Administration of thyroxine in treated Graves' disease. Effects on the level of antibodies to thyroid-stimulating hormone receptors and on the risk of recurrence of hyperthyroidism

BACKGROUND. Antibodies to thyroid-stimulating hormone (TSH) receptors that stimulate the thyroid gland cause hyperthyroidism in patients with Graves' disease, and their production during antithyroid drug treatment is an important determinant of the course of the disease. One factor that might contribute to the persistent production of antibodies to TSH receptors is stimulation of the release of thyroid antigens by TSH during antithyroid drug therapy. We therefore studied the effect of the suppression of TSH secretion by thyroxine on the levels of antibodies to TSH receptors after thyroid hormone secretion had been normalized by methimazole. METHODS AND RESULTS. The levels of antibodies to TSH receptors were measured during treatment with methimazole, either alone or in combination with thyroxine, in 109 patients with hyperthyroidism due to Graves' disease. The patients first received 30 mg of methimazole daily for six months. All were euthyroid after six months, and their mean (+/- SD) level of antibodies to TSH receptors decreased from 64 +/- 9 percent to 25 +/- 15 percent (P less than 0.01; normal, 2.9 +/- 1.4 percent). Sixty patients then received 100 micrograms of thyroxine and 10 mg of methimazole and 49 received placebo and 10 mg of methimazole daily for one year. In the thyroxine-treated group, the mean serum thyroxine concentration increased from 108 +/- 16 nmol per liter to 145 +/- 11 nmol per liter (P less than 0.01), and the level of antibodies to TSH receptors decreased from 28 +/- 10 percent to 10 +/- 3 percent after one month of combination therapy. In the patients who received placebo and methimazole, the mean serum thyroxine concentration decreased and the level of antibodies to TSH receptors did not change. Methimazole, but not thyroxine or placebo, was discontinued in each group 1 1/2 years after the beginning of treatment. The level of antibodies to TSH receptors further decreased (from 6.6 +/- 3.2 percent at the time methimazole was discontinued to 2.1 +/- 1.2 percent one year later) in the patients who continued to receive thyroxine, but it increased (from 9.1 +/- 4.8 percent to 17.3 +/- 5.8 percent during the same period) in the patients who received placebo. One patient in the thyroxine-treated group (1.7 percent) and 17 patients in the placebo group (34.7 percent) had recurrences of hyperthyroidism within three years after the discontinuation of methimazole. CONCLUSIONS. The administration of thyroxine during antithyroid drug treatment decreases both the production of antibodies to TSH receptors and the frequency of recurrence of hyperthyroidism.     

不同甲状腺功能绝经前女性血清饥饿素与全身骨量、肌肉量、体重的相关分析

目的:探讨不同甲状腺功能的绝经前女性血清饥饿素(ghrelin)水平与其身体成份骨量(BMC)、脂肪量(FM)、肌肉量(LM)的相互关系。方法:采用放射免疫分析法检测71例不同甲状腺功能的绝经前女性其中包括甲状腺机能亢进(甲亢)组33例、甲状腺机能减低(甲减)组18例、正常对照组20例的血清饥饿素水平,同时采用化学发光快速检测法检测其血清游离三碘甲状腺原氨酸(FT3)、游离甲状腺素(FT4)、灵敏促甲状腺激素(sTSH);并采用双能X线吸收法(DXA)测定其全身身体成份(骨量、脂肪量、肌肉量),同时记录体重(BW)。结果:(1)甲亢组血清饥饿素水平明显低于正常对照组(P0.01)和甲减组(P0.01),甲减组血清饥饿素水平与正常对照组之间无显著差别(P0.05)。血清饥饿素与其FT3(r=-0.318,P0.01)、FT4(r=-0.350,P0.01)呈负相关,与sTSH(r=0.281,P0.05)呈正相关。(2)血清饥饿素与全身骨量(r=0.284,P0.05)、肌肉量(r=0.259,P0.05)、体重(r=0.279,P0.05)存在正相关;与脂肪量不存在相关(P0.05)。结论:不同甲状腺功能的绝经前女性血清饥饿素可能影响其全身骨量、肌肉量、体重。     

Increased serum PIVKA-II levels in hyperthyroidism]

PIVKA-II has been practically used as a tumor marker of hepatocellular carcinoma. On the other hand, increased serum PIVKA-II concentration was reported in a Japanese patient who had hyperthyroidism without liver diseases. To evaluate whether thyroid hormone is related with serum PIVKA-II, we examined serum PIVKA-II concentrations in patients with various thyroid diseases. Eight patients with Hashimoto disease, 24 patients with Graves' disease, and 8 healthy subjects were studied. There was no significant difference of serum PIVKA-II levels among the three groups. However, serum PIVKA-II concentrations(mean +/- SD mAU/ml) in hyperthyroidism(37 +/- 27) were significantly higher than those in hypothyroidism(16 +/- 9) and normal controls(12 +/- 4) (p < 0.05 and p < 0.01, respectively). When hyperthyroid patients were treated by antithyroid drug or isotope, serum PIVKA-II concentrations decreased in accordance with the decrease of serum FT4 concentrations. Our data indicate that serum PIVKA-II concentration was increased in patients with hyperthyroidism, but further in vivo studies are necessary to clarify the mechanism related to increased serum PIVKA-II by thyroid hormone.     

胱抑素C在131I治疗甲亢中的应用价值

目的 探讨胱抑素C在131I治疗甲亢中的临床应用价值.方法 选择2011年2月至2012年10月在我院131I治疗的43例甲亢患者和40例健康者（对照组）进行甲状腺激素、血清胱抑素C（CysC）水平的比较;并观察甲亢患者131I治疗后3个月、6个月与治疗前的甲状腺激素、血清胱抑素C（CysC）与血清肌酐（Cr）水平变化.结果 甲亢患者血清CysC水平增高,随着甲亢患者131I治疗后甲状腺激素水平的恢复,血清CysC水平降低（P＜0.05）.结论 血清胱抑素C（CysC）可以作为甲亢的辅助检测项目和131I治疗后疗效判定的辅助诊治指标.     

Diagnosis of peripheral thyroid hormone effect using sex hormone-binding globulin (SHBG) and systolic time intervals (STI)

Only in rare cases with peripheral resistance to thyroid hormones, low T3 syndrome and inappropriate TSH secretion a laboratory determination of the effects of thyroid hormones on peripheral organs such as BMR, Achilles sinew reflex, cholesterol, SHBG, STI etc. is necessary. It was demonstrated that serum concentration of SHBG offered a clear and reliable parameter of the effects of thyroid hormones on liver cells. In a group of 31 patients with overt hyperthyroidism the level of SHBG being 136.5 nmol@l was significantly higher (p less than 0.001) than in control patients showing 36.3 nmol/l SHBG. The hypothyroid group (32 patients) showed a rather significant reduction (p less than 0.01) in SHBG level with a median of 27.5 nmol/l. Among the systolic time intervals the preejection period (PEP) and the LVET/PEP ratio were the most striking parameters. In the hyperthyroid group there was a highly significant shorter interval of PEP (p less than 0.001) and a significant rise of the LVET/PEP ratio (p less than 0.01) compared with the control patients. In the hypothyroid group a hardly perceptible extension of PEP (p less than 0.01) was observed, but a highly significant decrease of the LVET/PEP ratio (p less than 0.001) could be demonstrated.     

Increased serum soluble Fas ligand in hyperthyroid Graves' disease

The interaction of Fas with its ligand (FasL) regulates a number of physiological and pathophysiological process of cell death or apoptosis. Recent studies suggest that Fas and Fas ligand (FasL) interactions among thyrocytes from patients with Hashimoto disease which is caused by thyroid autoimmunity may contribute to clinical hypothyroidism. The role of Fas-FasL interaction in the pathophysiology of Graves' disease has not well been determined. The serum levels of soluble Fas (sFas) and FasL (sFasL) were measured in 48 Japanese patients with Graves' disease (U; untreated hyperthyroidism, T; hyperthyroidism under treatment, E; euthyroidism under treatment and R; remission), destructive thyroiditis (D), subacute thyroiditis (S) and 40 normal controls using commercially available ELISA kits. The levels of sFas (mean +/- SD, ng/ml) were 0.93 +/- 0.30 in normal controls (n = 32), 2.41 +/- 1.28 in U (n = 19), 2.44 +/- 0.79 in T (n = 16), 2.37 +/- 0.55 in E (n = 12), and 2.30 +/- 0.11 in R (n = 6), 2.42 +/- 0.37 in D (n = 3) and 2.68 +/- 0.17 in S (n = 3). There were no significant differences of sFas levels among any groups. While, the mean levels of sFasL (ng/ml) of normal controls were 0.058 +/- 0.02 (n = 40), and those of patients with hyperthyroid Graves' disease (U; 0.34 +/- 0.09 and T; 0.26 +/- 0.05), were significantly higher than those in normal controls (p < 0.005) and with subacute thyroiditis (0.097 +/- 0.001, vs U; p < 0.01, vs T; p < 0.05) but not different from those in E, R and D (E; 0.34 +/- 0.09, R; 0.25 +/- 0.07 and D; 0.31 +/- 0.11, respectively). There was a significant correlation between serum thyrotropin receptor antibody (TRAb) and free thyroxine levels (p < 0.01) while there were no correlation between sFas and sFasL levels and TRAb or free thyroxine levels. The results indicate that the Fas-FasL system contributes to the pathophysiology of hyperthyroid Graves' disease although serum sFas and sFasL levels do not appear to be useful indicators in evaluating disease activity.     

Increased need for thyroxine during pregnancy in women with primary hypothyroidism

BACKGROUND AND METHODS. Women with hypothyroidism have been thought not to require an increase in thyroxine replacement during pregnancy. To evaluate the effects of pregnancy on thyroxine requirements, we retrospectively reviewed the thyroid function of 12 women receiving treatment for primary hypothyroidism before, during, and after pregnancy. RESULTS. In all patients, the serum thyrotropin level increased during pregnancy. The mean (+/- SE) serum free-thyroxine index decreased from 111.0 +/- 5.8 before pregnancy to 86.5 +/- 5.2 during pregnancy (normal, 64 to 142; P less than 0.05), and the mean serum thyrotropin level increased from 2.0 +/- 0.5 mU per liter before pregnancy to 13.5 +/- 3.3 mU per liter during pregnancy (normal, 0.5 to 5.0 mU per liter; P less than 0.01). Because of high thyrotropin levels, the thyroxine dose was increased in 9 of the 12 patients. Among the three patients who did not require an increased thyroxine dose were two with low serum thyrotropin levels before pregnancy, suggesting excessive replacement at that time. The mean thyroxine dose before pregnancy was 0.102 +/- 0.009 mg per day; it was increased to 0.148 +/- 0.015 mg per day during pregnancy (P less than 0.01). The mean postpartum serum free-thyroxine index was 136.6 +/- 11.4 (P less than 0.05 as compared with values before and during pregnancy), and the mean postpartum serum thyrotropin level was 1.4 +/- 0.4 mU per liter (P less than 0.01 as compared with levels during pregnancy), demonstrating a decrease in the thyroxine requirement. The mean postpartum thyroxine dose was decreased to 0.117 +/- 0.011 mg per day (P less than 0.01 as compared with the dose during pregnancy). CONCLUSIONS. Our results indicate that the need for thyroxine increases in many women with primary hypothyroidism when they are pregnant, as reflected by an increase in serum thyrotropin concentrations. Although the effects of this modest level of hypothyroidism are not known, we think it prudent to monitor thyroid function throughout gestation and after delivery and to adjust the thyroxine dose to maintain a normal serum thyrotropin level.     

Impaired responses of plasma catecholamines to exercise in diabetic patients with abnormal heart rate reactions to tilt

The plasma catecholamine response to a standardized bicycle exercise test was evaluated in 24 insulin-dependent diabetic (IDDM) patients in whom the heart rate reactions to deep breathing (E/I ratio) and to tilt, the immediate acceleration and the transient deceleration (acceleration and brake indices), had been assessed as tests of autonomic neuropathy. Patients with an abnormal acceleration index (n = 8) showed, compared with non-diabetic (n = 18) controls who had participated in previous studies, an impaired increment in noradrenaline during exercise (80% of maximal working capacity) (MWC) (12.38 +/- 1.46 nmol l-1 vs. 18.74 +/- 1.45 nmol l-1; P less than 0.01) and adrenaline (50% of MWC: 0.25 +/- 0.04 nmol l-1 vs. 0.54 +/- 0.08 nmol l-1; P less than 0.05). Similarly, patients with an isolated abnormal brake index (n = 6), i.e. with a normal acceleration index and a normal E/I ratio, showed compared with controls an impaired increment in noradrenaline (9.53 +/- 1.66 nmol l-1 vs. 18.74 +/- 1.45 nmol l-1; P less than 0.01) and adrenaline (1.41 +/- 0.22 nmol l-1 vs. 2.92 +/- 0.51 nmol l-1; P less than 0.05) during 80% of MWC. IDDM patients with abnormal heart rate reactions to tilt, an abnormal acceleration index or an abnormal brake index show impaired catecholamine responses to exercise, which can be demonstrated also in patients without signs of parasympathetic neuropathy.     

Long-term growth in juvenile acquired hypothyroidism: the failure to achieve normal adult stature

It has been suggested that complete catch-up growth is achieved with treatment in patients with juvenile acquired hypothyroidism. We tested this assumption by examining long-term growth in 18 girls (mean [+/- SD] age, 11.4 +/- 2.7 years; bone age, 6.2 +/- 3.1 years) and 6 boys (age, 10.6 +/- 4.7 years; bone age, 6.4 +/- 2.7 years) with severe primary hypothyroidism (serum thyroxine level 1.1 +/- 0.3 micrograms per deciliter [13 +/- 4 nmol per liter]). At diagnosis, heights were 4.04 +/- 0.5 and 3.15 +/- 0.4 SD below the mean heights for age of normal girls and boys, respectively. The patients were treated with levothyroxine (3.4 +/- 0.3 micrograms per kilogram of body weight per day) to maintain normal thyroid function. During the first 18 months of therapy, the children's skeletal maturation exceeded the maturation expected for their statural growth, regardless of whether or not they were undergoing pubertal development. Predictions of decreased adult height were based on these observations. At maturity, girls and boys stood approximately 2 SD below normal adult stature, at 149 +/- 5.0 cm and 168 +/- 5.1 cm, respectively. Heights at maturity were also lower than midparental heights (P less than 0.01) and lower than pre-illness standard-deviation scores for height (P less than 0.01). The deficit in adult stature was significantly related to the duration of hypothyroidism before treatment (P less than 0.01). We conclude that despite treatment, prolonged juvenile acquired hypothyroidism results in a permanent height deficit related to the duration of thyroxine deficiency before treatment.     

The effect of iodine restriction on thyroid function in patients with hypothyroidism due to Hashimoto's thyroiditis

Lifelong thyroid hormone replacement is indicated in patients with hypothyroidism as a result of Hashimoto's thyroiditis. However, previous reports have shown that excess iodine induces hypothyroidism in Hashimoto's thyroiditis. This study investigated the effects of iodine restriction on the thyroid function and the predictable factors for recovery in patients with hypothyroidism due to Hashimoto's thyroiditis. The subject group consisted of 45 patients who had initially been diagnosed with hypothyroidism due to Hashimoto's thyroiditis. The subjects were divided randomly into two groups. One group was an iodine intake restriction group (group 1) (iodine intake: less than 100 micro g/day) and the other group was an iodine intake non-restriction group (group 2). The thyroid-related hormones and the urinary excretion of iodine were measured at the baseline state and after 3 months. After 3 months, a recovery to the euthyroid state was found in 78.3 % of group 1 (18 out of 23 patients), which is higher than the 45.5% from group 2 (10 out of 22 patients). In group 1, mean serum fT4 level (0.80 +/- 0.27 ng/dL at the baseline, 0.98 +/- 0.21 ng/dL after 3 months) and the TSH level (37.95 +/- 81.76 micro IU/mL at the baseline, 25.66 +/- 70.79 micro IU/mL after 3 months) changed significantly during this period (p < 0.05). In group 2, the mean serum fT4 level decreased (0.98 +/- 0.17 ng/dL at baseline, 0.92 +/- 0.28 ng/dL after 3 months, p < 0.05). In the iodine restriction group, the urinary iodine excretion values were higher in the recovered patients than in non-recovered patients (3.51 +/- 1.62 mg/L vs. 1.21 +/- 0.39 mg/ L, p=0.006) and the initial serum TSH values were lower in the recovered patients than in the non-recovered patients (14.28 +/- 12.63 micro IU/mL vs. 123.14 +/- 156.51 micro IU/mL, p=0.005). In conclusion, 78.3% of patients with hypothyroidism due to Hashimoto's thyroiditis regained an euthyroid state iodine restriction alone. Both a low initial serum TSH and a high initial urinary iodine concentration can be predictable factors for a recovery from hypothyroidism due to Hashimoto's thyroiditis after restricting their iodine intake.     

Effects of the phytoestrogen genistein on cardiovascular risk factors in postmenopausal women

OBJECTIVE: The phytoestrogen genistein has been shown to be the most efficacious in clinical and experimental studies. We studied whether genistein treatment affects some cardiovascular risk markers in postmenopausal women. DESIGN: Sixty healthy postmenopausal women, who were 52 to 60 years of age, were enrolled in a 6-month double-blind, placebo-controlled, randomized study. After a 4-week stabilization on a standard fat-reduced diet, participants were randomly assigned to receive either genistein (n = 30; 54 mg/d) or placebo (n = 30). At baseline and after a 6-month treatment, we measured fasting glucose, insulin, insulin resistance (HOMA-IR), osteoprotegerin (OPG), fibrinogen, and sex hormone-binding globulin (SHBG). RESULTS: By comparison with placebo, genistein treatment decreased significantly fasting glucose (genistein = -8.7 +/- 2.3%; placebo = 3.2 +/- 2.3%; P < 0.001), fasting insulin (genistein = -12 +/- 3.33%; placebo = 36 +/- 3.29%; P < 0.001), and HOMA-IR (genistein = -14 +/- 5.8%; placebo = 42 +/- 0.6%; P < 0.001). After genistein-treatment, fibrinogen decreased (genistein = 3.18 +/- 0.12 g/L; placebo = 3.83 +/- 0.04 g/L; P < 0.001) with respect to placebo. In the genistein group, serum OPG was lower (-2 +/- 0.3%) than in placebo (9 +/- 1.5%; P < 0.001), and serum SHBG was higher (63 +/- 3.8 nmol/L) compared with placebo (53 +/- 2.9 nmol/L; P < 0.05). CONCLUSION: Our study suggests that genistein may have a favorable effect on some cardiovascular markers.     

中青年男性血清睾酮水平变化的初步探讨

了解健康中、青年男性血清性激素水平的变化.选取126例健康男性分为20～29岁、30～39岁、40～49岁共3个年龄组.分别测定血清睾酮(T)、游离睾酮(FT)、性激素结合球蛋白(SHBG)、雌二醇(E2)、黄体生成素(LH)、卵泡刺激素(FSH),对各组测定值进行统计学分析.结果显示:血清T、FT水平在30～39岁组...     

Thyroid function tests in elderly Finnish men

Serum total thyroxine (T4), triiodothyronine (T3) and thyrotrophin (TSH) levels were determined among 65-84-year-old Finnish men living either in eastern Finland (n = 309) or in southwestern Finland (n = 389). The mean value for serum total T4 was 112.2 +/- 23.0 nmol/l in eastern Finland and 111.3 +/- 21.9 nmol/l in southwestern Finland. The mean value for serum T3 was 1.76 +/- 0.30 nmol/l in eastern Finland and 1.75 +/- 0.46 nmol/l in southwestern Finland. Serum TSH values showed the mean for men from eastern Finland to be 3.25 +/- 2.29 mU/l and the mean for men from southwestern Finland to be 3.11 +/- 1.83 mU/l. No differences were found in the means of the thyroid function tests between the two areas. Serum T4 levels were not related to age. Serum T3 values fell with age. In both areas, serum TSH levels were highest among men 70-74 years of age.     

甲亢和甲减患者血清PTH、CT水平的变化

目的：探讨了甲亢和甲减患者血清甲状旁腺素（PTH）和降钙素（CT）水平的变化。方法：应用放射免疫分析法测定了62例甲亢患者和32例原发性甲减患者血清中PTH、CT含量,并以35名健康人作对照。结果：甲亢组血清PTH水平低于正常人组（P＜0．05）、甲减组高于正常人组（P＜0．01）,CT水平两组均低于正常人组（P＜0．01）。结论：测定甲亢和甲减病人血清中PTH、CT水平的变化对了解病情,指导临床实践均有重要的临床意义 。     

Association between thyroid microsomal antibodies of subclass IgG-1 and hypothyroidism in autoimmune postpartum thyroiditis

The potential role of thyroid microsomal (Mic) antibodies in the development of postpartum hypothyroidism was investigated in 34 euthyroid women, whose sera were found to contain Mic antibodies in pregnancy. Additional serum samples were obtained 2. 5 and 10-12 months after delivery and analysed for IgG class and IgG subclass levels of Mic antibodies by ELISA techniques. Characteristically, Mic antibodies decreased from early pregnancy to 2 months postpartum, increased two-fold 5 months postpartum and had returned 10-12 months postpartum to the early pregnancy level. Mic antibodies were predominantly subclass IgG-1 or IgG-4 with only minor contributions from IgG-2 and IgG-3. In each individual the percentage contribution made by each IgG subclass to Mic antibody was essentially similar in early pregnancy and the postpartum period despite changes in total IgG class Mic antibody. During the year following delivery, thyrotoxicosis alone (Graves' disease) developed in 5 women. In the remaining 29 patients the absolute levels of Mic antibodies of IgG-4 subclass were similar 5 months postpartum in women with maximal serum thyrotropin (TSH) greater than 20 mU/1 (mean optical density in ELISA +/- s.d.; 0.84 +/- 0.538; n = 13) and in women with maximal TSH less than 10 mU/l (0.69 +/- 0.457; n = 16). In contrast, significantly higher values were observed for Mic antibody of IgG-1 subclass in patients with TSH greater than 20 mU/l (1.14 +/- 0.440) compared with women with maximal TSH less than 10 mU/l (0.65 +/- 0.289) (P less than 0.001 by t-test for groups). These results imply that the magnitude of Mic antibody levels of subclass IgG-1 but not IgG-4 is associated with the development of postpartum hypothyroidism and possibly with tissue destruction in autoimmune thyroid disease in general.     

Use of plasma iodine assay for diagnosing thyroid disorders.

AIMS--To examine the advantage of systematic plasma iodine assays in establishing the thyroid function of patients with thyroid disorders. METHODS--Iodine was determined by inductively coupled plasma mass spectrometry (ICPMS) in the plasma of 799 patients consulting for possible thyroid disorders, indicated by FT4 and TSH assays. RESULTS--Plasma iodine was below 40 micrograms/l in 57 (7%) patients, most of whom had hypothyroidism; 40-80 micrograms/l in 439 (55%) patients, most of whom had normal thyroid hormone function; 80-250 micrograms/l in 240 (30%) patients, most of whom had hyperthyroidism; and above 250 micrograms/l in 63 (8%) patients, almost all of whom had iodine overload caused by iodinated drugs, particularly amiodarone, resulting in euthyroidism (24%), hyperthyroidism (36%), and hypothyroidism (16%). Sixty five (7%) had been treated with amiodarone and 27 (3%) with other iodinated drugs. More than 10% of patients with thyroid disorders therefore had an iodine overload. CONCLUSIONS--The determination of total plasma iodine using the simple, accurate ICPMS technique, should be carried out in patients consulting for thyroid disorders, particularly for the detection of an iodine overload.     

Increased need for thyroxine in women with hypothyroidism during estrogen therapy

BACKGROUND: Women with hypothyroidism that is being treated with thyroxine often need higher doses when they are pregnant. Whether this need can be attributed solely to estrogen-induced increases in serum thyroxine-binding globulin or whether other factors are involved is not known. METHODS: In 11 postmenopausal women with normal thyroid function and 25 postmenopausal women with hypothyroidism treated with thyroxine, I assessed thyroid function before they started estrogen therapy and every 6 weeks for 48 weeks thereafter. The women with hypothyroidism included 18 women receiving thyroxine-replacement therapy and 7 women receiving thyrotropin-suppressive thyroxine therapy. On each occasion, serum thyroxine, free thyroxine, thyrotropin, and thyroxine-binding globulin were measured. RESULTS: In the women with normal thyroid function, the serum free thyroxine and thyrotropin concentrations did not change, whereas at 12 weeks the mean (+/-SD) serum thyroxine concentration had increased from 8.0+/-0.9 microg per deciliter (103+/-12 nmol per liter) to 10.4+/-1.5 microg per deciliter (134+/-19 nmol per liter, P<0.001) and the serum thyroxine-binding globulin concentration had increased from 20.3+/-3.5 mg per liter to 31.3+/-3.2 mg per liter, P<0.001). The women with hypothyroidism had similar increases in serum thyroxine and thyroxine-binding globulin concentrations during estrogen therapy, but their serum free thyroxine concentration decreased from 1.7+/-0.4 ng per deciliter (22+/-5 pmol per liter) to 1.4+/-0.3 ng per deciliter (18+/-4 pmol per liter, P<0.001) and their serum thyrotropin concentration increased from 0.9+/-1.1 to 3.2+/-3.1 microU per milliliter (P<0.001). The serum thyrotropin concentrations increased to more than 7 microU per milliliter in 7 of the 18 women in the thyroxine-replacement group and to more than 1 microU per milliliter in 3 of the 7 women in the thyrotropin-suppression group. CONCLUSIONS: In women with hypothyroidism treated with thyroxine, estrogen therapy may increase the need for thyroxine.     

Undetectable serum IgA and low IgM concentration in children with congenital hypothyroidism

Some studies suggest thyroid hormones may regulate the human immune system. In order to evaluate the effect of thyroid hormone deficiency on antibody production, we evaluated serum IgA and IgM concentrations in 83 children with congenital hypothyroidism (CH), diagnosed by neonatal screening. Patients were compared to two healthy, age-matched control groups. Patients with permanent CH had a significantly higher frequency of undetectable IgA concentrations (thyroid agenesis, P<10(-5); thyroid ectopy, P=0.013) and lower concentrations of IgA (thyroid agenesis, P<10(-6); thyroid ectopy, P<10(-5); dyshormonogenesis, P=0.0002) and IgM (thyroid agenesis, P=0.0002; thyroid ectopy, P<10(-6); dyshormonogenesis, P=0.0017) compared to control group. No difference was observed between patients with transient hypothyroidism and controls. A significant correlation was observed between serum IgA and IgM concentrations and fT4 levels. IgA and IgM deficiency is correlated with the severity of congenital hypothyroidism and may help to evaluate the duration and severity of thyroid hormone deficiency during prenatal life.     

甲状腺疾病与血清骨钙素的关系及其临床意义

观察各种甲状腺疾病治疗前、后血清骨钙素的变化，以探讨甲状腺功能异常与骨代谢的关系。本文对236例甲状腺疾病患者及52名健康志愿者为对照组，采用酶放大化学发光法测定了血清骨钙素(BGP)、FT3、FT4、TSH和人甲状腺球蛋白(HTG)。结果显示：正常人血清骨钙素水平随着年龄的增高而逐渐降低；甲亢患者治疗前。BGP浓度明显升高；甲减患者治疗前BGP浓度明显低于正常，经短期甲状腺紊替代治疗后，BGP浓度明显高于正常；治疗前的亚甲炎患者BGP浓度明显高于对照组，用糖皮质激素治疗后，BGP浓度反低于正常水平。相关统计表明，治疗前、后的甲亢、甲减和亚甲炎患者BGP与FT3、FT4之间呈明显的正相关；甲减患者BGP与TSH呈负相关。实验结果显示甲状腺激素可能直接参与加速骨转换过程，并以增加骨吸收过程为显著；糖皮质激素可使骨转换率减低，骨的形成降低，最终都可能导致骨矿丢失。     

Effect of vitamin D intake on seasonal variations in parathyroid hormone secretion in postmenopausal women

Vitamin D intake should be sufficient to maintain calcium absorption and prevent increased parathyroid secretion throughout the year. To determine the level of intake that achieved the latter in elderly women, we studied the interrelations among vitamin D intake, serum 25-hydroxyvitamin D (25(OH)D) levels, and parathyroid hormone concentrations in a cross-sectional study of 333 healthy, white, postmenopausal women with low median calcium (408 mg a day) and vitamin D (112 IU a day) intakes who lived in Massachusetts. The overall inverse relation between serum parathyroid hormone and 25(OH)D levels was found to be dependent on vitamin D intake. In women whose estimated intake of vitamin D was less than or equal to 220 IU a day, the mean (+/- SD) serum parathyroid hormone values were lowest in those studied between August and October (30 +/- 11 ng per liter; n = 72) and highest in those studied between March and May (37 +/- 16 ng per liter; n = 54); the respective serum 25(OH)D levels were 93 +/- 32 and 63 +/- 21 nmol per liter. At vitamin D intakes of more than 220 IU a day, the mean serum parathyroid hormone and 25(OH)D levels did not vary with the season. The correlation between vitamin D intake and serum 25(OH)D concentration, although significant in all women (r = 0.29; P less than 0.001), was highest in those studied between March and May (r = 0.65; P less than 0.001) and lowest in those studied between August and October (r = 0.13; P greater than 0.10). The estimated serum 25(OH)D level associated with a vitamin D intake of 220 IU a day between March and May was 95 nmol per liter. Mean serum calcium values were similar at all times in both groups. We conclude that the dietary intake of more than 220 IU of vitamin D a day by postmenopausal women in Massachusetts may be sufficient to maintain constant serum 25(OH)D and parathyroid hormone concentrations throughout the year. Such an intake prevents a seasonal increase in parathyroid hormone secretion, with its possible deleterious skeletal effects.