[Cushing's syndrome and pregnancy].
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Biomedical subjects
Publications and source records attributed to D Reinwein.
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The ratios of reverse triiodothyronine (rT3) to triiodothyronine (T3) concentrations were similar (0.89 +/- 0.09) in twenty-three autonomous thyroid nodules (fourteen decompensated, nine compensated) and paranodular tissues (0.82 +/- 0.08), whereas the serum ratio was significantly lower (0.098 +/- 0.014). This is compatible with the hypothesis that thyroidal rT3 and T3 production from mono- and diiodotyrosine may be a random process in contrast to non-random extrathyroidal rT3 and T3 formation.
Six patients with idiopathic isolated gonadotropin deficiency (IGD) were treated with 100 microgram LH-RH s.c. 3 times daily, leading to subnormal increases of serum gonadotropin (Gn) and testosterone (T) levels, and promoting puberty from stage I to stage II-III of TANNER. S.c. administration of 100 microgram of the more potent and longer-lasting analogue 6-D-Leu-10-Des-Gly-ethylamide-LH-RH induced LH and FSH rises after the very first application in these patients for more than 12 h. However, long-term therapy with the analogue (100 microgram s.c./day) did not improve hypogonadism. Paradoxically, on daily treatment (8 patients) with 6-D-Leu-10-Des-Gly-ethylamide-LH-RH the FSH serum levels fell after 1 week and the LH levels after 8 weeks of treatment.
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Thymus-derived peripheral blood lymphocytes were studied in untreated (n = 18), methimazole-treated (n = 28) thyrotoxicosis, after radioiodine (n = 14), in Hashimoto thyroiditis (n = 7) and in euthyroid goiter (n = 7). The results were compared with normal persons (n = 40) without thyroid disease. There was no significant difference in the total and relative counts of T-cells either between the different groups nor compared with the controls. These findings confirm that T-cells in peripheral blood cannot give any information about activity or prognosis of the various thyroid diseases. Thus T-cells give no further suggestion concerning the possible pathogenetic role of cell-mediated-immunity.
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In 27 thyrotoxic patients and in 177 healthy controls from the area of Essen we studied the total urinary iodine excretion. Whereas the iodine excretion was only 43.7 +/- 27.3 mug iodine per g creatine in the controls, the corresponding average value was significantly higher in thyrotoxic patients. It amounted to 193.3 +/- 201.7 mug iodine per g creatinine. This finding can not be explained by selection of patients with autonomous adenomas and contamination with iodine. Possible causes are an increased daily iodine uptake by increased dietary intake or iodine containing drugs that might not be remembered by the patients and increased renal clearance of iodine. Strong evidence for a contamination with iodine is the finding of increased differences between measured and calculated PBI, the latter being derived from T4 (D). The differences averaged in both groups 5.3 and 3.2 mug/100 ml. Our data can not exclude a basedowification of preexisting goiters. This unexpected finding gives rise to corresponding investigations in other thyroid centers.