Prelević, G.M. (7004326204)G.M. (7004326204)PrelevićWürzburger, M.I. (6603925241)M.I. (6603925241)WürzburgerPerić, L.A. (57017746600)L.A. (57017746600)Perić2025-06-122025-06-121989https://doi.org/10.1007/BF01560084https://www.scopus.com/inward/record.uri?eid=2-s2.0-0024315722&doi=10.1007%2fBF01560084&partnerID=40&md5=77c6abd4dd3200f515346fce7423935bhttps://remedy.med.bg.ac.rs/handle/123456789/2005To 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. © 1989 Springer-Verlag.C-peptideGonadotrophinsInsulin-dependent diabetes mellitus (IDDM)Residual beta cell activitySecondary amenorrhoea