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Hypothalamic-pituitary gonadal function is commonly altered in dialysis patients. Even though an improvement in general status and well-being has been noted after recombinant human erythropoietin supplementation, no significant changes were observed in the sex hormone profile. Pituitary gonadal axis as well as 5 alpha-reduced androgen glucosiduronates (i.e. 5 alpha-androstane,3 alpha,17 beta-diol and androsterone) profiles were studied in 23 young male stable dialyzed patients and compared to an age-matched group of healthy subjects. 5 alpha-Reduced androgen glucosiduronates are products of peripheral testosterone (T) metabolism and seem to be a useful tool in assessment of the male androgen status. Their polarity facilitates their urinary excretion, and their clearance is similar to the glomerular filtration rate in healthy men. We observed 1) a pituitary-Leydig cell dysfunction supported by normal serum estradiol and T levels, low free T, and increased LH levels; 2) an alteration of the dehydroepiandrosterone (DHEA) sulfate-DHEA interconversion, reflected by a dramatic decrease in DHEA while DHEA sulfate levels remained in the normal range; 3) an accumulation of 5 alpha-reduced androgen glucosiduronates, whose removal was impaired as shown by their very low sieving coefficients (< 0.012). Taken together, the above observations are consistent with alteration of spermatogenesis with respect to dialysis duration in which earlier elevated baseline serum LH levels indicate a primary defect in Leydig cell function.

Functional thyrotropin receptors (TSH-R) have recently been detected in fat cells but not in liver cells from rat, and it seems that in infant adipocytes stimulatory TSH-R antibodies (TSH-R-ab) act through this receptor pathway, resulting in increased triglyceride catabolism. We investigated the relationships between plasma TSH-R-ab and free thyroxine (FT4) levels and plasma lipid or lipoprotein values in 49 untreated adult women with Graves' disease, all positive for these antibodies. A simple positive correlation (p < 0.01) was found between TSH-R-ab levels and FT4 values (r = 0.40). Simple positive correlations (p < 0.001) were found between triglyceride levels and FT4 (r = 0.51) or TSH-R-ab (r = 0.52) values. Multiple regression analysis confirmed that both FT4 and TSH-R-ab are strong (p < 0.005) predictors of triglyceride (FT4: partial r = 0.40; TSH: partial r = 0.39). Simple negative correlations (p < 0.05, at least) were found between FT4 levels and total cholesterol (TC) (r = -0.45), low-density lipoprotein (LDL)-C (r = -0.46), apoprotein (apo)-B (r = -0.31) or high-density lipoprotein (HDL)-C (r = -0.55) values. Among these lipid parameters, only HDL-C levels (r = -0.31, p < 0.05) correlated to TSH-R-ab values. However, multiple regression analysis revealed that while FT4 is a strong predictor (p < 0.005) of TC (partial r = -0.42), LDL-C (partial r = -0.43) or HDL-C (partial r = 0.47), TSH-R-ab are not. Thus, the apparent positive relationship between TSH-R-ab and HDL-C results from the positive correlation between TSH-R-ab and FT4. In conclusion, this study suggests that stimulating TSH-R-ab are involved in triglyceride metabolism. In contrast to thyroid hormones, these antibodies seem not to be related to cholesterol metabolism.