Lower serum free thyroxine (T4) levels in painless thyroiditis compared with Graves' disease despite similar serum total T4 levels

Serum total T4 (T4), total T3 (T3), free T4 (FT4), free T3 (FT3), and T4-binding globulin concentrations and T3 resin uptake values were measured in 17 women with thyrotoxicosis due to painless thyroiditis (PT) and compared with the same parameters in 17 women with thyrotoxicosis due to Graves' disease (GD) with similar serum T4 levels. The mean serum T3 resin uptake value and T3, FT4, and FT3 concentrations in the PT patients were significantly lower than those in the GD patients. The mean serum T4-binding globulin concentration [20.2 +/- 4.2 (+/- SD) microgram/mL] in patients with PT did not differ significantly from those in patients with GD (18.0 +/- 2.6 micrograms/mL) and normal euthyroid women (21.9 +/- 4.0 micrograms/mL). The serum T3 to T4 (nanogram per microgram) ratio was higher than 20 in 14 GD patients, but lower than 20 in all patients with PT, whereas the individual serum FT3 to FT4 ratio values considerably overlapped in the 2 groups. In patients with PT, FT4 correlated well with T4 at various times during the clinical course. These findings indicate that the elevation in serum FT4 in patients with PT is mostly due to the increase in circulating T4 levels, whereas GD patients also have some diminution in T4 binding. The serum T3 to T4 ratio, but not the FT3 to FT4 ratio, may be helpful for differentiation between the two diseases.     

3,5,3'-Triiodothyronine thyrotoxicosis due to increased conversion of administered levothyroxine in patients with massive metastatic follicular thyroid carcinoma

OBJECTIVE: Some patients with massive metastatic thyroid carcinoma exhibit T(3) thyrotoxicosis. We investigated the prevalence and cause of T(3) thyrotoxicosis and the clues to the diagnosis. DESIGN: Serum free T(3) (FT(3)), free T(4) (FT(4)), and TSH were measured in patients with massive metastases from papillary, follicular, or medullary thyroid carcinomas (31, 20, and seven patients, respectively). Patients without recurrence served as controls. Thyrotoxic patients were reexamined 1 wk after withdrawal of levothyroxine. Type 1 and type 2 iodothyronine deiodinase (D1 and D2) activities were measured in three tumor tissues from thyrotoxic patients. MAIN OUTCOME: The serum FT(3) level and FT(3)/FT(4) ratio in the follicular carcinoma (FC) group were significantly higher than those in the papillary carcinoma group or patients without recurrence. Four patients (20%) in the FC group but none in the other groups demonstrated T(3) thyrotoxicosis or a FT(3)/FT(4) ratio greater than 3.5. One week after withdrawal of levothyroxine, both FT(3) and FT(4) levels decreased. Retrospective measurements of FT(3) in frozen stored sera demonstrated that FT(3) exceeded the upper normal limit when FT(4) began to decrease but remained within the normal range. Tumor tissues showed high D1 and D2 activities. CONCLUSIONS: Twenty percent of patients with massive metastatic FC exhibited T(3) thyrotoxicosis, most likely due to increased conversion of T(4) to T(3) by tumor expressing high D1 and D2 activities. Occasional measurement of serum FT(3) in addition to FT(4) and TSH is recommended in patients with massive metastatic FC, especially when serum FT(4) decreases on fixed doses of levothyroxine.     

THYROID HORMONES AND THE REGULATION OF THYROID FUNCTION IN MEN WITH COELIAC DISEASE

A specific pattern of thyroid hormone abnormalities was observed in twenty-seven men with coeliac disease which differed from that observed in patients with non-thyroidal illness (NTI). Serum free thyroxine (FT4) was reduced, but increased after gluten was withdrawn from the diet and jejunal morphology improved. Total T4 (TT4), total triodothyronine (TT3), free triiodothyronine (FT3) and reverse T3 (rT3) levels were unchanged, unlike the findings in nineteen men with Crohn's disease when TT3 fell, rT3 tended to rise but TT4, FT4 and FT3 levels were normal, except FT4 was significantly higher in a subgroup of patients who were more severely ill. The thyroid hormone changes in Crohn's disease are those expected in NTI. Basal serum thyrotrophin (TSH) was normal in all but one of the patients with coeliac disease but 45% of untreated coeliacs had exaggerated responses of TSH to thyrotrophin releasing hormone, an observation which cannot be explained as a feature of NTI. These changes in thyroid hormones in coeliac disease could not be attributed to abnormalities of thyroxine-binding globulin or thyroxine-binding prealbumin, and thyroid autoantibodies were not detected in these patients. Hence, different patterns of thyroid hormone abnormalities can occur in different diseases of the same organ in patients of equivalent nutritional status. Circulating gluten peptides may be involved in the hypothalamic-pituitary disturbance of coeliac disease.     

Serial changes in thyroid-stimulating antibody and thyrotropin binding inhibitor immunoglobulin at the time of postpartum occurrence of thyrotoxicosis in Graves' disease

Thyroid-stimulating antibody (TSAb) and TSH binding inhibitor immunoglobulin (TBII) were measured serially in 10 patients with Graves' disease at the time of postpartum onset (n = 2) or relapse (n = 8) of Graves' thyrotoxicosis and in 5 patients with Graves' disease who were in remission and had no postpartum relapse of Graves' thyrotoxicosis. TSAb was measured by a sensitive cAMP accumulation assay using FRTL-5 cells, and TBII was determined by radioreceptor assay. In no patient with either recurrent or new onset postpartum hyperthyroidism did the serum free T3 index (FT3I) rise before the free T4 index (FT4I). Of the 10 patients who had postpartum thyrotoxicosis, concomitant increases in serum FT4I and FT3I, and TSAb and TBII were observed in only 1 patient. Increases in TSAb and TBII after those in FT4I and FT3I occurred in 6 patients. In 1 patient, an increase in TBII was associated with the occurrence of thyrotoxicosis, but TSAb increased 1 month later. In the other 2 patients, a TSAb increase was followed by the development of thyrotoxicosis, but TBII increased later. In 3 of these 10 patients, the increased serum FT4I and FT3I values decreased spontaneously, whereas the TSAb and TBII levels increased continuously. No positive test or increase in TSAb or TBII was found in the 5 patients with Graves' disease who did not have a postpartum relapse of thyrotoxicosis. These data indicate that postpartum initiation of Graves' thyrotoxicosis is not always associated with an increase in circulating anti-TSH receptor antibodies and that such parameters are poor indicators of thyroid function. Intrathyroidal humoral or cell-mediated immunological mechanisms may also be involved in mediating thyrotoxicosis in Graves' disease.     

Thyroid hormone economy in response to extreme cold exposure in healthy factory workers

The effects of cold exposure on serum total T4 (TT4), total T3 (TT3), free T4 (FT4), free T3 (FT3), rT3, TSH, T4-binding globulin (TBG), and T3 resin uptake were investigated in 82 euthyroid factory workers. Twenty-five workers (group 1) were exposed intermittently (approximately 3.5 h daily) to extreme cold (-40 to -20 C) during the 8-h work shift, and 47 (group 2) were exposed to moderate cold (-10 to 8 C) for the entire 8 h. Ten individuals working at room temperature for the same period also were studied. After cold exposure, serum TT4 decreased in group 1 and did not change in group 2, whereas FT4 did not change in group 1 and increased in group 2. After exposure, serum TT3 and rT3 decreased significantly in both groups, while FT3 did not change in either. The basal serum TT4 levels in groups 1 and 2 were significantly lower than those in the control group, whereas those of FT4 and FT3 were higher. Thus, cold exposure had opposite effects on total thyroid hormones and their free fractions, consistent with a cold-induced decrease in thyroid hormone-binding capacity. A postexposure decrease in serum TBG was found in women in group 2, but not in men in either group 2 or group 1, suggesting that factors other than decreased TBG are also involved. The results suggest the possibilities that 1) decreased thyroid hormone-binding capacity is an adaptive response to cold exposure, and/or 2) increased free thyroid hormone levels in response to cold exposure result in a new higher equilibrium between extracellular and intracellular FT4 and FT3.     

Clinical study on thyroid hormone levels in tuberculous patients]

The article reported the results of serum total thyroxine (TT4), triiodothyronine (TT3), reverse triiodothyronine (rT3), triiodothyronine resin uptake ratio (T3RU) thyroid stimulating hormone (TSH), free thyroxine index (FT4I), and ratio of T3/rT3 in 103 tuberculous patients. The results showed the levels of serum TT4, TT3 and ratio T3/rT3 in tuberculous patients were lower than those of 50 healthy subjects (total P less than 0.01), rT3, T3RU and TSH were higher than those (total P less than 0.01). FT4I has no significant difference between the two groups (P greater than 0.05).     

Total and free thyroxine and triiodothyronine in normal and complicated pregnancy.

Serum concentrations of total and free thyroxine (T4 and FT4) and total and free triiodothyronine (T3 and FT3) were measured in normal pregnant women, in patients with toxemia of pregnancy, and in patients with gestational trophoblastic disease (GTD). In normal pregnancy, FT4 and FT3 levels remained normal while T4 and T3 levels were elevated. In patients with pre-eclampsia, the mean serum T3 concentration was significantly lower than that of normal pregnancy and the serum FT3 concentrations in three out of nine patients were below the normal pregnancy range. The mean serum T4 and FT4 concentrations in patients with pre-eclampsia were, however, significantly higher than those in normal pregnant women. In patients with GTD without signs of hyperthyroidism, the mean serum total and free T4 concentrations were 43 and 92% higher than those in normal pregnancy (P less than 0.02), and many patients had levels above the range of values observed in normal pregnant women. The mean serum total and free T3 concentrations in GTD patients without signs of hyperthyroidism were not different from those of normal pregnancy (P less than 0.05). In the single GTD patient with hyperthyroid crisis, the s. erum FT4 concentration was within the range seen in GTD patients without signs of hyperthyroidism. Her serum FT3 concentration was, however, much higher than the ranges in normal pregnancy or in GTD patients without clinical hyperthyroidism. Higher than normal FT4 levels were found in patients with and without elevated hCG levels.     

The role of serum binding proteins in determining free thyroid hormone concentrations during development in quail

Japanese quail were used as a model for studying the role of binding proteins in determining free T4 (FT4) and free T3 (FT3) concentrations during development. Adults were used to characterize thyroid hormone binding; developmental stages studied were late embryonic, perinatal, hatchling, and juvenile. Total and free hormones were determined directly by RIA, and free hormones were determined indirectly by equilibrium dialysis. Binding proteins were identified by electrophoresis of serum preincubated with labeled hormones. Serum FT4 and FT3 concentrations in adult quail were equivalent to those in humans. T4 bound principally to albumin and secondarily to prealbumin; T3 bound principally to alpha-globulin and secondarily to albumin and gamma-globulin. A specific T4-binding globulin, as in mammals, was not present. The relative affinity of stripped serum was greater for T4 than for T3. In late embryos, FT4 concentrations rise as a result of a marked increase in total T4 (TT4) and modest increases in binding proteins. The perinatal peak in FT4 reflects the perinatal surge of TT4 without a change in binding proteins. From days 1-6 posthatching, FT4 decreases as a consequence of TT4 decreasing faster than the decrease in binding. In juveniles, FT4 concentrations stabilize as increases in TT4 are paralleled by increases in serum binding. T3 binding shows few significant differences from adult values during development, so FT3 concentrations follow closely the pattern of TT3 changes. These results demonstrate that developmental changes in serum binding proteins play a significant role in determining the pattern of free thyroid hormones, especially for FT4, by modulating the total hormone concentrations controlled by the hypothalamic-pituitary axis.     

妊娠一过性甲状腺毒症的临床研究

目的 调查沈阳地区既往健康的妇女妊娠早期妊娠一过性甲状腺毒症(GTT)的患病率及其病因.方法 对来自沈阳地区10家医院的534例妊娠早期妇女进行问卷调查、体格检查、血清促甲状腺素(TSH)、游离T4(FT4)、游离T3(FT3)、甲状腺过氧化物酶抗体(TPOAb)、促甲状腺素受体抗体(TRAb)和人绒毛膜促性腺激素(hCG)水平的检测.结果 (1)妊娠早期甲状腺毒症总患病率为9.75%,GTT的患病率为7.86%,占甲状腺毒症的80.77%;88.89%临床GTT表现为单纯FT3升高.(2)妊娠6、8～10和12周孕妇血清hCG水平逐渐升高,中位数分别为25300、85220和81780IU/L(P=0.000).血清TSH中位数依次降低(P＜0.01),分别为1.45、1.10和0.84mIU/L.(3)当妊娠妇女血清hCG水平＞50 000 IU/L时,GTT的比例明显升高;当血清hCG水平在80 000～110000IU/L时发生亚临床GTT的比例明显升高;当血清hCG水平＞110 000IU/L时发生临床CTT的比例明显升高.相关分析结果 显示,妊娠早期血清hCG与TSH显著负相关(r=-0.402,P=0.000),与FT3正相关(r=0.165,P=0.000),而与FT4无相关.结论 GTT是妊娠早期甲状腺功能亢进症的首要病因,占妊娠早期甲状腺毒症的80.77%,其血清学特点主要表现为血清FTT升高.妊娠早期血清hCG水平与GTT严重程度相关.     

Red blood cell thyroxine in nonthyroid illness and in heparin-treated patients

Red blood cell T4 concentrations (RBC T4) were measured in 15 normal subjects, 13 patients with hypo- or hyperthyroidism, and 10 patients with elevated or decreased serum thyroid hormone binding. In each case, RBC T4 was compared with the serum concentration of free T4 measured by equilibrium dialysis ( FT4D ). RBC T4 correlated significantly with FT4D in these subjects (r = 0.90; P less than 0.001). The normal range for RBC T4 was 0.27-0.83 ng/ml. RBC T4 was below the normal range in all 8 patients with hypothyroidism and above the normal range in all 5 patients with hyperthyroidism. It was within the normal range in all 4 subjects with absent or low T4-binding globulin (TBG) and in 5 of the 6 subjects with elevated TBG or familial dysalbuminemic hyperthyroxinemia. The sixth subject (increased TBG) had elevated RBC T4 and FT4D . RBC T4 was similarly measured in 10 patients with severe nonthyroid illness (NTI), 5 of whom had decreased serum concentrations of total T4. RBC T4 was normal in 8 of these patients, elevated in 1, and decreased in 1; in comparison, FT4D was normal in 4, elevated in 5, and decreased in 1. Eight patients receiving continuous iv infusions of heparin were also studied because of previously described similarities in the in vitro thyroid tests of heparin-treated and euthyroid sick patients. FT4D was elevated in 7 of the heparin-treated patients, whereas RBC T4 was elevated in only 2. Furthermore, for any given value of FT4D , RBC T4 was lower in heparin-treated patients than in normal subjects, indicating the presence of an inhibitor of cellular T4 binding in these patients. This putative inhibitor, demonstrated by an elevated FT4D to RBC T4 ratio, was present in 6 of the 8 heparin-treated patients and in 5 of the 10 patients with NTI. The findings of this study support the hypothesis that an inhibitor of cellular T4 binding is present in the serum of some patients with NTI and in most heparin-treated individuals.     

Serum thyroid hormone abnormalities in psychiatric disease

Psychiatric illness is a cause of “euthyroid sick syndrome” (ESS), defined as abnormal concentrations of circulating iodothyronines in euthyroid subjects with nonthyroidal illness (NTI). We describe a prospective study of 150 consecutive psychiatric admissions studied by endocrine and psychologic techniques. Based on 150 admission blood samples, we found a 7% incidence of ESS and with serial samples (74 patients) the incidence was 27%, demonstrating that ESS can develop after hospital admission. Of the 20 patients with ESS, 11 had elevation of both serum total T4 concentrations (T4) and free thyroxine index (FTI) while their serum total T3 concentrations (T3) remained normal; 5 had elevation of FTI without elevation of T4 or T3; and 4 had low T4 and low FTI and normal TSH. In 2 of the 4 patients in the last category, the T3 was also low. The free T3 index (FT3I) was normal in all but 1 patient who had low FT3I and FTI, low T4 and T3, and normal TSH. The serum thyroid hormone abnormalities were transient in the ESS patients during the 10 day period with 2 exceptions; 1 patient had persistently elevated T4 and FTI with normal T3 and FT3I values while another patient had persistently depressed T4 and FTI without abnormality of FT3I or TSH. Multivariate statistical analysis demonstrated a difference (P < .06) in the psychologic attributes of somatic and autonomic symptoms in ESS patients compared to controls. We conclude that ESS is as common amongst psychiatric admissions as in general hospital patients previously studied and that blood thyroid function tests should be interpreted cautiously in all hospitalized patients.     

二甲双胍对糖尿病患者血清促甲状腺激素水平的影响

目的探讨二甲双胍对未服用甲状腺激素的糖尿病患者血清甲状腺激素和促甲状腺激素水平的影响。方法测定未服用甲状腺激素的糖尿病患者的血清游离三碘甲腺原氨酸（FT3）、游离甲状腺素（FT4）、总三碘甲腺原氨酸（TT3）、总甲状腺素（TT4）和促甲状腺激素（TSH）的水平，并分析其与是否服用二甲双胍的关系。结果未服用二甲双胍组与服用二甲双胍组的血清FT3（4.65±0.68vs4.59±0.67pmol/L）、FT4（17.88±3.26vs17.75±2.85pmol/L）、TT3（1.79±0.42vs1.77±0.38nmol/L）、TT4（107.9±22.1vs109.2±22.1nmol/L）和lnTSH（0.49±0.83vs0.47±0.87mU/L）之间的差异无统计学意义（P〉0.05）。结论未服用甲状腺激素的糖尿病患者在服用二甲双胍期间促甲状腺激素的水平不受影响。     

SERUM IODOTHYRONINE CONCENTRATIONS DURING INTRODUCTION OF THYROXINE REPLACEMENT THERAPY IN HYPOTHYROIDISM

Serum concentrations of total and free T4 (TT4 and FT4), total and free T3 (TT3 and FT3), rT3, T4 binding globulin (TBG), T3 uptake (T3U) and TSH were measured in 12 patients with severe hypothyroidism before and during the introduction of replacement therapy with oral T4. The dose of T4 was increased by increments of 50 micrograms at intervals of 4 weeks to a total of 200 micrograms daily. There was a linear correlation between the concentrations of FT3 and FT4 (FT3 = 1.35 + 0.23FT4, r = 0.916, P less than 0.001). The correlation between TT3 and TT4 was more complex: the data were best fitted by the expression TT3 = 0.195 square root TT4, (r = 0.936, P less than 0.001). The relatively greater rise in TT3 initially may reflect a greater binding of T3 by TBG when the concentration of T4 is low. TBG concentration fell after 50 and 100 micrograms of T4 but did not change at the higher doses. There was a simple linear relation between TT4 and rT3 (rT3 = -0.022 + 0.0027TT4, r = 0.921, P less than 0.001). The expected inverse relation between TSH concentration and the thyroid hormones was seen, the three closest correlations being between the logarithm of the TSH concentration and FT3, the ratio T4/TBG and FT4 (r = 0.927, -0.917 and -0.900 respectively). These correlations were significantly better (P less than 0.05) than the correlations with untransformed TSH values. Suppression of TSH occurred while FT3 tended to remain within normal limits, but FT4 was often raised.(ABSTRACT TRUNCATED AT 250 WORDS)     

Basal oxygen uptake: a new technique for an old test

To assess the metabolic effects of T4 and T3, we measured serum total T4 (TT4), free T4 (FT4), total T3 (TT3), TSH, and basal oxygen uptake (VO2) in eight normal subjects in the basal state and after treatment with L-T3 (T3) and sodium ipodate for 2 weeks. T3 treatment resulted in a rise of serum TT3 from a baseline of 137 +/- 16 (+/- SE) to a peak of 239 +/- 15 ng/dl. Serum TT4 declined from 8.14 +/- 0.56 to 6.08 +/- 0.43 micrograms/dl, FT4 from 1.59 +/- 0.13 to 1.03 +/- 0.05 ng/dl, and TSH from 1.74 +/- 0.24 to 0.56 +/- 0.16 microU/ml. Basal VO2 increased from 2.66 +/- 0.11 to 3.15 +/- 0.09 ml/kg X min. Ipodate, on the other hand, led to a lower serum TT3 concentration (102 +/- 21 ng/dl), higher serum TT4 and FT4 (9.59 +/- 0.5 micrograms/dl and 1.91 +/- 0.13 ng/dl, respectively), and elevated TSH (3.64 +/- 0.14 microU/ml). Basal VO2 was reduced to 2.44 +/- 0.06 ml/kg X min. Linear regression analysis revealed an excellent positive correlation between serum TT3 and basal VO2 (n = 25; r = 0.747; P less than 0.001) and a significant negative correlation between serum TT3 and TSH (n = 26; r = -0.526; P less than 0.01). Serum TT4 and FT4 correlated negatively with VO2 and positively with serum TSH. The higher T4 level during ipodate treatment was associated with lower VO2 and higher TSH, and vice versa when T4 was suppressed while receiving T3. When ipodate was given concomitantly with T3 to five subjects, only the effects of T3, characterized by increased VO2 and decreased TSH, were evident. These data indicate that both basal VO2 and serum TSH are sensitive indices of thyroid hormone activities. The latter gives only the directional change (hyper- or hypothyroidism), while the former more accurately quantitates the magnitude of the derangement. Moreover, it appears that in man, T3, and not T4, is the primary hormone that regulates thermogenesis and TSH secretion.     

Minor alterations in thyroid-function tests associated with diabetes mellitus and obesity in outpatients without known thyroid illness

Thyroid function tests might be affected by diabetes and obesity. To evaluate the influence of these parameters in routine conditions, 72 diabetic and 53 non-diabetic outpatients without known thyroid diseases or severe chronic illness were recruited over a 7-month period. For each patient, dosages of thyrotropin (TSH), total and free thyroxine (TT4 and FT4, respectively), total and free triiodothyronine (TT3 and FT3) and T3 resin uptake (T3RU) were performed by radioimmunoassays. The simultaneous influence of various parameters known to affect thyroid-function tests was evaluated by multivariate linear regression. The studied variables included gender, age, glucosteroids, estrogens, tobacco habits, iodine contacts, body mass index (BMI) and diabetes mellitus. Tobacco habits and iodine contacts did not influence any tests. As expected, estrogens induced an increase in TT4 and TT3 values (p < 0.001 and 0.020, respectively) associated with a decrease in T3RU (p < 0.001). Consequently, females had lower T3RU than males (p < 0.0001). Corticotherapy was associated with decreased TSH values (p = 0.022). TT3 and FT3 decreased with age (p < 0.001), whereas T3RU and FT4 increased (p = 0.020 and 0.004, respectively). In contrast to an increase in TSH (p = 0.006), TT4 and FT4 decreased at higher BMI levels (p = 0.018 and 0.004, respectively), which is consistent with subclinical hypothyroidism. In diabetic patients, TSH was lower than in nondiabetic subjects (p = 0.039). Thus, the present study indicates that besides known parameters such as age and drugs, thyroid-function tests can also be altered by diabetes mellitus and obesity.     

Thyroid function in hyperemesis gravidarum

Plasma total T4 (TT4), T3 (TT3), free T4 (FT4), free T3 (FT3), thyroxine binding globulin, hCG, and erythrocyte zinc content were measured in 43 women with uncomplicated pregnancy and in 71 patients admitted with hyperemesis gravidarum. Plasma concentration of thyroid hormones in hyperemesis subjects showed wide variability and 32% of subjects had high TT4 (higher than mean +2 SD of normal pregnant subjects), 33% had high FT4, 20% had high TT3, and 20% had high FT3. Red cell zinc content, a tissue marker of thyroid status, in the hyperthyroxinemic subjects was not different from that of normothyroxinemic hyperemesis subjects or of subjects with uncomplicated pregnancy. The elevated TT4 concentration decreased spontaneously in all but two of the hyperemesis subjects to normal pregnant levels. The plasma FT4 concentration at presentation correlated with plasma hCG in hyperemesis gravidarum (partial correlation coefficient r = 0.411, P less than 0.01), but not in normal pregnancy (partial correlation coefficient r = 0.043) after allowing for the effect of gestational age. We conclude that approximately one third of hyperemesis subjects show transient hyperthyroxinemia and suggest that hCG or a molecular variant of hCG may stimulate the thyroid gland.     

Factors affecting suppression of endogenous thyrotropin secretion by thyroxine treatment: retrospective analysis in athyreotic and goitrous patients

Factors affecting TSH suppression by L-T4 administration were retrospectively evaluated in 452 patients: 180 who were athyreotic after total thyroidectomy and remnant radioiodine ablation for differentiated thyroid carcinoma and 272 with nontoxic diffuse or nodular goiter. All patients were considered clinically euthyroid. TSH secretion was assessed by iv TRH stimulation testing. The T4 dose associated with an undetectable basal serum TSH level and no increase in serum TSH after TRH administration (suppressive dose) averaged 2.7 +/- 0.4 (SD) micrograms/kg body weight (BW)/day in athyreotic patients and 2.1 +/- 0.3 micrograms/kg BW/day in goitrous patients (P less than 0.001). The 25th-75th percentile intervals were 2.5-2.9 micrograms/kg BW/day for athyreotic patients and 1.9-2.3 micrograms/kg BW/day for goitrous patients. The suppressive dose of T4 was dependent in both groups on patient age, younger patients needing higher doses than older patients. The duration of treatment also proved to be an important parameter, since in both groups the percentage of patients with suppressed TSH secretion increased if TRH testing was carried out after at least 6 months after the initiation of therapy. Serum total T4, total T3, free T3 (FT3), free T4 (FT4) index, and FT3 index values did not differ in the two groups and were significantly higher (P less than 0.001) than in normal subjects. Mean serum FT4 was significantly higher in athyreotic patients than in goitrous patients with suppressed TSH secretion. Among athyreotic patients with suppressed TSH secretion, 24% had elevated serum FT4 and FT3, and 47% had elevated serum FT4 alone. Of goitrous patients with suppressed TSH secretion, 20% had elevated serum FT4 and FT3, and 27% had elevated serum FT4 alone. On the other hand, 35% of athyreotic patients and 14% of goitrous patients whose TSH secretion was not suppressed had elevated serum FT4. Serum sex hormone-binding globulin concentrations were measured in 3 groups of goitrous women. Values above normal limits were found in 13/26 patients (50%) with high serum FT4 and FT3, in 4/30 patients (13%) with elevated serum FT4 alone, and in 1/25 patients (4%) with normal FT4 and FT3. In conclusion: TSH suppression requires daily doses of T4 between 2.5 and 2.9 micrograms/kg BW in athyreotic patients and between 1.9 and 2.3 micrograms/kg BW in goitrous patients, with appropriate adjustments in relation to the age of the patient; Assessment of the adequacy of treatment should not be carried out before 6 months after the institution of therapy.     

急性乙型肝炎患者血清甲状腺激素水平变化

目的研究急性乙型肝炎患者血清中甲状腺激素水平变化情况,观察患者甲状腺激素水平的动态变化和甲状腺激素水平异常与发病时间的关系。方法急性乙型肝炎患者36例作为观察对象,健康体检的36人作为对照组。检测其入院时的甲状腺激素水平：血清总甲状腺素（TT4）、血清总三碘甲腺原氨酸（TT3）、血清游离甲状腺素（FT4）、血清游离三碘甲腺原氨酸（FT3）、促甲状腺激素（TSH）,并与对照组比较。对异常者1周后复查甲状腺激素水平,以后每周复查1次,直至正常,观察其动态变化。结果急性乙型肝炎患者血清甲状腺激素TT4、TT3、FT4、FT3水平较对照组增高,差异具有统计学意义（P〈0.05）。TSH较对照组降低,但TSH均在正常值范围内,差异无统计学意义（P〉0.05）。入院时TT4、TT3、FT4、FT3高于正常值者在第三周全部转为正常。结论急性乙型肝炎患者血清甲状腺激素TT4、TT3、FT4、FT3水平升高,对于升高超过正常值者不需要治疗,随着肝功能逐渐好转,短期可恢复正常。     

Serum levels of thyrotropin, thyroid hormones and their response to thyrotropin releasing hormone in infective febrile illnesses.

In 25 patients suffering from fever of infection, serum levels of thyrotropin (TSH), thyroxine (T4), triiodothyronine (T3), and thyroxine binding globulin (TBG) were estimated on two consecutive days during the febrile period and again 3 to 10 days after the fever had subsided. The serum TSH and T3 responses to 100 mug iv TRH were also studied during fever. Hormones were estimated by specific radioimmunoassays and TBG by radioligand binding assay. As compared with age and sex matched normal controls, patients with fever of infection had significantly lowered levels of total serum T3 and TBG. The serum TSH and total T4 concentrations were not significantly altered. During fever both % FT4 and absolute FT4 were significantly elevated, whereas only % FT3 was significantly increased and due to lowered serum total T3 levels the absolute FT3 were not significantly altered as compared to that in normal subjects. After the fever had subsided, the serum T3 levels returned to normal and the serum TBG levels increased. There was no correlation between basal serum levels of T3 and TSH during fever. Although in response to iv TRH the mean rise in serum TSH during fever was comparable to that in normal subjects, the overall TSH response showed an inverse correlation with serum TT3 levels. Following iv TRH there was a significant increase in serum T3 levels and the T3 response in fever was comparable to that in normal subjects. These data suggest that hormone secretion by the thyroid and its responsiveness to endogenous TSH are maintained during fever. The lowered T3 levels are not suggestive of a hypothyroid state, but perhaps could be due to decreased peripheral conversion of T4 to T3 and to decreased binding of T3 to serum proteins. The exact mechanism or significance of these alterations in thyroid function during febrile illness remains to be elucidated.     

FREE THYROXINE (FT4) AND FREE TRIIODOTHYRONINE (FT3) IN AUTONOMOUS THYROID NODULES

Total and free thyroid hormones (T3, T4, FT3 and FT4), TSH and its response to TRH were determined in sixty-three patients affected by autonomous thyroid nodules: mean concentrations of free T3 (FT3) were significantly higher in hot nodules (suppressing extranodular tissue on the scan) as compared to warm ones, even in those cases where total T3 and T4 were within normal ranges (hot nodules, group as a whole: 8.8 +/- 3.5 pg/ml; warm nodules: 5.3 +/- 1.2; hot nodules with normal total T3 and T4 concentrations: 7.5 +/- 3). Also the clinical condition of thyrotoxicosis appeared to be correlated with FT3 concentrations (toxic patients, group as a whole: 9.6 +/- 4.0 pg/ml; euthyroid patients: 6.8 +/- 3.1; toxic patients with normal values of T3 and T4; 8.3 +/- 2.8). On the contrary the correlation of total and free thyroid hormone concentrations with the response of TSH to TRH was not significant.