LH, FSH responses to GnRH in lepromatous leprosy.
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Biomedical subjects
Publications and source records attributed to G K Rastogi.
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The circulating levels of TSH, its metabolism, and its response to synthetic TRH were studied in five euthyroid menstruating rhesus monkeys before and during treatment with estradiol monobenzoate (E2B, 50 microgram/kg BW/day sc). The pre-E2B treatment mean plasma TSH level was 1.4 +/- 0.12 (SE) microunit/ml. A significant increase in mean plasma TSH (P less than 0.01) to 1.54 +/- 0.29 microunit/ml was observed as early as 48 h after intiation of E2B treatment; it continued to rise progressively to day 28 when it plateaued around a mean concentration of 3 microunit/ml. It normalized within 10 days after cessation of E2B therapy. After iv TRH (5 microgram/kg BW), a consistent rise in plasma TSH was observed before and on days 11 and 56 of E2B therapy. The peak TSH level and maximum rise over the basal level (deltaTSH) during the three tests were not significantly different. During E2B therapy there were remarkable changes in TSH kinetics. These alterations included a significant decrease (P less than 0.01) in metabolic clearance rate, contraction of the distribution space, and expansion of the extrapituitary TSH pool, but there was no appreciable change in TSH production rate. Although a definite trend towards the above alterations was discernible on day 17 of treatment, they were well established by day 66. These data suggest that the estrogen-induced rise in circulating TSH was caused mainly by decreased degradation and not by increased production.
The effects on carbohydrate and lipid metabolism in 24 healthy female subjects of the long-acting steroid contraceptives norethisterone oenanthate (200 mg) (11 subjects) and depo-medroxyprogesterone acetate (150 mg) (13 subjects) were studied. The subjects were between the ages of 18 and 25 years, with a history of normal menstrual periods. Pretreatment levels of plasma cholesterol, plasma triglycerides, phospholipids, blood glucose, insulin, and growth hormone were compared with those obtained 3 weeks and 12 weeks after the initial injections. There were no statistically significant differences from the pretreatment levels in any of the values obtained at 3 weeks and 12 weeks in either group.
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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 alterations in serum levels of T3, T4, TSH and TBG, TSH response to 100 mug iv TRH, and urinary excretion of T3 and T4 were studied in 8 healthy men at sea level (SL), on days 1, 2, 4, 8 and 16 after arrival by air at high altitude (3,700 m, HA), and during days 5 to 7 after their return to SL. No significant alterations in serum levels of TSH and TBG or TSH response to TRH were observed during exposure to HA or on return to SL. There was, however, an acute elevation in both serum total T3 and T4. Serum total T3 from a mean basal+/-SE value of 128+/-13 ng/dl increased to 320+/-18 on day 1 and remained significantly elevated at 225+/-48 up to day 8 after arrival at high altitude. Similarly serum total T4 increased from basal level of 9+/-0.92 mug/dl to 15.2+/-1.2 and remained elevated till day 16 and it was 11+/-1.19 mug/dl during days 5 to 7 after return to SL. The urinary excretion of both T3 and T4 was decreased. These changes perhaps were the result of complex physiologic adjustments on acute exposure to high altitude, like shrinkage of the T3 and T4 distribution pools, altered binding capacities of thyroid hormones binding proteins, and a reduction in clearance of thyroid hormones from the plasma compartment; and were probably not suggestive of an enhanced thyroid activity. Their actual significance in high altitude adaptation in man is not clearly understood.
Sera from twenty six patients of various types of leprosy were tested for the detection of circulating auto-antibodies and nuclear components against thyroid using various methods. Four patients of lepromatous leprosy had higher levels of thyroid auto-antibodies by latex agglutination. Three patients showed the presence of anti-nuclear antibodies, two belonged to the TT and one to the LL group.
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Twenty six patients of different types of leprosy were studied for radio active iodine uptake (I131) and serum levels of triiodothyronine (T3), thyroxine (T4) and thyroid stimulating hormone (TSH). None of the patients had clinical evidence of thyroid involvement. No significant difference was found between the values obtained in patients and normals and in different varieties of leprosy.