Paget's disease of the vulva: A challenge for the gynaecologist.

Paget's disease of the vulva is a rare form of extramammary Paget's disease mainly affecting postmenopausal women. Its pathophysiology remains largely unknown. Up to fairly recently, the only treatment for this disease was surgery, often mutilating the vulva, with significant psychosexual repercussions without the assurance of complete therapeutic efficacy. New therapeutic approaches -topical treatments, radiotherapy or chemotherapy- have emerged in recent years but lack consensual guidelines. We present a literature review of the recent results published in this field.

Vulvar intraepithelial neoplasia: Classification, epidemiology, diagnosis, and management.

Vulvar intraepithelial neoplasia (VIN) is classified into two entities: differentiated (dVIN) and vulvar high-grade squamous intraepithelial lesions (vH-SIL). dVIN is a premalignant lesion that develops on an existing vulvar lesion such as lichen sclerosus, while vH-SIL is associated with HPV infection. The two entities differ in terms of pathophysiology, background, prognosis, and management. The incidence of VIN in young women is rising and recurrence is common, even after radical surgery, which can cause significant disfigurement. Alternative strategies include topical treatments, ablation, and a watch-and-wait approach. There is currently no consensus on how these lesions should be managed. We review the literature in this field.

Cellular function and control of volume-regulated anion channels.

Restoration of cell volume after cell swelling in mammalian cells is achieved by the loss of solutes (K+, Cl-, and organic osmolytes) and the subsequent osmotically driven efflux of water. This process is generally known as regulatory volume decrease (RVD). One pathway for the swelling induced loss of Cl- (and also organic osmolytes) during RVD is the volume-regulated anion channel (VRAC). In this review, we discuss the physiological role and cellular control of VRAC. We will first highlight evidence that VRAC is more than a volume regulator and that it participates in other fundamental cellular processes such as cell proliferation and apoptosis. The second part concentrates on the Rho/Rho kinase/myosin phosphorylation cascade and on compartmentalization in caveolae as modulators of the signal transduction cascade that controls VRAC gating in vascular endothelial cells.