The effect of residual beta cell activity on menstruation and the reproductive hormone profile of insulin-dependent diabetics.

To investigate the cause of secondary amenorrhoea in insulin-dependent diabetes gonadotrophins, sex steroid hormone levels and residual beta cell activity (C-peptide index) were estimated in a group of 43 women with IDDM. Among 26 women with residual insulin secretion, the C-peptide positive (CpP) group, 5 had secondary amenorrhoea (CpP-Am); among 17 women without endogenous beta cell activity, the C-peptide negative (CpN) group 6 had secondary amenorrhoea (CpN-Am). In this study two different types of secondary amenorrhoea in insulin-dependent diabetics were observed. All CpP-Am women have the classical hormone profile of the polycystic ovary syndrome (increased (LH/FSH ratio, increased serum testosterone, decreased SHBG) together with a history of oligomenorrhoea and excess weight before the onset of diabetes. On the other hand, all CpN-Am women had decreased LH levels as well as low LH/FSH ratio and testosterone levels. These results strongly suggest that a lack of residual pancreatic beta cell activity influences hypothalamus-pituitary function in insulin-dependent diabetes. It might be concluded that PCOS is independent of diabetes while low LH amenorrhoea seems to be the consequence of diabetes and is strongly associated with a lack of residual insulin secretion.