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One of the aims in reproductive medicine is to differentiate between couples that have favourable chances of conceiving naturally and those that do not. Since the development of the prediction model of Hunault, characteristics of the subfertile population have changed. The objective of this analysis was to assess whether additional predictors can refine the Hunault model and extend its applicability. Consecutive subfertile couples with unexplained and mild male subfertility presenting in fertility clinics were asked to participate in a prospective cohort study. We constructed a multivariable prediction model with the predictors from the Hunault model and new potential predictors. The primary outcome, natural conception leading to an ongoing pregnancy, was observed in 1053 women of the 5184 included couples 120%). All predictors of the Hunault model were selected into the revised model plus an additional seven Ivvoman's body mass index, cycle length, basal FSH levels, tubal status, history of previous pregnancies in the current relationship [ongoing pregnancies after natural conception, fertility treatment or miscarriages), semen volume, and semen morphology. Predictions from the revised model seem to concur better with observed pregnancy rates compared with the Hunault model; c-statistic of 0.71 195% CI 0.69 to 0.731 compared with 0.59 195% CI 0.57 to 0.61). (C) 2017 Published by Elsevier Ltd on behalf of Reproductive Healthcare Ltd

The incidence of familial cases of premature ovarian failure varies from 4 to 31%. Recall bias may explain part of the variance. Thorough evaluation of alleged affected relatives showed a lower incidence than the original family history suggested. In the present study the incidence of familial cases was 12.7%. Pedigree studies on affected families showed a mode of inheritance suggestive of autosomal dominant sex-limited transmission or X-linked inheritance with incomplete penetrance. An adequate family history can distinguish between familial or sporadic premature ovarian failure. The risk of female relatives developing premature ovarian failure may be as high as 100% in familial premature ovarian failure, or as low as 1% in sporadic cases.

Objective: To determine the effect of corticosteroids on ovarian responsiveness to exogenous gonadotropins in patients with idiopathic premature ovarian failure (POF). Design: Placebo-controlled, randomized, double-blind, multicenter study. Setting: Two tertiary care academic centers for reproductive endocrinology and fertility and two general teaching hospitals. Patient(s): One hundred patients with idiopathic POF intended to enter the study. The study was discontinued after 36 patients failed to ovulate. Intervention(s): Endocrine and immune parameters were tested on days 1 and 15. On day 1, subjects were randomized to receive either 9 mg of dexamethasone daily or placebo. From day 5 onward, 300 IU of hMG daily was added for 10 days in both groups. The dosage of dexamethasone was decreased stepwise in the second week and discontinued after day 15. Patients were monitored by transvaginal ultrasonography and by determining serum E 2 levels. Main Outcome Measure(s): Ovulation rate. Fifty patients would have to be included in each study group to detect a statistically significant difference of 20% in the ovulation rate between the two groups with α = 0.05 and β = 0.1 (one-tailed test). Result(s): No ovulation was recorded in the first 36 patients. Interim analysis showed that the 95% confidence intervals of an ovulation rate of 0 were 0–17% for the dexamethasone arm (n = 19) and 0–19% for the placebo arm (n = 17). Because the preset objective (a difference of 20%) would never be reached, the study was discontinued. Conclusion(s): Corticosteroids do not influence ovarian responsiveness to gonadotropins in patients with idiopathic POF.