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BackgroundDyspareunia affects approximately half of postpartum women and is attributed to multiple factors. Despite its high prevalence and resultant negative effects, data are lacking regarding the causes and different pain components, the usefulness of recommended treatments, and the prognosis.AimTo evaluate causes of postpartum dyspareunia, targeted treatment modalities, and their effectiveness.MethodsA retrospective observational study was conducted of women diagnosed with postpartum dyspareunia between September 2008 and January 2017 at a single designated vulvovaginal disorder clinic. The inclusion criterion was complaint of painful intercourse commencing postdelivery. The cohort was divided into 4 groups based on the causes of dyspareunia: muscle hypertonicity, scar tenderness, vestibular tenderness, and atrophy.OutcomesThe following were assessed for each group: patient background demographics, clinical and obstetric data, physical findings, recommended therapy, adherence to the suggested treatment, level of improvement at follow-up visits, and length of time until maximal improvement.ResultsA hundred women met the inclusion criterion; the majority (n = 60) presented with >1 causative factor. The most common finding was vestibular tenderness (n = 78, 78%), which was significantly associated with atrophy (adjusted odds ratio [aOR], 15.08; 95% CI, 2.45-93.35), contraceptive usage (aOR, 4.76; 95% CI, 1.07-21.39), and primiparity (aOR, 4.89; 95% CI, 1.01-23.88). Episiotomy was the only risk factor for scar tenderness (aOR, 5.43; 95% CI, 1.20-24.53), while the existence of a spontaneous perineal tear was not. No specific correlation was found with pelvic floor muscle hypertonicity. Targeted treatment resulted in significant improvement in most patients.Clinical ImplicationsA targeted diagnostic and treatment approach for postpartum dyspareunia is effective and can be beneficial for caregivers treating postpartum women.Strengths and LimitationsA uniform and consistent protocol for patient selection and management is a major strength, which magnifies the clinical implication of our findings. The retrospective nature of the study is the primary limitation.ConclusionPostpartum dyspareunia is a common problem; however, many women refrain from discussing it with their providers. Therefore, it is important to assess this condition with all women during the postpartum visit as targeted diagnosis and treatment can significantly improve outcomes.

The development of autoimmune diseases in genetically susceptible individuals is probably caused by a combination of environmental exposure, hormonal changes, and immune defects. Autoantibodies (aAbs) play variable and inconsistent roles in cause, prediction, diagnosis, classification, pathogenesis, and prognostication of autoimmune diseases. Mucocutaneous autoimmune diseases are usually categorized into two major groups based on the localization of the autoantigen (aAg). Type I is characterized by autoimmunity to self-antigens (Ag) expressed at both cutaneous and extracutaneous sites. Type I aAbs usually target ubiquitous aAgs, most of which were characterized in systemic diseases (Sjogren syndrome, scleroderma, dermatomyositis, etc.) before their detection in dermatologic disease. Many, such as anti-Ro/SSA and La/SSB, serve as diagnostic markers for specific diseases, and, therefore, no attempts were made to link them pathogenetically to mucocutaneous manifestations. By contrast, in type II autoimmune diseases, the aAbs are restricted to mucocutaneous tissues and are found mostly in immunobullous dermatoses and vitiligo. Unlike type I Abs, they target self-Ags presented exclusively by mucocutaneous cells and are directly related to the pathogenesis of the diseases. Type II mucocutaneous autoimmune diseases can be further divided by the predominant cutaneous (epidermal or dermal) localization of the Ags. Epidermal Ags are produced by keratinocytes and are involved in the formation of blisters, as in the major disease groups of pemphigus and pemphigoid, although they may also be found in some nonblistering diseases such as vitiligo. In pemphigus diseases (intraepidermal blistering), the aAbs are directed to the keratinocyte cell surface, producing a fishnet-like staining of the epidermis on DIF microscopy, whereas in the pemphigoid group (subepidermal blistering), the aAbs target self-Ags associated with the basal keratinocytes attached to the epidermal basement membrane, forming a linear staining pattern on DIF microscopy. Dermal Ags are also associated with blistering disease. They are found either at the dermal half of the epidermal–dermal junction, as in epidermolysis bullosa acquisita, or in the dermal papillae, as in dermatitis herpetiformis. The aim of this chapter is to present the important new data that have emerged in recent years on the pathophysiologic role of aAbs in type II mucocutaneous autoimmune diseases. First, we focus on diseases in which an epidermal Ag is the main target protein, followed by diseases in which a dermal Ag is the main target protein. A detailed discussion on the aAbs produced by patients with type I mucocutaneous autoimmune diseases can be found in other chapters of this book.

Objectives In 2013 the American Task force on Hypertensive diseases defined new criteria for preeclampsia (pet) without proteinuria and excluded the severity of proteinuria from criteria defining pet with severe signs. Still, the majority of women presenting with pet also exhibit proteinuria. It remains disputed whether isolated proteinuria is part of the pet continuum or whether it is a physiological alternation in kidney function in pregnancy. Our aim was to examine maternal and neonatal outcomes of isolated proteinuria and define risk factors for progression to pet. Methods Retrospective cohort study. Data from all hospitalized pregnant women with isolated proteinuria of over 300 mg/24 h at admission between 2009 and 2014, was obtained. We followed this study group from the time of admission to the hospital to the time of discharge postpartum, obtaining maternal and neonatal outcomes. Results During the 5 year period 99 women were diagnosed with isolated proteinuria. 13 women developed pet during pregnancy, and an additional 8 developed pet postpartum (21%). No risk factors for proteinuria were found, however the earlier the diagnosis of proteinuria the higher were the maximal values of proteinuria reached. Risk factors for progression of pet were primiparity (p = 0.01) and greater values of proteinuria (p = 0.005). Among women who developed pet, an earlier diagnosis was made for those with early onset proteinuria (p = 0.002), well established risk factors for pet (p = 0.01) and multiple gestations (p = 0.002). Neonatal outcome was equivocal regardless of progression to pet and levels of proteinuria. Conclusions To date this is the largest series of women with isolated proteinuria followed to term. We conclude that isolated proteinuria is a risk factor for pet, with greater chances of developing pet among primiparous women with higher values of proteinuria. While proteinuria itself is negligible, chances of pet are high and close follow-up is recommended until after delivery. Disclosures S. Shinar: None. A. Schwartz: None. M. Ram-Weiner: None. M. Kupferminc: None. A. Many: None.