Current Women's Health Reviews - Volume 3, Issue 4, 2007

Recurrent pregnancy loss is classically described as three or more consecutive miscarriages occuring before the 20th weeks of gestation. The overall incidence of spontaneous miscarriage varies between 15% and 25%, whereas recurrent miscarriage affects around 1% of fertile couples. First trimester losses consist of 75% of recurrent miscarriages and second trimester losses the remaining 25%. Genetic, anatomical, endocrine, immune, infective and environmental factors are believed to play important roles in the pathophysiology of recurrent pregnancy losses. However, the majority of recurrent miscarriage cases are idiopathic and no identifiable cause is found. In this review we aim to summarize the identifiable causes of recurrent pregnancy losses and discuss the current treatment modalities.

The multifactorial etiology of preeclampsia is contrasted by the fact that at the same time the presence of the placenta is a prerequisite for its development. Preeclampsia is related to a failure of the differentiation pathway of the villous trophoblast leading to an abnormal release of material into the maternal circulation. These factors shed from the placenta are involved in finally causing an inflammatory response of the mother. But the underlying cause and the developmental changes within the placenta leading to the placental dysfunction are unclear. Here we want to shed light on putative placental origins of preeclampsia, new markers that may be able to predict this syndrome already in the first trimester of pregnancy, and new strategies for putative therapeutics. These new therapies may be used to reduce the severity of the syndrome or even to stop the development of the clinical symptoms. Preeclampsia is a disease of placentation with a cause somewhen very early in gestation and the maternal systemic inflammatory response is the subject of clear debate and has led to the proposal of new treatment paradigms.

The lack of elimination of potentially toxic compounds due to impaired bile formation by the maternal liver results in deleterious effects for the trio formed by the foetal liver, the placenta and the maternal liver, which constitutes a key excretory pathway during gestation. One of the most frequent causes of this condition is intrahepatic cholestasis of pregnancy (ICP). This is a pregnancy-specific disorder that mainly occurs during the third trimester of pregnancy and is characterised primarily by pruritus, altered serum levels of liver enzymes and, less frequently, jaundice. ICP has been associated with spontaneous preterm labour and increased foetal morbidity and mortality. Although the pathogenesis of the disease remains obscure, significant advances have been made. These include the investigation of the repercussions of the accumulation of biliary compounds on the structure and function of the foetal liver, the placenta and the maternal liver. The present review provides an overview of current information on this topic as well as on the pharmacological remedies used to treat these patients.

Female genital tract malformations are frequently a cause of reproductive problems. Besides, complex malformations also frequently generate serious gynecological problems, often ones with inappropriate surgical solutions, as the gynecologist does not think of the malformation as either the cause of the symptoms or of its embryonary origin. Apart from analyzing the embryological bases in the development of the female genital tract and insisting on the well known mullerian origin of the uterus, the ratification of the embryological hypothesis about the origin of the human vagina from the Wolff ducts and the Muller tubercle allows us to not only advance in knowledge but to use that knowledge for better clinical management of the problems generated by the complex malformations of the female genital tract. In this review we study the methods and means for the diagnosis of female genital-urinary malformations, their classification and clinical findings, and especially those cases involving unilateral renal agenesis, vaginal ectopic ureter and other complex malformations. We also analyze the related obstetric and gynecologic pathology, and especially that cases of complex genital malformations. We review the related literature and some interesting case reports, as well as our experimental studies in rats. After re-asserting our hypothesis about the embryology of the human vagina as derived from the Wolff ducts and the Muller tubercle, we suggest different recommendations for a better approach and management of the malformations of the female genital tract according to the findings observed in different diagnostic procedures.

Objective: To review recent literature regarding the potential causes of impaired fertility in women with polycystic ovary syndrome. Design: Medline review and cross-reference of published literature. Results: The underlying pathophysiology of polycystic ovary syndrome has significant negative impact on reproductive potential. Yet no single pathogenic alteration can completely account for its negative reproductive impact. Excessive LH secretion increases the follicular androgen concentration and in combination with hyperinsulinemia alters the follicular fluid microenvironment. These endocrine aberrations may result in a reduction in oocyte quality. Conclusion: Infertile PCOS patients have unique alterations in the underlying physiology that results in impaired fertility. Recent data from ART cycles is leading to an improved understanding of the underlying abnormalities and may direct future therapy to improve reproductive outcomes among these patients.