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BACKGROUND: Predictive factors of women who are unable to quit prolonged hormonal therapy (HT) are largely unknown. We sought to identify predictors for the resumption of HT after the discontinuation of treatment. METHODS: A cohort prospective study was conducted allocating menopausal women treated with HT for over 3 years. Menopausal symptoms were monitored periodically after HT cessation by the Greene climacteric scale. RESULTS: Eighty-two women participated in the study. Age, the age of menopause, BMI, HT duration, the type of regimen, reasons cited to discontinue HT and the method of discontinuation did not differ between the subjects who successfully discontinued HT and those who failed to quit HT. Only the prevalence of vasomotor symptoms when HT was first prescribed significantly differed between the groups (P = 0.03). Comparable maximal Greene score was recorded in both groups. Over time, the subjects who returned to HT had higher Greene score [Hazard ratio 1.25, confidence interval (CI) 95% (1-1.07)] and significantly higher vasomotor score [Hazard score 1.22, CI 95% (1.02-1.46)]. CONCLUSIONS: The history of hot flashes and the duration of menopausal symptoms upon HT discontinuation predict the resumption of HT. Thus, the return to HT is expected in individuals who are intolerant of prolonged climacteric syndrome.

The objective was to study the pathophysiology of the dyslipidaemia hi polycystic ovarian syndrome (PCOS) patients, and to determine how it is related to hyperinsulinaemia, hyperandrogenism and dehydroepiandrosterone sulphate (DHEA-S) concentrations. The lipoprotein lipid profile, anthropometric measurements, endocrine profile and the presence of insulin resistance were evaluated hi 31 PCOS patients and 20 age-matched healthy women, who served as controls. PCOS patients had higher fasting insulin concentrations, higher body mass indexes (BMI) and were hyperlipidaemic, with higher total cholesterol, low density lipoprotein (LDL) and triglyceride (TG) concentrations. There were no relationships between plasma lipids and anthropometric variables hi the patient group as a whole. Insulin-resistant (IR) and non-ER (NIR) PCOS patients were then evaluated separately. Obesity with marked hyperandrogenism were the predominant features hi patients with IR. NIR patients were not obese and had significantly less hyperandrogenism. The adrenal androgen DHEA-S was at the upper limit of its normal range in both groups. However, both PCOS subgroups exhibited similar significant abnormalities hi terms of then- lipid parameters. Insulin and DHEA-S concentrations were positively correlated with total cholesterol, LDL and TG, and negatively correlated with high density lipoprotein, hi IR patients. In NIR subjects, insulin was not correlated with any of the lipids and DHEA-S was negatively related to cholesterol and LDL. Anthropometric variables were related to lipids hi only the NIR patients. Thus PCOS subjects as a group exhibit dyslipidaemia, characterized by increased total cholesterol, LDL and TG concentration s. When divided into IR and NIR subjects, there were no differences hi the degree of lipid abnormalities, despite significant variations hi the BMI and androgen status. Thus, hi PCOS subjects, dyslipidaemia may occur irrespective of insulin resistance. Insulin and DHEA-S concentrations were positively correlated with an atherogenic lipid profile hi the IR group only. As distinct from syndrome X when IR was present, dyslipidaemia was not related to body weight or the waist:hip ratio. In the NTR group there was no relationship 1848 between lipids and insulin; DHEA-S, on the other hand, was negatively related to cholesterol and LDL concentrations. Thus, dyslipidaemia hi PCOS patients may occur irrespective of insulin resistance, and may have different metabolic aetiologies depending on DHEA-S metabolism. It remains to be seen whether the two types of PCOS are associated with different risks for ischaemic heart disease.

We studied the clinical and endocrine features of 35 patients with polycystic ovary syndrome (PCOS) who are either insulin resistant or non-insulin resistant. The occurrence of insulin resistance was determined by measuring insulin and glucose concentrations following a standard 75 g oral glucose load. All patients were evaluated by anthropometric measurements: body mass index (BMI), percentage of body fat (BCF) and waist-to-hip ratio (W/H), degree of hirsutism (Ferriman-Gallwey method) and endocrine profile. Fourteen patients had insulin resistance of unknown origin whereas four were due to a type A insulin receptor mutation, and 17 were non-insulin resistant. The insulin resistant patients were significantly more obese (higher BMI P < 0.0001, BCF P < 0.002 and W/H ratio P < 0.005) and were more hirsute (P < 0.002) than the non-insulin resistant patients. Testosterone concentrations were significantly higher in the insulin resistant group than in the non-insulin resistant group (2.65 versus 1.37 nmol/l; P < 0.027), whereas sex hormone-binding globulin was lower in insulin resistant patients (30.61 versus 19.48 nmol/l; P < 0.02). Non-insulin resistant patients showed a high luteinizing hormone to follicle stimulating hormone ratio, while a normal ratio was found in the insulin resistant subpopulation (2.94 versus 1.34; P < 0.0001). We concluded that PCOS comprises two subpopulations, one with insulin resistance of different aetiologies and the other which has no insulin resistance. These two groups differ in their anthropometric and endocrine features. The diagnosis of insulin resistance in PCOS can be easily determined by the insulin response to an oral glucose tolerance test.

A seasonal distribution in human natural conception and birth rates has been consistently demonstrated by epidemiological studies in several geographical areas. Possible hypotheses abound to explain this seasonality. Though a seasonal effect on reproduction is well-documented and has been extensively investigated in mammals, information concerning the influence of seasonal variation and its mechanism on human and primate reproduction is scarce. Recent evidence suggests that deterioration in sperm quality during the host summer in sub-equatorial areas, may result in lower conception rates leading to a reduction in the birth rate in spring. In northern countries, however, in regions where a strong seasonal contrast in luminosity exists, activity of the anterior pituitary-ovarian axis and the conception rate are decreased during the dark winter months. In these areas, inversely, a peak in conception rate during summer leading to a maximum in birth rate in spring has been observed. It is believed that seasonality in the ovulation rate may cause this variability. However, changes in the quality of the ovum or in endometrial receptivity which may lead to a greater waste of ovulated eggs and peri-implantation conceptuses at specific times of the year, have also been suggested. These phenomena might have important implications for in-vitro fertilization and gamete intra-Fallopian transfer as well as infertility in general. The seasonal effects, which may influence primate and human fertility and reproduction and its possible mediators, are critically reviewed.