A case of hypothyroidism with simultaneous presence of stimulating type anti-thyrotropin (TSH) receptor antibodies and anti-thyroxine (T4) autoantibodies.

We have examined a hypothyroid patient with stimulating type anti-thyrotropin (TSH) receptor antibodies and without blocking type anti-TSH receptor antibodies. Although she had high serum TSH (240 microU/ml) and low free triiodothyronine (FT3, 0.49 pg/ml) concentrations, which agree with physical findings of hypothyroidism, she had an unusually high free thyroxine (FT4) concentration (3.56 ng/dl). Incubation of her serum with 125I-T4, followed by precipitation with 12.5% polyethylene glycol (PEG) disclosed a higher binding of 125I-T4 (34.4%) than in normal controls, being 5-7%. In addition, binding of 125I-T4 to her serum gamma-globulin was completely displaced by the addition of unlabelled T4. From these results it was concluded that her serum contained anti-T4 autoantibodies. Treatment with synthetic T4 was begun and her thyroid function was monitored by sensitive TSH radioimmunoassay (RIA) and RIA of FT4 after PEG treatment. Since both sensitive TSH RIA and FT4 RIA results after PEG treatment give results concordant with the physical findings, it was concluded that both of the RIA results are useful for the evaluation of thyroid function in patients with thyroid hormone autoantibodies.     

Serum TSH, T4, T3, FT4, FT3, rT3, and TBG in youngsters with non-ketotic insulin-dependent diabetes mellitus

Several parameters of thyroid function were studied in 112 non-ketoacidotic youngsters with insulin-dependent diabetes mellitus (IDDM). Levels of thyroxine (T4), reverse triiodothyronine (rT3), thyroxine-binding globulin (TBG) and T3 were lower than in controls, whereas FT4, and FT3 were normal. T4 levels in IDDM patients were positively related to T3, rT3 and TBG, and inversely related to haemoglobin A1 (HbA1). However, only 4 patients showed biochemical hypothyroidism (T4 less than 5 micrograms/100 ml), whereas their FT4, FT3 and thyroid-stimulating hormone (TSH) levels were normal. Concurrent variations of T3 and rT3 levels were found in IDDM patients; thus, their T3/rT3 ratios were stable or higher than in controls, indicating that peripheral deiodination of T4 is preferentially oriented to production of rT3 only during ketoacidosis. Although changes in thyroid function may reflect the degree of metabolic control of diabetes in a large population, the clinical usefulness of serum thyroid hormone measurements in an individual case still appears to be limited.     

The pituitary-thyroid axis in patients with pituitary disorders

The pituitary-thyroid axis of 12 patients, exposed to transsphenoidal pituitary microsurgery because of nonfunctioning adenomas (6), prolactinomas (3) and craniopharyngioma (1), or to major pituitary injury (1 apoplexy, 1 accidental injury), was controlled more than 6 months following the incidents. The patients did not receive thyroid replacement therapy and were evaluated by measurement of the serum concentration of thyroxine (T4), 3,5,3'-triiodothyronine (T3), 3,3',5'-triiodothyronine (rT3), T3-resin uptake test and thyrotropin (TSH, IRMA method) before and after 200 micrograms thyrotropin releasing hormone (TRH) iv. The examination also included measurement of prolactin (PRL) and cortisol (C) in serum. Apart from 1 patient with pituitary apoplexy all had normal basal TSH levels and 9 showed a significant TSH response to TRH. Compared to 40 normal control subjects the 12 patients had significantly decreased levels of T4, T3 and rT3 (expressed in free indices), while the TSH levels showed no change. Five of the patients, studied before and following surgery, had all decreased and subnormal FT4I (free T4 index) after surgery, but unchanged FT3I and TSH. The levels of FT4I were positively correlated to both those of FT3I and FrT3I, but not to TSH. The TSH and thyroid hormone values showed no relationship to the levels of PRL or C of the patients exposed to surgery. It is concluded that the risk of hypothyroidism in patients exposed to pituitary microsurgery is not appearing from the TSH response to TRH, but from the thyroid hormone levels.     

Variations in the serum levels of thyroid hormones and TSH after intake of a dose of L-thyroxine in euthyroid subjects and in adequately-treated hypothyroid patients

The aim of the present study was to determine whether the temporary variations in blood thyroid hormone levels secondary to a therapeutic dose administration of L-thyroxine observed in adequately treated hypothyroid patients also occur in spontaneously euthyroid subjects under analogous conditions. Serum levels of T3, T4, FT3, FT4 and TSH were measured over 6 hours following a single oral administration of L-thyroxine (dosage 85 mcg/mq body surface area) in a group of 18 euthyroid volunteers and 8 hypothyroid patients adequately compensated with replacement therapy. In the euthyroid subjects there was a significant increase in T4 and a significant fall in TSH values at 60', while a significant decrease in FT3 and FT4 as compared to initial values was observed at 120'. In the treated hypothyroid patients serum T3 and T4 increased at 120', while FT4 concentrations, already significantly higher at 120', still remained higher than initial levels at 360'. The different behaviour of the hypothyroid patients, in spite of being compensated with therapeutic doses of L-thyroxine, reflects the persistence of a thyroid-metabolic condition substantially different to the physiological feature, which appears to be realized by means of a reduced iodothyronine clearance and a lower sensitivity in TSH feedback.     

Visfatin Levels in Subclinical Hypothyroidism

Alterations in thyroid function are associated with changes in body weight, metabolism, and low-grade inflammation abnormal thyroid function may be associated with disturbances in the production of adipokines also. Although there have been studies showing changes in visfatin levels in thyroid dysfunction, exact relationship between them was still unclear. Our aim was to evaluate serum concentrations of visfatin in patients with subclinical thyroid dysfunction before and after normalization of thyroid function tests. The study included 43 patients (mean age 50.1 ± 10.6 years) with subclinical hypothyroidism. Serum insulin, visfatin, TSH, free T4 (FT4) and free T3 (FT3) levels of subjects were analyzed. Visfatin levels were measured in all patients before starting therapy and after normalization of thyroid function. Serum visfatin levels of subclinical hypothyroid patients were 0.99 ± 0.45 and they were similar after normalization of thyroid function (p = 0.394). Serum visfatin levels were negatively correlated with FT4 levels before treatment (r = ?0.329 p < 0.05). There was no significant correlation between serum levels of visfatin and the serum levels of TSH and FT3. Serum visfatin levels did not correlate with insulin, fasting blood glucose, total cholesterol, HDL cholesterol, LDL cholesterol and triglyceride levels. In this study, it was shown visfatin levels did not change after replacement therapy in patients with subclinical hypothyroidism. Subclinical hypothyroid state may be an earlier stage regarding the changes of adipocytokines specifically the visfatin secretion as seen in overt hypothyroidism.     

Thyroid hormone levels during a 3-week professional road cycling competition

AIMS: The aim of this investigation was to examine the thyroid hormone levels of professional cyclists during a 3-week stage competition (Vuelta a Espa?a 1998). METHODS: The study population was made up of 16 male cyclists from two world-leading professional teams. Four blood samples were drawn (between 07:00 and 09:00 a.m.) from each participant before and at the end of the 1st, 2nd and 3rd weeks of competition. 3,5,3'(-Triiodothyronine (T(3)), free T(3) (FT(3)), thyroxine (T(4)), free T(4) (FT(4)) and thyroid-stimulating hormone (TSH) were determined in each blood sample by radioimmunoassay. RESULTS: Serum T(4), FT(4) and FT(3) levels showed a significant increase (p < 0.05) by the last week of competition while concentrations of TSH and T(3) remained unchanged. CONCLUSION: In conclusion, 3 weeks of competition provokes changes in basal thyroid hormone concentrations in professional road cyclists.     

Serum T3, T4, FT3, TSH and TBG in Turner's syndrome]

Turner's syndrome was originally reported as sexual infantilism, short stature, webbed neck and cubitus valgus. Subsequent investigations, however, have disclosed many other abnormalities both in chromosomal and physical features occurring in this syndrome. An increased prevalence of Hashimoto's thyroiditis in patients with Turner's syndrome has been well documented and molecular defects of the TBG have been described. In our study we examined serum T3, T4, FT3, FT4, TSH and TBG levels in 18 girls with Turner's syndrome, in 18 healthy control girls and in the parents of both groups. We reported significant elevated levels of T3 and FT3 in the Turner's group (P 0.01). We did not find any quantitative abnormalities of immunoreactive TBG in the same patients.     

Common genetic variation in CYP1B1 is associated with concentrations of T4, FT3 and FT4 in the sera of polycystic ovary syndrome patients

CYP1B1 encodes an estrogen enzyme that oxidizes 17β-estradiol to 4-hydroxyestradiol. The evidence demonstrates there may be a relationship between CYP1B1 and thyroid function. To date, no study has evaluated if genetic polymorphisms that regulate concentrations of serum FT3 and FT4 contribute to Polycyctic Ovary Syndrome (PCOS). To identify polymorphisms in the CYP1B1 locus associated with PCOS, we genotyped three common polymorphisms across the CYP1B1 locus in 226 patients. A test for association of common variants with susceptibility to PCOS was conducted in a large cohort of 609 subjects. The functional polymorphism CYP1B1 L432V (rs1056836) is associated with serum T4 (P = 0.003), serum FT3 (P < 0.001) and serum FT4 concentrations (P < 0.001). Our study provides the first evidence that genetic variants in CYP1B1 can be associated with serum T4, FT4 and FT3 levels in PCOS. These findings imply novel pathophysiological links between the CYP1B1 locus and thyroid function in PCOS.     

Clinical evaluation of accuracy in determining serum free thyroxine and free triiodothyronine in patients with non-thyroidal illness: immunoglobulin effect on T3/TBG ratio and T4/TBG ratio

We examined the effect of endogenous immunoglobulins (G, A and M) and albumin on the measurement of thyroid hormones by different methods, including a new non-isotopic immunoassay of free thyroxine (FT4) and free triiodothyronine (FT3), in a large number of patients with non-thyroidal illness (NTI). Variations in serum protein concentrations can affect the results of radioimmunoassay of human thyroid hormones and thyroxine binding globulin (TBG). Our data revealed that in patients with non-thyroidal illness, when fluctuations in serum gamma-globulin occurred the T3/TBG and T4/TBG ratios altered. Consequently, when patients are suffering from non-thyroidal illness with changing gamma-globulin levels, clinical scientists should take care when they use T3/TBG and T4/TBG ratios as a substitute for FT3 or FT4 estimation. We found FT4 and FT3 (determined with Amerlex-M kits) T3 and the T3/TBG ratio were altered inversely due to the difference in the serum gamma-globulin levels. A recently developed enhanced luminescence enzyme immunoassay for FT3 and FT4 (Amerlite FT3 and FT4 kits) provides more reliable and accurate results, because of its resistance to interference, especially from albumin and gamma-globulin.     

Serum thyroid hormone profile and trace elements in children receiving valproic acid therapy: A longitudinal and controlled study

Valproic acid (VPA) may affect thyroid hormone profile, causing alteration in serum trace elements concentrations. The aim of this study was to prospectively investigate this relationship in children receiving VPA monotherapy for a period up to 6 months. Serum thyrotropin (TSH), free thyroxine (FT4), free triiodothyronine (FT3), thyroxine (T4), triiodothyronine (T3), thyroglobuline (TG), selenium (Se), zinc (Zn), and copper (Cu) levels were evaluated at baseline and at the 6th month in all the patients and in the control group. The mean Cu concentration in the 6th months of VPA therapy was significantly lower than that of the control group. TSH level was significantly increased in the patient group whereas FT4 was significantly decreased. The mean TSH level in the 6th month of VPA therapy was significantly higher than that of the control group, whereas mean T4 level was significantly lower. The Cu level in the 6th months of VPA therapy was positively correlated with T4 level. Δlog Cu and ΔTSH were negatively correlated. This study suggests that the alteration in the serum thyroid hormone profile during VPA therapy may result from the reduction in serum Cu levels.     

Levothyroxine monotherapy cannot guarantee euthyroidism in all athyreotic patients

Context

Levothyroxine monotherapy is the treatment of choice for hypothyroid patients because peripheral T4 to T3 conversion is believed to account for the overall tissue requirement for thyroid hormones. However, there are indirect evidences that this may not be the case in all patients.

Objective

To evaluate in a large series of athyreotic patients whether levothyroxine monotherapy can normalize serum thyroid hormones and thyroid-pituitary feedback.

Design

Retrospective study.

Setting

Academic hospital.

Patients

1,811 athyreotic patients with normal TSH levels under levothyroxine monotherapy and 3,875 euthyroid controls.

Measurements

TSH, FT4 and FT3 concentrations by immunoassays.

Results

FT4 levels were significantly higher and FT3 levels were significantly lower (p<0.001 in both cases) in levothyroxine-treated athyreotic patients than in matched euthyroid controls. Among the levothyroxine-treated patients 15.2% had lower serum FT3 and 7.2% had higher serum FT4 compared to euthyroid controls. A wide range of FT3/FT4 ratios indicated a major heterogeneity in the peripheral T3 production capacity in different individuals. The correlation between thyroid hormones and serum TSH levels indicated an abnormal feedback mechanism in levothyroxine-treated patients.

Conclusions

Athyreotic patients have a highly heterogeneous T3 production capacity from orally administered levothyroxine. More than 20% of these patients, despite normal TSH levels, do not maintain FT3 or FT4 values in the reference range, reflecting the inadequacy of peripheral deiodination to compensate for the absent T3 secretion. The long-term effects of chronic tissue exposure to abnormal T3/T4 ratio are unknown but a sensitive marker of target organ response to thyroid hormones (serum TSH) suggests that this condition causes an abnormal pituitary response. A more physiological treatment than levothyroxine monotherapy may be required in some hypothyroid patients.     

Analysis of overall pathophysiological relationships between serum levels of TSH and thyroid hormones using a large laboratory database

Factors associated with the basal level of serum thyrotropin (TSH) were analyzed over a wide range of pathophysiological conditions by means of a large laboratory database on thyroid function. When data were analyzed two-dimensionally, serum TSH showed significant inverse correlations with total triiodothyronine (T3), free T3 index (FT3I), total thyroxin (TT4) and free T4 index (FT4I) in the order of increasing intensity. The three-dimensional analysis, however, revealed that 1) total hormone levels were actually unrelated to serum TSH when the levels of free hormone indices were held constant, 2) the relation between FT3I and TSH became obscure when the influence of FT4I was similarly removed. On the other hand, 3) the relation of FT4I with TSH was unaffected by the level of FT3I. These results suggest that free T4 is the main determinant of the serum TSH level. This study also implies that it is possible to use large amounts of laboratory data to elucidate the overall profile of a given patho-physiological system, whose structure is only partially revealed by conventional clinical or animal studies.     

Decreased levels of ionized calcium one year after hemithyroidectomy: importance of reduced thyroid hormones

BACKGROUND: Previously we have found reduced levels of total serum calcium and 1,25(OH)2D3 despite an unaltered stimulated parathyroid hormone (PTH) secretion 1 year after hemithyroidectomy. The present study was undertaken to elucidate the possible relationship between calcium homeostasis, thyroid hormones and bone resorption in a group of 45 consecutive patients subjected to hemithyroidectomy because of a solitary nodule. All patients had free T4 and T3 levels within normal range preoperatively. METHODS: Thyroid hormones, bone mineral and biochemical variables known to reflect calcium homeostasis were studied. Patients were divided into three separate groups depending on their pre- and postoperative thyroid hormone status. RESULTS: One year postoperatively, serum levels of free T4 were decreased and that of thyrotropin (TSH) increased in the entire group of patients. The concentration of ionized calcium was reduced from 1.25 +/- 0.05 to 1.22 +/- 0.04 (p < 0.001) despite an unaltered PTH value (2.8 +/- 1.0 vs. 3.1 +/- 1.5, p = 0.50). A significant reduction in C-terminal telopeptide type 1 collagen (1CTP) indicated decreased bone resorption 1 year after surgery (p < 0.05). Subgroup analysis showed that a reduction in ionized calcium was seen only among patients with a postoperative decrease in free T4. Patients with subclinical hyperthyroidism preoperatively presented the lowest postoperative levels of ionized calcium, significantly reduced levels of 1CTP and increased levels of phosphate and creatinine. Multiple linear regression analysis showed that age (p < 0.05) and postoperatively changed serum levels of TSH (p < 0.05), creatinine (p < 0.05), phosphate (p < 0.001) and FT4 (p < 0.01) were independently associated with altered levels of ionized calcium. CONCLUSION: We conclude that the reduction in ionized calcium 1 year after hemithyroidectomy was not due to PTH deficiency. Instead our results suggest that the reduced effects of thyroid hormones on bone and kidney function is essential.     

Prenatal exposure of the fetal rat to excessive L-thyroxine or 3,5-dimethyl-3'-isopropyl-thyronine produces persistent changes in the thyroid control system

Studies were conducted to determine if brief exposure, in utero, to high levels of T4 or to the synthetic thyromimetic agent 3,5-dimethyl-3'-isopropyl-L-thyronine (DIMIT) can produce permanent disruption of the thyroid control system in a manner analogous to the changes in the "set point" reported to occur due to neonatal T4 exposure in the "neo-T4 syndrome". If such a change were to occur, it could explain the persistent thyroid disturbances seen in the progeny of hypothyroid mother rats. These latter progeny are exposed in utero to both low and high serum T4 levels. Maternal T4 treatment produced a 4-fold elevation in fetal serum T4 accompanied by a large decrease in serum TSH levels. The brief treatment in utero with high doses of T4 or of DIMIT resulted in higher neonatal mortality and the T4-treatment produce subsequent growth stunting. These treatments resulted in suppression of the fetal/neonatal thyroid which was very apparent at 5 days of age. At 30 days post-partum, the thyroid control system of the progeny of the T4 and DIMIT-treated animals was still abnormal with low serum T4 levels accompanied with normal serum TSH and T3 levels. At 60 days of age, serum T4 levels remained low in the progeny of the T4-treated animals and the TSH response to TRH was subnormal in both the progeny of the T4-treated and the DIMIT-treated animals. However, serum and pituitary TSH and serum T3 were normal. The thyroid control system of the rat is sensitive to prenatal exposure to hyperthyroxinemia as it is to postnatal exposure.(ABSTRACT TRUNCATED AT 250 WORDS)     

Thyroid Physiology in Pregnancy

ObjectiveVarious physiological changes occur in maternal thyroid economy during pregnancy. This review focuses on the events taking place during gestation that together strongly influence maternal thyroid function.MethodsScientific reports on maternal thyroid physiology in pregnancy.ResultsDuring the 1^st trimester, human chorionic gonadotropin (hCG) induces a transient increase in free thyroxine (FT4) levels, which is mirrored by a lowering of thyroid-stimulating hormone (TSH) concentrations. Following this period, serum FT4 concentrations decrease of approximately 10 to 15%, and serum TSH values steadily return to normal. Also starting in early gestation, there is a marked increase in serum thyroxine-binding globulin (TBG) concentrations, which peak around midgestation and are maintained thereafter. This event, in turn, is responsible for a significant rise in total T4 and triiodothyronine (T3). Finally, significant modifications in the peripheral metabolism of maternal thyroid hormones occur, due to the expression and activity of placental types 2 and 3 iodothyronine deiodinases (D2 and D3, respectively).ConclusionIn line with these variations, both free thyroid hormone and TSH reference intervals change throughout pregnancy, and most scientific societies now recommend that method-and gestation-specific reference ranges be used for interpreting results in pregnancy.The maternal iodide pool reduces during pregnancy because of increased renal clearance of iodine and transfer of iodine to the feto-placental unit. This results in an additional requirement of iodine during pregnancy of ~ 100% as compared to nonpregnant adults. In accordance, the recommended iodine intake in pregnancy is 250 μg/day. A daily iodine intake below this threshold poses risks of various degrees of thyroid insufficiency for both the mother and the fetus. (Endocr Pract. 2014;20:589-596)     

Euthyroid hyperthyrotropinemia secondary to hyperestrogenemia in a male with congenital adrenal hyperplasia.

A 10-year-old boy with congenital adrenal hyperplasia and associated hyperplastic testicular adrenal rests had high serum concentrations of 17-OH progesterone (17-OHP), estradiol (E2), testosterone (T), and basal and TRH-stimulated TSH and PRL, but normal thyroid hormones (T3, T4, FT3, FT4) and thyroxine-binding globulin (TBG). Upon dexamethasone therapy, steroid hormones returned progressively toward normal as did both PRL and TSH; PRL declined faster than TSH. Serum E2 correlated better with PRL than with TSH. Therefore, the responsiveness of the thyrotrophs to the ambient concentration of E2 is lower and slower than that of the lactotrophs. In the context of the inconclusive data on the role of estrogens in controlling the secretion of TSH in humans, our case suggests that E2 does stimulate the secretion of basal and TRH-elicited both TSH and PRL, and that this positive action is unopposed by T. In contrast, T antagonizes the estrogen-induced increase in serum TBG. We also postulate that E2 might impair the bioactivity of TSH, in order to explain (i) the approximate 3-fold increase in serum TSH coexisting with a normally sized (rather than enlarged) thyroid and normal (rather than increased) serum thyroid hormones, and (ii) the inability of TRH-stimulated TSH to acutely raise FT3 serum levels.     

3,5-diiodo-L-thyronine increases resting metabolic rate and reduces body weight without undesirable side effects

Recently, it was demonstrated that 3,5-diiodo-L-thyronine (T2) stimulates the resting metabolic rate (RMR), and reduces body-weight gain of rats receiving a high-fat diet. The aim of this study is to examine the effects of chronic T2 administration on basal metabolic rate and body weight in humans. Two euthyroid subjects volunteered to undergo T2 administration. Body weight, body mass index, blood pressure, heart rate, electrocardiogram, thyroid and liver ultrasonography, glycemia, total cholesterol, triglycerides, free T3 (FT3), free T4 (FT4), T2, thyroid stimulating hormone (TSH) and RMR were evaluated at baseline and at the end of treatment. RMR increased significantly in each subject. After continuing the T2 treatment for a further 3 weeks (at 300 mcg/day), body weight was reduced significantly (p<0.05) (about 4 percent), while the serum levels of FT3, FT4 and TSH, were unchanged. No side effects were observed at the cardiac level in either subject. No significant change was observed in the same subjects taking placebo.     

131I对男性甲状腺功能亢进症血清性激素及甲状腺球蛋白水平影响研究

目的:探讨~(131)I对男性甲状腺功能亢进症患者血清性激素及甲状腺球蛋白水平的影响。方法:收集我院收治的男性甲状腺功能亢进症患者74例,随机分为对照组和实验组,每组各37例,对照组患者给予他巴唑口服,20-30 mg/次,每日口服1次。实验组患者在对照组基础上给予~(131)I治疗。治疗结束后,检测并比较两组患者血清游离三碘甲状腺素(FT3)、游离甲状腺素(FT4)、促甲状腺激素(TSH)、睾酮(T)、雌二醇(E2)、甲状腺球蛋白(TG)水平的变化以及临床疗效。结果:与治疗前相比,两组患者血清FT3、FT4、T、E2、TG水平均显著下降,TSH水平明显升高(P0.05);与对照组相比,实验组患者血清FT3、FT4、T、E2、TG水平较低,TSH水平以及临床治疗有效率较高(P0.05)。结论:~(131)I能够显著降低男性甲状腺功能亢进症血清FT3、FT4、T、E2、TG水平,升高TSH水平,临床效果较好。     

Influence of perinatal factors and sampling methods on TSH and thyroid hormone levels in cord blood.

To evaluate the effect of perinatal factors and sampling methods on thyroid stimulating hormone (TSH) and thyroid hormone levels in cord blood, serum TSH, free thyroxine (FT4) and free triiodothyronine (FT3) concentrations were measured in 124 healthy term neonates. Eighty-eight infants were born in normal vaginal deliveries, 25 were delivered by vacuum extractor and 11 by Cesarean section. There was no significant difference among the three infant groups in the mean TSH levels. Birth weight, the infant's sex, duration of labor and uterotonic agents had no effect on cord serum TSH and free thyroid hormone levels in the neonates born by normal vaginal delivery. To assess the adequacy of specimen collection, mixed cord blood samples, obtained by a direct application of cord on a filter paper, and venous blood withdrawn with a plastic syringe were collected in another 200 infants. There was a significant linear correlation in the TSH concentration in mixed cord blood and cord venous serum from the same individuals, while a poor correlation was found in T4 values from two specimens. Our results suggest that the TSH value in cord blood is less influenced by perinatal factors, including the sampling method, and the mixed cord blood collected by this technique might be a feasible alternative specimen for a TSH screening program with cord blood which is useful in countries where neonatal blood is not available.     

Response of thyrotropin, prolactin and free thyroid hormones to graded exercise in normal male subjects

Serum levels of thyrotrophin (TSH), prolactin (PRL), free thyroxine (FT4) and free triiodothyronine (FT3) were determined before and after physical exercise in 21 normal male subjects. The subjects were divided into 3 groups as follows: group I--light exercise (exercise on the Mijnhardt bicycle ergometer at 100 Watts for 15 min); group II--moderate exercise (a 5 km marathon); group III--heavy exercise (a 10 km marathon). In group I, TSH level rose from 1.96 +/- 0.42 mu u/ml (mean +/- SEM) to 2.52 +/- 0.30 mu u/ml (p less than 0.01), and PRL levels rose from 11.0 +/- 2.0 ng/ml to 19.0 +/- 5.2 ng/ml (p less than 0.01). In group II, TSH rose from 2.11 +/- 0.51 mu u/ml to 2.62 +/- 0.56 mu u/ml (p less than 0.05), and PRL rose from 11.2 +/- 1.6 ng/ml to 24.0 +/- 5.2 ng/ml (p less than 0.01). In group III, TSH rose from 2.01 +/- 0.41 mu u/ml to 2.36 +/- 0.45 mu u/ml (p less than 0.02), and PRL rose from 12.1 +/- 2.0 ng/ml to 47.7 +/- 9.3 ng/ml (p less than 0.01). The serum levels of FT4 showed different results among the three groups: Group I showed an increased response from 1.60 +/- 0.12 ng/dl to 1.72 +/- 0.12 ng/dl (p less than 0.01); Group II showed no significant difference; and group III demonstrated a diminished response from 1.61 +/- 0.14 ng/dl to 1.45 +/- 0.16 ng/dl (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)