INCREASED 17-OH-PROGESTERONE LEVELS FOLLOWING HCG STIMULATION IN MEN WITH IDIOPATHIC OLIGOZOOSPERMIA AND RAISED FSH-LEVELS

Leydig cell function was investigated in 71 men with idiopathic oligospermia and compared to 14 fertile controls by assessing the steroidogenic response to GnRH and the repetitive administration of hCG (1500 IU x3). The oligospermic men were divided into two groups according to their basal serum FSH values (FSH<8, n=35; FSH>8, n=36), this level being defined by the mean + 3 SD of the levels in normal men (3.71+4.08 mIU/ml). Oversecretion of LH was supported by the findings of: (a) higher basal LH levels (p<0.0001) in both oligospermic groups, although still within the normal range; (b) higher D-max LH and area LH (p<0.0001) levels in the FSH>8 group; (c) a strong position correlation (p<0.001) of the above parameters with the respective levels of FSH. No difference in basal testosterone levels was observed between the three groups, whereas basal levels of 17-OHP were significantly higher (p<0.05) in the group with FSH>8. The testosterone/LH ratio was significantly (p<0.0001) lower in the FSH>8 group, and was correlated inversely to the basal blood levels of FSH (p<0.0001) and to the area LH (p<0.04). After the hCG test, there was no difference in the testosterone and oestradiol response between the groups, whereas the secretion of 17-OHP and the ratio of 17-OHP/testosterone was significantly higher (p<0.0001) in the group with FSH>8 compared with the other two groups. Using multiple regression, the total production of 17-OHP and the 17-OHP/testosterone ratio were found to be correlated positively with FSH levels. These results support the view that in men with idiopathic oligozoospermia associated with severe Sertoli cell dysfunction there is parallel oversecretion of LH and compensated dysfunction of the Leydig cells, as indicated by oversecretion or accumulation of 17-OHP after hCG administration, and also by the low testosterone/LH ratio. This is possibly due to alterations in intratesticular paracrine factors deriving from the Sertoli cells, as suggested by the positive correlation between the altered steroidogenic indices and blood FSH levels

THE CONTRIBUTION OF HYPOGONADISM TO THE DEVELOPMENT OF OSTEOPOROSIS IN THALASSEMIA MAJOR - NEW THERAPEUTIC APPROACHES

OBJECTIVE The osteoporosis seen in thalassaemia major is of multifactorial origin. The aim of the study was to evaluate the contribution of hypogonadism to the development of this osteoporosis and to assess the efficacy of new sex hormone replacement therapy regimens. DESIGN AND PATIENTS Sixty-seven patients were studied: 12 were hypogonadal, 32 had been on previous hormone replacement therapy (conjugated oestrogens plus medroxyprogesterone for females, depot testosterone esters for males); 10 had received continuous courses of treatment and 22 3-monthly on/off courses, and 22 were eugonadal without previous replacement therapy. Twenty-seven of the above patients were evaluated prospectively at 16 and 32 months during different therapeutic approaches (12 without treatment, 7 on continuous replacement and 8 on/off schemes followed by continuous therapy during the second observation period). The continuous schemes comprised either transdermal oestradiol (100 mu g) plus medroxyprogesterone for females or hCG to produce serum testosterone concentrations within normal range, for males. MEASUREMENTS Bone mineral density (BMD) end bone mineral content (BMC) of lumbar spine and distal end of radius were measured by dual-energy X-ray absorptiometry. RESULTS Spinal BMD was found to be more than 30% lower than that of controls matched for sex and age with no difference between sexes. Radial BMD was less impaired and showed significantly (P < 0.01) higher levels in males (decrease of 5.8% +/- 2.3, mean +/- SD) than in females (- 14.5 +/- 3.4%, mean +/- SD). In the retrospective evaluation it was found that the hypogonadal group had the lowest (P < 0.0001) BMD levels (0.62 +/- 0.01, mean +/- SE) and the highest were observed on the continuous replacement group (0.83 +/- 0.04), whereas the values of the other groups were similar. In a multiple regression analysis model it was found that only sex steroid levels were related to the BMD measurements (for oestradiol t = 2.6, P = 0.01 and for testosterone t = 6.5, P = 0.0001), whereas parameters related to haemolytic anaemia and desferrioxamine treatment were not. In the prospective study the continuous replacement group increased BMD and BMC values more than the on/off treatment courses (P = 0.01). CONCLUSIONS Hypogonadism seems to play an important role in the development of osteopenia-osteoporosis in thalassaemia major; continuous hormone replacement therapy with transdermal oestrogen for females or hCG for responding males best improves the bone density parameters

Cold thyroid nodule as the sole manifestation of Rosai-Dorfman disease with mild lymphadenopathy, coexisting with chronic autoimmune thyroiditis

A case of thyroid Rosai-Dorfman disease (RDD) without apparent lymphadenopathy in a 49-year-old woman with underlying euthyroid chronic autoimmune thyroiditis, as indicated by high thyroid autoantibodies titers, is presented. The initial presentation was that of a cold, hypoechogenic nodule of left thyroid lobe which increased in size during the two years of follow up, together with new ultrasonographic findings of the right lobe. No biochemical abnormalities were found apart from mild hypercalcemia. A near total thyroidectomy was performed. Histologically, the left robe nodule as well as the right lobe lesions consisted of typical RDD cellular population, with the pathognomonic phenomenon of emperipolesis. Infiltration to the periphery of the gland was observed and three adjacent lymph nodes were also involved. The uninvolved thyroid parenchyma showed changes compatible with chronic autoimmune thyroiditis. No other localizations or systemic manifestations of RDD were revealed. Normocalcemia was restored promptly and the patient remains free of clinically overt disease one year post-operatively. (J. Endocrinol. Invest. 22: 866-870, 1999) (C) 1999, Editrice Kurtis