We report three patients who developed hypopituitarism as a late complication of hemorrhagic fever with renal syndrome (HFRS). Their past history, physical examination, and endocrine investigation confirmed hypopituitarism. Magnetic resonance imaging of the pituitary revealed atrophic pituitary gland with an empty sella. Hemorrhagic fever is endemic in certain regions of the Balkans, and this preliminary report suggests the importance of investigating the endocrine status in every patient who survived HFRS.
The study was conducted to assess leptin levels and insulin sensitivity in obese and non-obese patients with polycystic ovary syndrome (PCOS). Twenty-two women with PCOS and 19 control healthy women were included in the study, divided into obese and non-obese groups. Leptin was determined using Linco Research radio-immunoassay while insulin sensitivity was calculated from intravenous glucose tolerance tests with frequent blood sampling using MINMOD analysis. Significantly higher basal leptin levels were found in obese compared to non-obese PCOS (31.76 +/- 3.06 vs. 10.42 +/- 2.31 ng/ml; p < 0.05) as well as in obese in comparison to non-obese controls (29.16 +/- 5.06 vs 8.51 +/- 0.88 ng/ml; p < 0.05). A negative correlation was found between insulin sensitivity and leptin levels in both obese (r = -0.2480; p > 0.05) and non-obese PCOS groups (r = -0.4620; p > 0.05). In conclusion, high serum leptin, insulin and testosterone levels together with reduced insulin sensitivity were found in obese PCOS women, suggesting that high leptin levels could be a characteristic of the obese PCOS phenotype.
Ten patients in acute exacerbation of multiple sclerosis were treated with 1000 mg of methylprednisolone for 7 days, followed by abrupt cessation of therapy. The function of hypothalamic-pituitary-adrenal (HPA) axis was assessed by the response of ACTH and cortisol to insulin tolerance test (ITT). ITT was performed 1 day before and 1, 3, 8, 13 and 23 days after the termination of the therapy (days 0, 8, 10, 15, 20 and 30 of the study, respectively). The response of these hormones to insulin-induced hypoglycemia prior to therapy was normal. There was no suppression of the ACTH response to hypoglycemia after the methylprednisolone therapy based on the 100% rise of ACTH after ITT. Cortisol response during ITT was suppressed at day 8 (1 day after ending of therapy) but recovered on day 10 (3 days after ending of therapy). In conclusion, 7 day-therapy with 1000 mg methylprednisolone does not result in the permanent suppression of the HPA axis, suggesting that no regular supplemental corticosteroid coverage is required. The observed transitory suppression of the HPA axis recovered spontaneously after the therapy.
The sequential administration of GHRH in normal subjects and of hexarelin 120 minutes later provides separate information regarding pituitary GH reserve, of both secretagogues without mutual interference. There were not false negative results to the combined test. This sequentially delayed test may be of some value in the clinical setting for assessing pituitary GH reserve.
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