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OBSERVATIONS Range 11–325), Ruling out a Condition of References Iron Overload LETTERS were 14, 82, and 113 pmol/l (normal ●●●●●●●●●●●●●●●●●●●●●●● OBSERVATIONS range 11–325), ruling out a condition of References iron overload. 1. Escobar-Morreale HF, Luque-Ramı´rez M, Forty-eight of the patients (61.5%) Alvarez-Blasco F, Botella-Carretero JI, and 24 of the control subjects (55.8%) Sancho J, San Milla´n JL: Body iron stores are increased in overweight and obese Mutations in the had one or more mutated alleles of the Hereditary women with polycystic ovary syndrome C282Y and H63D genotype alleles, (Brief Report). Diabetes Care 28:2042– Hemochromatosis whereas all other women were homozy- 2044, 2005 gous for wild-type alleles of both HFE 2. Sanchez M, Bruguera M, Bosch J, Rodes J, Gene Are Not 2 mutations (␹ ϭ 0.377, P ϭ 0.539). The Ballesta F, Oliva R: Prevalence of the Associated With the HFE mutations studied here did not influ- Cys282Tyr and His63Asp HFE gene mu- Increased Body Iron ence serum ferritin levels when consider- tations in Spanish patients with heredi- ing PCOS patients and control subjects as tary hemochromatosis and in controls. Stores Observed in a whole (C282C [n ϭ 110] 109 Ϯ 94 J Hepatol 29:725–728, 1998 Overweight and pmol/l vs. C282Y [n ϭ 11]110 Ϯ 115 Obese Women With pmol/l [F ϭ 0.122, P ϭ 0.728]; H63H [n ϭ 57] 108 Ϯ 98 pmol/l vs. H63D and Polycystic Ovary D63D [n ϭ 64] 110 Ϯ 94 pmol/l [F ϭ Syndrome 0.499, P ϭ 0.481]; and interaction be- On the Weighted- tween both genotypes [Fϭ 0.834, P ϭ 0.363]) or separately (data not shown). Average e recently reported (1) that se- Finally, a multivariate stepwise linear Relationship rum ferritin levels are increased regression analysis model retained BMI Between Plasma W in overweight and obese women (␤ϭ0.263, P ϭ 0.003) and PCOS status with polycystic ovary syndrome (PCOS) (␤ϭ0.238, P ϭ 0.007) as predictive vari- Glucose and HbA1c independently of inflammation. This ables of serum ferritin levels (R2 ϭ 0.127, finding suggested increased body iron F ϭ 8.557, P Ͻ 0.001), whereas carrier stores in these women, raising the possi- status for C282Y and/or H63D mutations, bA1c (A1C) is widely used to assess bility that genes related to iron metabo- as well as having oligo/amenorrhea com- glycemic control in clinical and re- lism are altered in PCOS. pared with having regular cycles, were ex- H search settings, but the precise rela- Classic hereditary hemochromatosis cluded as predictors. tionship between A1C and preceding self- is an autosomal recessive disorder caused In summary, PCOS is not associated monitored plasma glucose measurements by mutations in the HFE gene, resulting in with the C282Y and H63D mutations in is recognized to be complex. It has been increased intestinal iron absorption and HFE, and these mutations did not influ- reported that measuring plasma glucose iron accumulation in several organs. In ence serum ferritin levels in our series. As levels in the 120 days before an A1C mea- the study by Sanchez et al. (2), Ͼ80% of discussed earlier (1), other mechanisms surement has a nonuniform effect on the the Spanish patients with hereditary are possibly related to the increase in result depending on the time that has hemochromatosis were homozygous for body iron stores observed in overweight elapsed between the glucose level and the HFE C282Y mutation or compound and obese PCOS patients. subsequent A1C measurement (1). heterozygotes for the HFE C282Y and Tahara and Shima (2) attempted to model 1 this weighted-average relationship between H63D mutations. JOSE´ I. BOTELLA-CARRETERO, MD, PHD 1 plasma glucose and A1C by measuring de- Although hereditary hemochromato- MANUEL LUQUE-RAMı´REZ, MD 1 creases in glucose and corresponding sis has low penetrance in young women, FRANCISCO A´ LVAREZ-BLASCO, MD 2 decreases in A1C in patients admitted to we studied the HFE genotypes of 78 JOSE´ L. SAN MILLAN´ , PHD 1 the hospital. Their model gives maximum PCOS patients and 43 control subjects HECTOR´ F. ESCOBAR-MORREALE, MD, PHD characterized in our previous report of in- weighting to glucose measurements im- 1 mediately before the A1C measurement, creased body iron stores in PCOS (1). From the Department of Endocrinology, Hospital Genotyping was conducted by PCR/ Ramo´n y Cajal, Madrid, Spain; and the 2Department with the weighting linearly decreasing for restriction fragment–length polymor- of Molecular Genetics, Hospital Ramo´n y Cajal, Ma- glucose measurements further back in phism methods using the PmlI and BclI drid, Spain. time, reaching zero weighting for plasma Address correspondence to He´ctor F. Escobar- glucose Ͼ120 days before the A1C. restriction enzymes for the C282Y and Morreale, Department of Endocrinology, Hospital H63D mutations, respectively. The ethics Ramo´n y Cajal, Carretera de Colmenar km 9Ј1, Trevin˜ o (3) reported that this weighted- committee of the Hospital Ramo´n y Cajal Madrid E-28034, Spain. E-mail: hescobarm.hrc@ average relationship leads to an anoma- approved the study, and informed con- salud.madrid.org. lous relationship between the exponential sent was obtained from all participants. DOI: 10.2337/dc06-1655 decay rates of glucose (G ) and A1C. We © 2006 by the American Diabetes Association. t We did not find homozygosity for the have reviewed this result and believe that C282Y substitution in HFE in any PCOS no such anomaly exists. Trevin˜ o sub- patient or control subject. Three patients Acknowledgments— This study was sup- tracted A1C calculated from the Tahara with PCOS but no control subjects were ported by grants FIS PI050341, PI050551, model (Ht) from “the mean of patient- compound heterozygotes for the C282Y and RGDM G03/212 from the Fondo de Inves- admission A1C values” (Hstart), obtaining 2 and H63D mutations (␹ ϭ 1.696, P ϭ tigacio´n Sanitaria, Instituto de Salud Carlos the counterintuitive result that a faster de- 0.552), but their serum ferritin levels III, Spain. cay in blood glucose results in a slower 2556 DIABETES CARE, VOLUME 29, NUMBER 11, NOVEMBER 2006 Letters Ϫ decay in (Hstart Ht). However, this “in- Is Pregnancy with type 2 diabetes and 532 consecutive verted” decay is likely to be due to sub- Outcome Worse in singleton pregnancies in women with tracting H from a constant value. His type 1 diabetes referred to the Diabetes t Type 2 Than in Type expression for Ht is an absolute A1C and Pregnancy Unit at University Hospi- value, not a change in A1C. An initial 1 Diabetic Women? tal La Paz from 1984 to 2004. value, Gs, has been specified for Gt, and Women with type 2 diabetes were hence an initial value is implicit in his significantly older ([means Ϯ SD] 31.8 Ϯ calculations. Subtracting H from a con- ost research on pregestational di- 5.5 vs. 29.4 Ϯ 4.7 years, P Ͻ 0.001), were t Ͻ stant would not be expected to give a valid abetes has focused on type 1 dia- more frequently obese (45.2 vs. 9%, P A1C estimate. betes, and surprisingly little 0.001), and had a shorter duration of di- M Ϯ Ϯ Ͻ To verify this conclusion, we simu- knowledge exists concerning outcomes of abetes (5.7 6 vs. 11.8 7.1 years, P pregnancies of women with type 2 diabe- 0.001). The rate of preconceptional care lated a patient with a constant glucose ϭ level followed by an exponential decay tes. A dearth of published data suggest (16.1 vs. 22.6%, P 0.175) and gesta- outcomes similar to those of type 1 dia- tional age at first visit (12.1 Ϯ 6.8 vs. upon admission to the hospital. During Ϯ ϭ the preadmission time period, the simu- betic women (1,2), although recent stud- 11.5 6.9 weeks’ gestation, P 0.529) did not differ between type 2 and type 1 lated A1C reached a steady state under the ies report poorer outcomes in women with type 2 diabetes (3–7). diabetic women. Maternal and perinatal constant glucose conditions, which We retrospectively compared mater- outcomes are shown in Table 1. Insulin avoided any ambiguity over the initial nal and perinatal outcomes of 93 consec- requirements and HbA (A1C) were value (H ) of A1C. In this simulation, 1c start utive singleton pregnancies in women lower during all three trimesters of preg- the decay rates of Ht then varied in the same way as those for the glucose data, as would be intuitively expected. The use of Table 1—Maternal and perinatal outcomes two initial values by Trevin˜ o, one for H and one for G, appears to have led to the anomalous result previously reported, Type 2 Type 1 rather than any inherent defect in the diabetes diabetes P weighted-average relationship proposed n* 93 532 by Tahara and Shima. Prepregnancy BMI (kg/m2) 28.9 Ϯ 6.5 23.3 Ϯ 3.1 Ͻ0.001 Maternal weight gain during 11.7 Ϯ 5.0 13.7 Ϯ 4.2 Ͻ0.001 pregnancy (kg) OLIVER J. GIBSON, MENG Glycemic control during pregnancy PATRICK E. MCSHARRY, DPHIL A1C at admission (%) 6.4 Ϯ 1.19 7.2 Ϯ 1.19 Ͻ0.001† LIONEL TARASSENKO, DPHIL A1C second trimester (%) 5.8 Ϯ 0.84 6.3 Ϯ 0.9 Ͻ0.001† A1C third trimester (%) 5.8 Ϯ 0.76 6.2 Ϯ 0.8 0.001† Insulin requirements From the Department of Engineering Science, Uni- Ϯ Ϯ Ͻ versity of Oxford, Oxford, U.K. First trimester (units/kg) 0.38 0.19 0.68 0.18 0.001† Address correspondence to Oliver J.
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