In white women in their mid-30s, the prevalence of the metabolic syndrome is 3- to 5-fold increased in those with a history of PIH in their first pregnancy. This emphasizes the importance of long-term follow-up assessment for cardiovascular risk factors in these women.

No abstract

Many of the biological changes occurring in the endometrium during the menstrual cycle bear a striking resemblance to those associated with inflammatory and reparative processes. Hence, it would not be surprising to find that cytokines known for their proinflammatory properties, such as interleukin-1 (IL-1), could play a key role in the physiology of this tissue and that their action would be tightly controlled by local mechanisms. In the present study, immunohistochemical and Western blot analyses show that in normal women (n ‫؍‬ 39), the endometrial tissue expresses, in a cycle-dependent manner, the IL-1 receptor type II (IL-1RII), a molecule of which the only biological property known to date is that of capturing IL-1, inhibiting thereby its binding to the functional type I IL-1 receptor. IL-RII immunostaining was particularly intense within the lumen of the glands and at the apical side of surface epithelium. Interestingly, the intensity of staining was markedly less pronounced in the endometrium of women with endometriosis (n ‫؍‬ 54), a disease believed to arise from the abnormal development of endometrial tissue outside the uterus, especially in the early stages of the disease (stages I and II). This study is the first to show the local expression in endometrial tissue of IL-1RII, a potent and specific down-regulator of IL-1 action and its decreased expression in women suffering from endometriosis. Uterine endometrium, one of the most dynamic tissues of the human body, is an active site of cytokine production and action. During each menstrual cycle and throughout the reproductive phase of women's life, the endometrial tissue undergoes a series of dynamic physiological processes of regeneration, remodeling, and differentiation, followed by necrosis and menstrual shedding at the end of the cycle should implantation not occur. It is well established that these complex events are orchestrated by the coincident variations of estrogen and progesterone levels in the peripheral circulation. However, many of the biological changes occurring in the human endometrium during the menstrual cycle bear a striking resemblance to those associated with inflammatory and reparative processes. Hence, it is not surprising to find that pro-inflammatory cytokines can be involved at autocrine, paracrine, and endocrine levels in the modulation of a variety of endometrial functions.