The aim of this study was to obtain evidence for the genetic basis of polycystic ovaries (PCO) and premature male pattern baldness (PMPB) by screening first-degree relatives of women affected by polycystic ovary syndrome (PCOS). Because of the high prevalence of PCO in the general population, we also studied first-degree relatives of ten asymptomatic control volunteers of reproductive age. The probands were recruited prospectively from infertility and endocrine clinics, where they presented with various clinical symptoms of PCOS. Each had PCO, on transvaginal ultrasound scan. The families of 29 probands and 10 volunteers agreed to take part in the study. Clinical, ultrasound, and biochemical parameters were used to define PCO/PCOS. All female relatives had an ovarian ultrasound scan and hormone profile performed. History was used to assign status in postmenopausal women. All male relatives were assessed for early onset (<30 yr old) male pattern baldness, by photographs. All relatives were assigned affected (PCO/PMPB) or nonaffected status, and segregation analysis was performed. Of the relatives of 29 PCOS probands, 15 of 29 mothers (52%), 6 of 28 fathers (21%), 35 of 53 sisters (66%), and 4 of 18 brothers (22%) were assigned affected status. First-degree female relatives of affected individuals had a 61% chance of being affected. Of the first-degree male relatives, 22% were affected. Of a total of 71 siblings of PCOS probands, 39 were affected, giving a segregation ratio of 39/32 (55%), which is consistent with autosomal dominant inheritance for PCO/PMPB. In the control families, 1 of 10 probands (10%), 1 of 10 mothers (10%), no fathers, 2 of 13 sisters (15%), and 1 of 11 brothers (9%) were affected. Of a total of 24 siblings, 3 were affected (13%), giving a segregation ratio (observed/expected) of 3/12, which was significantly different from autosomal dominant inheritance. The inheritance of PCO and PMPB is consistent with an autosomal dominant inheritance pattern in PCOS families, perhaps caused by the same gene. There was no such genetic influence in families of women without PCOS. Sisters of PCOS probands with polycystic ovarian morphology were more likely to have menstrual irregularity and had larger ovaries and higher serum androstenedione and dehydroepiandrosterone-sulfate levels than sisters without PCO. This suggests a spectrum of clinical phenotype in PCOS families. Men with PMPB had higher serum testosterone than those without. Collectively, these data are consistent with a role for genetic differences in androgen synthesis, metabolism, or action in the pathogenesis of PCOS.
Postpartum haemorrhage remains a signi®cant complication of childbirth in the UK and worldwide. The most common cause of postpartum haemorrhage is uterine atony, but placent accreta is becoming more frequent. In these situations tamponade may be required. The successful use of the in¯ated stomach balloon (300ml) of a Sengstaken±Blakemore tube has been reported previously. We describe an innovative method of`tamponade' which is simple and effective, using the Ru Èsch urological hydrostatic balloon catheter. In two cases of failed medical therapy for PPH, where the catheter has been tried, further surgical interventions have been avoided.
Objective To evaluate the efficacy of progesterone and progestogens in the management of premenstrual syndrome. Design Systematic review of published randomised, placebo controlled trials. Studies reviewed 10 trials of progesterone therapy (531 women) and four trials of progestogen therapy (378 women). Main outcome measures Proportion of women whose symptoms showed improvement with progesterone preparations (suppositories and oral micronised). Proportion of women whose symptoms showed improvement with progestogens. Secondary analysis of efficacy of progesterone and progestogens in managing physical and behavioural symptoms. Results Overall standardised mean difference for all trials that assessed efficacy of progesterone (by both routes of administration) was − 0.028 (95% confidence interval − 0.017 to − 0.040). The odds ratio was 1.05 (1.03 to 1.08) in favour of progesterone, indicating no clinically important difference between progesterone and placebo. For progestogens the overall standardised mean was − 0.036 ( − 0.014 to − 0.060), which corresponds to an odds ratio of 1.07(1.03 to 1.11) showing a statistically, but not clinically, significant improvement for women taking progestogens. Conclusion The evidence from these meta-analyses does not support the use of progesterone or progestogens in the management of premenstrual syndrome.
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