Reviews in Gynaecological and Perinatal Practice最新文献

Accurate diagnosis is important to ensure optimal management of dysmenorrhoea—for women whose dysmenorrhoea does not respond to first line treatments, diagnostic laparoscopy is often useful. Randomised trials have confirmed the effectiveness of a wide and varied array of treatments: conservative approaches including aerobic exercise, topical heat, relaxation therapy, high frequency transcutaneous electrical nerve stimulation (TENS) and timely diagnostic ultrasound; drug treatments including paracetamol and non-steroidal anti-inflammatory drugs, hormonal drug treatments for endometriosis, progestogen drug treatment for unexplained chronic pelvic pain; alternative and newer drug treatments including Vitamin B1, Vitamin E, magnesium, fish oil, toki-shakuyaku-san; surgical treatments including laparoscopic excision and laparoscopic ablation for endometriosis, laparoscopic ovarian cystectomy for endometriomas, the levonorgestrel intrauterine system as a post-operative adjunct for endometriosis, and laparoscopic uterine nerve ablation for primary dysmenorrhoea. The future research agenda has been defined by gaps in randomised trial evidence where data are insufficient or conflicting.

Epithelial ovarian cancer is the leading cause of gynecologic cancer death. Strategies for risk modifications must begin with an accurate assessment of risk factors, the most important of which is family history. Approximately 10% of ovarian cancer is related to familial syndromes, including hereditary breast/ovarian cancer syndrome and hereditary non-polyposis colorectal carcinoma syndrome, otherwise known as Lynch syndrome type II. Individuals at high-risk for ovarian cancer may avail themselves of several methods to attempt to decrease their chances for developing ovarian cancer, including chemoprophylaxis, intensive cancer surveillance, and prophylactic oophorectomy, though surgery remains the most effective prevention method currently available.

Pre-eclampsia (PE) and intra-uterine growth restriction (IUGR) cause significant maternal and perinatal morbidity and mortality. Placental dysfunction is central to the development of both conditions. Although the pathophysiology of these conditions is unknown, there is common placental pathology with an increase in apoptotic cell death seen within the trophoblast. In addition, in pre-eclampsia, apoptotic fragments of syncytiotrophoblast have been detected in the maternal circulation. Both hypoxia and reactive oxygen species have been proposed as potential mediators of the insults to the placenta in pre-eclampsia and IUGR resulting in apoptosis. Cell proliferation and apoptosis are tightly regulated by oncoproteins. The increased apoptosis observed within trophoblast is associated with an alteration in oncoprotein expression within placental tissue. Further investigation of these oncoproteins capable of detecting or responding to cell damage may improve understanding of the pathophysiology of pre-eclampsia and IUGR.

The placenta is actively involved in transporting nutrients to the fetus, it has both direct and indirect effects on fetal cardiovascular function and has endocrine influences on the mother and fetus. As such, a properly functioning placenta is crucial for normal fetal development and plays a central role in mediating effects of the maternal environment on the fetus. An altered external environment or abnormal placental function can induce developmental changes in the fetus and may have important consequences for the risk of cardiovascular and metabolic disease in adult life.

The developmental origins hypothesis proposes that the early environment, from the periconceptional period until early childhood, can predispose an individual to adult cardiovascular and metabolic disease. This hypothesis is supported by epidemiological studies and by work in animals. These effects do not just act in low birth weight babies but have been shown to occur within the normal range of birth weight. It is thought that fetal adaptations to an impaired intra-uterine environment may enhance survival in early life but have deleterious effects in later life.

Experimental studies suggest that maternal diet and body composition can alter placental structure and function, and we have recently demonstrated associations between a woman's nutritional state before pregnancy and placental function at term. To elucidate these relationships, further work is needed to define markers of placental function and to characterize their relation to rates of fetal growth.

Understanding how the placenta mediates maternal influences will be crucial in determining the mechanisms underlying developmental programming. This will allow the design of targeted public health interventions, both before and during pregnancy, to enhance placental function and thereby improve the health of the offspring throughout life.