Thyroid hormones changes in infants and children with metabolic acidosis.

The influence of the acidotic state on the thyroxine (T4) peripheral metabolism was studied in two different forms of metabolic acidosis, ie infantile diarrhea and diabetic ketoacidosis. The serum concentrations of T4, free T4 (FT4), triiodothyronine (T3), reverse T3 (rT3), thyrotropin (TSH) and thyroxine-binding globulin (TBG) were measured and compared to healthy control groups. Lower T4 and T3 and higher rT3 serum concentrations were found in both tested groups of patients in relation to the control groups. In infants with severe metabolic acidosis FT4 values were lower than those observed in the control group. In addition, serum TBG levels were lower in diabetic patients as compared to control subjects. Despite the reduced serum T3 and T4 concentrations in both groups of patients, TSH concentrations, were within the normal range. Therefore, we concluded that acidosis caused either by diarrhea (not so far described) or by diabetes mellitus (well documented up to now) affects the thyroid hormones metabolism in a similar way, at least as far as the thyroid hormones blood levels are concerned.     

The effect of growth hormone on the plasma levels of T4, free-T4, T3, reverse T3 an TBG in hypopituitary patients

The plasma concentrations of thyroxine (T4), free thyroxine (free-T4), triiodothyronine (T3), reverse triiodothyronine (rT3), TSH and thyroxine-binding globulin (TBG) were measured in 19 children suffering from idiopathic growth hormone deficiency. Blood was taken before and one month after growth hormone treatment. Ten patients were hypothyroid (group 1) and 9 were euthyroid (group 2). The basal T3 and rT3 levels correlated well with the T4 concentrations. Free-T4 levels were very low in all the hypothyroid patients and proved to be the most reliable index of TSH deficiency. TBG concentration was high in th hypopituitary patients regardless of their thyroid function. Following growth hormone treatment T4, free-T4 and rT3 levels fell in both groups. The T3 concentration rose in group 1 but no change was seen in group 2. There was a significant correlation between the changes of T4 and T3, such that the increase in T3 level was greatest in those with only a slight reduction of T4 concentration and no T3 increase was seen with more marked T4 decreases. The plasma TBG concentration is enhanced in growth hormone deficiency causing relatively high T4 values. Growth hormone treatment reduces T4 secretion and affects the peripheral metabolism of thyroid hormones resulting in an increase of T3 and a reduction of rT3 concentration.     

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).     

Human fetal and cord serum thyroid hormones: developmental trends and interrelationships

Thyroid hormone is essential for fetal and neonatal development in particular of the brain, but little is known about regulation of fetal thyroid hormone levels throughout human gestation. The purpose of this study was to clarify developmental trends and interrelationships among T(4), free T(4) (FT4), thyroxine-binding globulin (TBG), TSH, T(3), rT(3), and T(4) sulfate (T4S) levels in cord and fetal blood sera (n = 639, 15-42 wk gestation) and correlate infant levels (23-42 wk gestation) to maternal values (n = 428, 16-45 yr) and those of nonpregnant women (n = 233, 16-46 yr). In cord and fetal serum, T(4), T(3), and TBG levels increase with gestation until term; TSH, FT4, T4S, and rT(3) levels increase and peak in the late second/early third trimester and then decline to term; T(4)/TBG ratios increase until late second trimester and plateau to term. Term cord sera TSH, TBG, and all iodothyronine levels, except T(3), are higher than nonpregnant women. In the third trimester, cord serum FT4, TSH, rT(3), and T4S levels are also higher than corresponding maternal levels, but T(4), T(3), and TBG levels are lower than maternal values. The late second/early third trimester is a critical transition period in fetal thyroid hormone metabolism, which may be interrupted by preterm birth and contribute to postnatal thyroid dysfunction.     

Early adaptation of thyrotropin and thyroglobulin secretion to experimentally decreased iodine supply in man.

Five healthy male volunteers (aged 25 to 28 years) were studied both after 4 weeks of treatment with 200 micrograms iodine/d orally (PO) and following experimental iodine depletion by treatment with 3 x 300 mg perchlorate/d PO over a 4-week period, in an attempt to better define the early adaptive responses to an alteration in iodine supply in thyroid function. Intrathyroidal iodine, serum triiodothyronine (T3), free T3 (FT3), thyroxine (T4), free T4 (FT4), reverse T3 (rT3), thyroxine-binding globulin (TBG), thyroglobulin (Tg), and thyrotropin (TSH) levels (10-minute sampling over 24 hours) were measured at the end of iodine administration and at the end of perchlorate treatment. Thyroid volume was determined by sonography, and iodine content was determined by fluorescence scintigraphy. TSH pulses were analyzed by computer-assisted programs. Comparing both experimental situations, perchlorate treatment significantly reduced intrathyroidal iodine concentration (4.0 +/- 1.3 to 3.0 +/- 1.2 nmol/mL, P less than .05), but thyroid volume and total serum T4, T3, FT3, and TBG levels were not altered. Mean 24-hour serum TSH levels (1.8 +/- 0.3 to 1.0 +/- 0.3 mU/L, P less than .001), amount of TSH secreted/pulse (0.5 +/- 0.1 to 0.3 +/- 0.1 mU/L, P less than .001), and FT4 levels (15.7 +/- 1.7 to 14.3 +/- 1.4 pmol/L, P less than .005) were significantly diminished, whereas Tg levels (18.6 +/- 10.0 to 35.1 +/- 14.0 ng/mL, P less than .01) were significantly increased. Thyroid-specific antibodies were normal and were not altered by treatment.(ABSTRACT TRUNCATED AT 250 WORDS)     

老年人血管性痴呆与甲状腺轴功能关系的研究

目的　探讨老年人血管性痴呆（VD）与甲状腺轴功能的关系。　方法　采用放射免疫分析法检测31例VD患者、22例不伴有痴呆的脑血管病（CVD）患者及22例同龄对照的血清三碘甲状腺原氨酸（T     

Euthyroid sick syndrome in acute ischemic syndromes

The purposes of this study were to assess the occurrence of euthyroid sick syndrome in patients with acute myocardial infarction (AMI) or unstable angina (UA), and the relationship with beta-blocker or thrombolytic therapy. Plasma triiodothyronine (T3), reverse T3 (rT3), free T3 (FT3), thyroxine (T4), free T4 (FT4), thyroid-stimulating hormone (TSH), thyroxine-binding globulin (TBG), and albumin (ALB) levels were determined in 95 patients (59 males, 36 females, aged 58.4+/-9) with AMI and 19 patients (13 males, 6 females aged 54.7+/-12.3) with UA for 5 consecutive days from the onset of the acute syndrome and 1 month later. Patients were divided according to beta-blocker therapy and thrombolytic therapy. There was a significant T3 decrease and rT3 increase in all patients during the first 5 days following admission (p < 0.05). FT3 and FT4 remained unchanged during the study. In patients with complicated infarctions, the rT3 increase and the T3 decrease were significantly greater compared to those with uncomplicated infarctions (p<0.03). TSH, T4, TBG, and ALB were significantly (p<0.05) decreased only in complicated infarctions. No differences were observed between patients with or without thrombolysis or patients with or without beta-blocker treatment. The apparent decrease in T3, the increase in rT3 levels and the decreased TSH and T4 levels, show clearly that the euthyroid sick syndrome (low T3) occurs not only in AMI but also in UA. In addition, these hormonal changes are not affected by beta-blocker therapy and thrombolysis does not influence the occurrence of the syndrome. The degree of T3 decrease is proportional to the severity of cardiac damage and may have a possible prognostic value.     

Changes in serum thyroid hormones levels and their mechanisms during long-term growth hormone (GH) replacement therapy in GH deficient children

OBJECTIVE: The effects of GH therapy on thyroid function among previous reports have shown remarkable discrepancies, probably due to differences in hormone assay methods, degree of purification of former pituitary-derived GH preparations, dosage schedules, diagnostic criteria, patient selection, duration of treatment and study design. These considerations motivated us to investigate whether and how GH replacement therapy changes serum thyroid hormone levels, including the much less studied rT3 levels, in a group of unequivocally GH-deficient children receiving long-term recombinant human GH therapy. PATIENTS AND DESIGN: Twenty clinically and biochemically euthyroid children were studied in two therapeutic conditions: on GH replacement therapy for at least 6 months and without GH replacement, either before GH was started or after GH was withdrawn for 30-60 days. Eight patients were on thyroxine replacement treatment and thyroxine doses were kept constant during the study. Blood was collected before and after 15, 20 and 60 minutes of TRH administration in both therapeutic conditions (with GH and without GH). MEASUREMENTS: Concentrations of thyroid hormone levels were determined only in sera obtained before TRH administration. FT4, T3 and TSH were measured by immunoflourimetric assays and rT2 was measured by immunoradioassay. RESULTS: Patients were classified into two groups, according to basal TSH levels: group I (TSH > 0.4 mU/l, n = 12) and group II (on thyroxine and TSH < 0.05 mU/l, n = 8). In both groups, serum FT4 levels decreased (17. 0 +/- 1.1 vs. 14.3 +/- 0.9 mU/l, P < 0.001, and 18.0 +/- 1.7 vs. 14. 2 +/- 1.7 mU/l, P < 0.01, respectively), serum T3 levels increased (1.8 +/- 0.1 vs. 2.4 +/- 0.2 nmol/l, P < 0.001, and 1.9 +/- 0.3 vs. 2.4 +/- 0.2 nmol/l, P < 0.05, respectively), and serum rT3 levels decreased (0.35 +/- 0.03 vs. 0.25 +/- 0.03 nmol/l, P < 0.01, and 0. 48 +/- 0.06 vs. 0.34 +/- 0.06 nmol/l, P < 0.01, respectively). Basal (3.2 +/- 0.50 vs. 2.6 +/- 0.72 mU/l, P = 0.28, paired t-test), TRH-stimulated peak TSH levels (13.9 +/- 5.3 vs. 15.9 +/- 8.0 mU/l, P = 0.35, paired t-test) and TRH-stimulated TSH secretion, expressed as area under the curve (609 +/- 97 vs. 499 +/- 53 mU/l.minutes-1, P = 0.15, paired t-test), remained unchanged during GH replacement in group I patients. Low serum FT4 and high serum T3 levels were observed in only one patient each, but low serum rT3 levels were found in six patients (four in group I and two in group II) during GH replacement. CONCLUSIONS: These results show that long-term GH replacement therapy in children with unequivocal GHD significantly decreases serum FT4 and rT3 levels and increases serum T3 levels; that these changes are independent of TSH and result from increased peripheral conversion of T4 to T3 and that GH replacement therapy in GH deficient children does not induce hypothyroidism, but simply reveals previously unrecognized cases whose serum FT4 values fall in the low range during GH replacement.     

Effects of evening vs morning thyroxine ingestion on serum thyroid hormone profiles in hypothyroid patients

OBJECTIVE: Standard drug information resources recommend that l-thyroxine be taken half an hour before breakfast on an empty stomach, to prevent interference of its intestinal uptake by food or medication. We observed cases in which TSH levels improved markedly after changing the administration time of l-thyroxine to the late evening. We therefore conducted a pilot-study to investigate whether l-thyroxine administration at bedtime improves TSH and thyroid hormones, and whether the circadian rhythm of TSH remains intact. DESIGN Patients were studied on two occasions: on a stable regimen of morning thyroxine administration and two months after switching to night-time thyroxine using the same dose. On each occasion patients were admitted for 24 h and serial blood samples were obtained. PATIENTS: We investigated 12 women treated with l-thyroxine because of primary hypothyroidism, who used no medication known to interfere with l-thyroxine uptake. MEASUREMENTS: Patients were admitted to hospital and blood samples were obtained at hourly intervals for 24 h via an indwelling catheter. Following this first hospital admission, all women were asked to switch the administration time from morning to bedtime or vice versa. After 2 months they were readmitted for a 24-h period of hourly blood sampling. Blood samples were analysed for serum TSH (immunometric assay), FT4 and T3 (competitive immunoassay), T4 and rT3 (radioimmunoassay), serum TBG (immunometric assay) and total protein and albumin (colourimetric methods). RESULTS: A significant difference in TSH and thyroid hormones was found after switching to bedtime administration of l-thyroxine. Twenty-four-hour average serum values amounted to (mean +/- SD, morning vs bedtime ingestion): TSH, 5.1 +/- 0.9 vs 1.2 +/- 0.3 mU/l (P < 0.01); FT4, 16.7 +/- 1.0 vs 19.3 +/- 0.7 pmol/l (P < 0.01); T3, 1.5 +/- 0.05 vs 1.6 +/- 0.1 nmol/l (P < 0.01). There was no significant change in T4, rT3, albumin and TBG serum levels, nor in the T3/rT3 ratio. The relative amplitude and time of the nocturnal TSH surge remained intact. CONCLUSIONS: l-thyroxine taken at bedtime by patients with primary hypothyroidism is associated with higher thyroid hormone concentrations and lower TSH concentrations compared to the same l-thyroxine dose taken in the morning. At the same time, the circadian TSH rhythm stays intact. Our findings are best explained by a better gastrointestinal uptake of l-thyroxine during the night.     

Transient stimulatory effects on pituitary-thyroid axis in patients treated with interleukin-2.

It has been shown that various cytokine therapies may influence thyroid hormone parameters that may lead to serious side effects including nonthyroidal illness. Interleukin-2 is effective in increasing CD4-T cell numbers in human immunodeficiency virus (HIV)-infected patients and it is used in the treatment of various malignant tumours. However, the association of interleukin-2 (IL-2) therapy and thyroid function is not clearly established as serial systematic measurements of thyroid parameters have not been performed with interleukin-2 as the sole therapeutic agent. Therefore, it was the aim of this study to examine prospectively the impact of a 5-day interleukin-2 therapy on thyroid parameters in asymptomatic HIV-infected patients. Twenty male euthyroid patients (mean age, 42.6 +/- 3.2 years; body weight, 73.4 +/- 3.0 kg) received 9,000,000 IU/d interleukin-2. Thyroid function was evaluated by measurements of serum thyrotropin (TSH), triiodothyronine (T3), thyroxine (T4), free thyroxine (FT4), reverse T3 (rT3), thyroglobulin (Tg), thyroxine-binding globulin (TBG), and anti-thyroid-peroxidase (TPO)-antibodies from day 1-4 and on days 7, 14, 20, 40, 60, 80, and 100. All results are given as mean +/- SD. On day 4, we observed a significant increase that was still within normal range of T4 and T3 (p < 0.05). TSH increased from 1.33 +/- 0.57 to 4.53 +/- 1.39 mU/l (p = 0.0001) and FT4 from 18.1 +/- 4.2 to 48.9 +/- 10.9 pmol/L (p = 0.0001) on day 4 with a gradual decrease thereafter. Normalization to baseline levels for TSH (1.45 +/- 0.75 mU/L) and FT4 (18.1 +/- 3.0 pmol/L) was achieved only on day 14. The increase of FT4 was more pronounced (well in the hyperthyroid range) than the increase in total T4 in the presence of normal TBG and albumin concentrations whereas TBG was not affected. We did not observe changes in anti-TPO-antibody levels up to day 100. Our data clearly demonstrate that the administration of interleukin-2 has a stimulatory effect on the pituitary-thyroid axis. The increase of TSH suggests a central stimulation directed by the action of IL-2 as the major mechanism.     

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.     

THE INFLUENCE OF CARBAMAZEPINE ON THYROID HORMONES AND THYROXINE BINDING GLOBULIN IN HYPOTHYROID PATIENTS SUBSTITUTED WITH THYROXINE

Carbamazepine (CBZ) decreases the serum concentration of thyroid hormones. It is proposed that CBZ increases the extra-thyroidal metabolism of thyroid hormones. In order to test this hypothesis CBZ was given to nine hypothyroid patients substituted with thyroxine (T4). A significant decrease in serum concentrations of T4, calculated free T4 (FT4), triiodothyronine (T3), and calculated free T3 (FT3) was found after 3 weeks of CBZ medication. The serum concentrations of TSH and the T4:T3 ratios were unaltered, while the serum concentrations of T4-binding globulin (TBG) increased markedly in eight of the nine patients. These findings support the hypothesis of a CBZ induced increase in the extra-thyroidal metabolism of thyroid hormones.     

Prenatal diagnosis of a thyroglobulin synthesis defect in goats

Seven families, ascertained through probands with undetectable levels of thyroxine binding globulin (TBG) were studied from clinical and genetic points of view. The blood levels of TBG, thyroxine binding prealbumin (TBPA), thyroid-stimulating hormone (TSH), triiodothyronine (T3), and thyroxine (T4) were determined in altogether 128 family members. The concentration of free thyroxine (FT4) was calculated from the concentrations of T4, TBG and TBPA. Only men (n = 15) were found to have total TBG deficiency. Their TSH levels were within normal range and they did not show any clinical symptoms of thyroid dysfunction. The mothers and daughters of the affected men had significantly lower TBG levels than control women. Segregation analysis performed on 46 nuclear families showed significant evidence for an X-linked additive mode of transmission and an additional multifactorial component with heritability 0.47.     

Circulating thyroid hormones in progressive renal failure in the baboon (Papio ursinus)

In order to examine the effects of developing renal failure on circulating thyroid hormones, serum concentrations of thyroxine (T4), free T4 (FT4), triiodothyronine (T3) and reverse T3 (rT3) and TBG capacity were measured in 9 baboons before and during the progress of acute (mean survival 12 days), subacute (32 days) and chronic (120 days) renal failure following allogeneic renal transplantation. Irrespective of the rate of development of renal failure, there were significant, non linear (power functions) negative correlations between serum creatinine or urea concentrations and levels of T4, FT4 and T3; rT3 levels remained unchanged, but the T4: rT3 molar ratio fell from 236.5 +/- 61 (+/- SE) to 121.8 +/- 30.9 (p less than 0.05). T4 and T3 levels were invariably subnormal at creatinine concentrations greater than 250 mumol/l (2.8 mg/dl), but FT4 was subnormal only in chronic renal failure. Thyroxine binding globulin (TBG) capacity did not change significantly; thus the TBG: T4 ratio increased from 3.4 +/- 0.2 (basal) to 10.4 +/- 3.4 before death (p less than 0.05). In animals which survived for greater than 25 days after transplantation, a significant linear correlation between FT4 and T3 was found as uremia progressed. Polyacrylamide gel electrophoresis (pH 7.4) of (125I)-T4 labelled preoperative and uremic serum showed a consistent decline in the proportion of tracer bound to TBG, from 67.0 +/- 0.8% to 58.9 +/- 1.0% (p less than 0.001), with a 48% reduction in TBG saturation (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

The effect of surgical operation of moderate severity on thyroid function

The effect of surgery on thyroid hormone transport was studied in ten subjects undergoing vagotomy and pyloroplasty for chronic duodenal ulceration. Measurements of the serum protein bound iodine (PBI), thyrotrophic hormone (TSH), T4 binding capacities of the thyroxine binding proteins (TBPA and TBG), percentage and absolute free thyroxine (T4) and percentage free triiodothyronine (T3) were made before and after operation. Operation produced a sharp reduction in the maximal binding capacity of TBPA with no apparent change in TBG. There were significant increases in percentage and absolute free T4 and in percentage free T3. There was no change in PBI and no increase was demonstrated in TSH after operation. The changes appeared to be unrelated to the increase in adrenocortical hormones associated with injury. It is suggested that thyroid hormones may have an important role in post-injury metabolism.     

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.     

The effect of iodide on serum thyroid hormone levels in normal persons, in hyperthyroid patients, and in hypothyroid patients on thyroxine replacement.

OBJECTIVE: To clarify the duration and the extent of the antithyroid effect of iodides in hyperthyroidism, and to investigate whether iodides have an additional peripheral effect on the metabolism of thyroid hormones, as has been reported for some organic iodine compounds. DESIGN: The effect on the peripheral thyroid hormone levels of 150 mg of potassium iodide daily (equivalent to 114 mg of iodide) for 3-7 weeks was compared in 21 hyperthyroid patients and 12 healthy controls. A possible effect of iodide on the peripheral metabolism of thyroid hormones was investigated by assessing the serum levels of thyroid hormone in 12 hypothyroid patients on thyroxine replacement for 2 weeks. PATIENTS: There were 21 thyrotoxic patients, 12 healthy hospital controls, and 12 patients with complete or near-complete hypothyroidism, on thyroxine replacement. MEASUREMENTS: The following were measured before and at weekly intervals after iodide administration: (1) pulse rate, (2) serum T4, (3) serum T3, (4) serum TSH, (5) serum thyroxine-binding capacity (TBC), (6) serum rT3, (7) serum thyroxine-binding globulin (TBG), (8) the free-T4 Index, calculated as T4/TBC. RESULTS: In the hyperthyroid patients serum T4, T3 and rT3 decreased, whereas serum thyroxine-binding globulin and thyroxine binding capacity increased. Serum T3, however, did not become completely normal in all cases. After 21 days, serum T4 and T3 started increasing again in some cases, but other patients remained euthyroid even after 6 weeks. In the normal controls there was a small but significant and consistent decrease in serum T4, T3 and rT3 and an increase in serum TSH. Finally, in the T4-treated hypothyroid patients there was no consistent change, except for an increase of serum T4 at 1 and 14 days and a decrease of serum TSH the first day. CONCLUSION: Iodides in hyperthyroidism have a variable and unpredictable intensity and duration of antithyroid effect. Their antithyroid effect is smaller in normal controls. They have no important effect on the peripheral metabolism of thyroid hormones.     

The effect of prednisone on serum thyrotropin, thyroxine and triiodothyronine concentrations in hypothyroid patients.

The effect of exogenous prednisone on serum thyrotropin (TSH), thyroxine (T4), and triiodothyronine (T3) concentrations was investigated in four patients with non-functioning thyroid glands receiving T4 replacement therapy. Orally administered prednisone, in a dose of 20 mg each day for nine days, resulted in a significant decrease in mean serum TSH levels (p less than 0.01) without significant changes in levels of serum T4, T3, and thyroxine binding globulin (TBG). These findings suggest an inhibitory action of relatively low pharmacologic doses of prednisone on TSH release without changes in circulating thyroid hormone concentrations or inhibition of the peripheral conversion of T4 to T3.     

Lacking evidence for release of thyroid hormones from circulating thyroglobulin during subtotal thyroidectomy

The effect of subtotal thyroid resection for thyrotoxicosis on concentrations of serum thyroid hormones and thyroglobulin (Tg), was determined in 10 patients during operation and the subsequent 18 days. Mean serum Tg responded drastically, increasing from a pre-operative value of 0.30 nmol/l to a peak value of approximately 26 nmol/l during operation followed by a gradual decline to levels lower than before surgery on day 18. Mean serum total thyroxine was 114 nmol/l pre-operatively and free thyroxine index (FT4I) 105 units. Both fluctuated only slightly during operation. Postsurgically, the mean values decreased to below 50% of the pre-operative level. Mean serum total triiodothyronine (TT3) was 1.46 nmol/l pre-operatively. It decreased during operation, reaching a nadir of 0.55 nmol/l on day 2, whereafter the concentration increased slightly. Mean serum reverse T3 (rT3) was 0.45 nmol/l pre-operatively, increased 62% during surgery, and decreased postsurgically. The mean value of serum thyroid stimulating hormone (TSH) was 0.61 mU/l pre-operatively and remained below 1 mU/l during and after operation, but from day 10 concentration began to rise steadily. It is concluded that the vast release of Tg during thyroid resection did not contribute to the concentration of serum T4 to an extent of clinical relevance.