ABSTRACT
OBJECTIVE: A scoping review of discharge instructions for women undergoing cesarean section (c-section) in sub-Saharan Africa (SSA). METHOD: Studies were identified from PubMed, Globus Index Medicus, NiPAD, EMBASE, and EBSCO databases. Eligible papers included research based in a SSA country, published in English or French, and containing information on discharge instructions addressing general postnatal care, wound care, planning of future births, or postpartum depression targeted for women delivering by c-section. For analysis, we used the PRISMA guidelines for scoping reviews followed by a narrative synthesis. We assessed quality of evidence using the GRADE system. RESULTS: We identified 78 eligible studies; 5 papers directly studied discharge protocols and 73 included information on discharge instructions in the context of a different study objective. 37 studies addressed wound care, with recommendations to return to a health facility for dressing changes and wound checks between 3 days to 6 weeks. 16 studies recommended antibiotic use at discharge, with 5 specifying a particular antibiotic. 19 studies provided recommendations around contraception and family planning, with 6 highlighting intrauterine device placement immediately after birth or 6-weeks postpartum and 6 studies discussing the importance of counselling services. Only 5 studies provided recommendations for the evaluation and management of postpartum depression in c-section patients; these studies screened for depression at 4-8 weeks postpartum and highlighted connections between c-section delivery and the loss of self-esteem as well as connections between emergency c-section delivery and psychiatric morbidity. CONCLUSION: Few studies in SSA directly examine discharge protocols and instructions for women following c-section. Those available demonstrate wide variation in recommendations. Research is needed to develop structured evidence-based instructions with clear timelines for women. These instructions should account for financial burden, access to resources, and education of patients and communities.
ABSTRACT
Mast cells and basophils have long been implicated in the pathogenesis of IgE-mediated hypersensitivity reactions. They express the high-affinity IgE receptor, FcϵRI, on their surface. Antigen-induced crosslinking of IgE antibodies bound to that receptor triggers a signaling cascade that results in activation, leading to the release of an array of preformed vasoactive mediators and rapidly synthesized lipids, as well as the de novo production of inflammatory cytokines. In addition to bearing activating receptors like FcεRI, these effector cells of allergy express inhibitory ones including FcγR2b, an IgG Fc receptor with a cytosolic inhibitory motif that activates protein tyrosine phosphatases that suppress IgE-mediated activation. We and others have shown that food allergen-specific IgG antibodies strongly induced during the course of oral immunotherapy (OIT), signal via FcγR2b to suppress IgE-mediated mast cell and basophil activation triggered by food allergen challenge. However, the potential inhibitory effects of IgA antibodies, which are also produced in response to OIT and are present at high levels at mucosal sites, including the intestine where food allergens are encountered, have not been well studied. Here we uncover an inhibitory function for IgA. We observe that IgA binds mouse bone marrow-derived mast cells (BMMCs) and peritoneal mast cells. Binding to BMMCs is dependent on calcium and sialic acid. We also found that IgA antibodies inhibit IgE-mediated mast cell degranulation in an allergen-specific fashion. Antigen-specific IgA inhibits IgE-mediated mast cell activation early in the signaling cascade, suppressing the phosphorylation of Syk, the proximal protein kinase mediating FcεRI signaling, and suppresses mast cell production of cytokines. Furthermore, using basophils from a peanut allergic donor we found that IgA binds to basophils and that activation by exposure to peanuts is effectively suppressed by IgA. We conclude that IgA serves as a regulator of mast cell and basophil degranulation, suggesting a physiologic role for IgA in the maintenance of immune homeostasis at mucosal sites.