of elevated free thyroid hor- algorithm is to measure free thyroxine (free T ) and mones that produce the symptoms and signs of thyrotoxicosis. 4 thyrotropin (TSH). When the former is higher than normal This review describes these rarer conditions and includes 14 il- lustrative patients. Thyrotropin and free thyroxine should be but the latter is suppressed, thyrotoxicosis is diagnosed. measured and, when the latter is normal, the free triiodothyronine When the former is normal but TSH is low, it is valuable to 123 level should be obtained. Measurement of the uptake of Iis measure free triiodothyronine (free T3); when the latter is recommended for most patients. abnormally high, the diagnosis is T3 toxicosis (2–4). When Key Words: thyrotoxicosis; Graves’ disease; thyroiditis; thyroid both free hormones are normal but TSH is low, the term hormones ‘‘subclinical thyrotoxicosis’’ can be applied (5). Once it has J Nucl Med 2008; 49:265–278 been determined that thyrotoxicosis is present, measure- DOI: 10.2967/jnumed.107.041202 ment of 123I uptake can differentiate among several disor- ders (Table 1).
    [Show full text]
  • Subacute Thyroiditis: Diagnostic Difficulties and Simple Treatment
    SUBACUTE THYROIDITIS: DIAGNOSTIC DIFFICULTIES AND SIMPLE TREATMENT Joel I. Hamburger Northland Thyroid Laboratory, Southfield, Michigan Subacute thyroiditis (SAT) constitutes 0.8% produce the systemic manifestations of hyperthyroid of referrals to Northland Thyroid Laboratory ism, usually mild. and is one tenth as common as hyperthyroidism. The laboratory abnormalities are readily under The peak age is 30—SOyears, and women pre standable in terms of the underlying pathophysiology. dominated by a factor of 4.5. Two thirds of the As a consequence of the diffuse inflammation, the patients presented in typical fashion with a thyroidal uptake of radioactive iodine (RAI) is im painful tender goiter, but for one third the paired (1—9). The discharge of thyroid hormone presentation was atypical in that there was no elevates serum thyroxine values (ST4) (1—9). The pain, the principal complaint in most cases erythrocyte sedimentation rate (ESR) is elevated being painless goiter, thyroid nodule, or fea as a nonspecific response to inflammation (1—9), and tures of hyperthyroidism. Elevated erythrocyte occasionally there is an increase in the white blood sedimentation rates were found in all typical cell count (WBC) as well (3,6—9). patients and in 11 of 14 atypical patients. As the disease progresses the local and systemic Serum thyroxine iodide values were elevated in features decline until full recovery is realized, usually two thirds of the patients, typical and atypi within 2—4months. In some instances there is a cal. The radioactive iodine uptake was sub temporary hypothyroid phase (2,3) which rarely nornwl for all and responded subnormally to may prove permanent (10) .
    [Show full text]