Pre-eclampsia is a significant complication that may occur during gestation. It elevates blood pressure and harms organs, typically the liver and kidneys. It often commences after 20 weeks of gestation, and if not promptly identified and addressed, it can have severe repercussions for both the mother and the infant. Extensive research in Saudi Arabia has indicated that pregnant women had limited knowledge on the signs, risk factors, and complications associated with pre-eclampsia. This narrative review aims to provide a comprehensive review about the efficacy of educational interventions, particularly educational videos, in enhancing women's understanding of pre-eclampsia. Audiovisual tools significantly enhance comprehension, engagement, and retention compared to conventional methods such as pamphlets or verbal communication. This review emphasizes how different educational intervention, and instructional videos assist mothers in acquiring knowledge, facilitate early symptom recognition, and enhance pregnancy outcomes.
Asthma and allergy are two prevalent immune-mediated disorders caused by an excess of T-helper (TH) cell activity, i.e., an example of TH2 predominance with elevated IgE, eosinophilia and chronic airway inflammation. Of special importance, immune checkpoint receptor cytotoxic T lymphocyte–associated antigen 4 (CTLA-4) were observed to regulate T-cell regulation and TH1/TH2 immunobalance of immunity through competitive blocking of CD28 interaction with B7 ligands on antigen-presenting cells to inhibit T-cell activation. Functional polymorphisms like +49 A/G (rs231775), −318 C/T (rs5742909) and CT60 A/G (rs3087243) of the CTLA4 gene have been associated with regulated CTLA-4 expression and function with implications for asthma and allergy susceptibility. This review collates contemporary understanding of CTLA-4 structure biology, its TH1/TH2 polarizing immunomodulatory roles, and genetic variants' effects on allergic phenotypes across diverse populations. Some CTLA-4 polymorphisms disrupt immune regulation, promoting TH2 dominance, IgE synthesis, airway hyperresponsiveness, and atopic disease progression by undermining regulatory mechanisms. Ethnic variation in CTLA-4 variants may serve as biomarkers for disease susceptibility and treatment response, potentially even to corticosteroids and biologics. Rising preclinical data also show the potential of CTLA-4–targeted therapies to regulate allergic inflammation. Current evidence is hampered by small cohorts, limited ethnic diversity, and replication constraint in genome-wide studies. We conclude by outlining areas of unknowns and proposing future research directions to determine genotype–phenotype relationships and integrate CTLA-4 findings into individualized interventions for allergy and asthma. Understanding the immunogenetic landscape of CTLA-4 will enhance precision immunology and inform new treatments against these global disease burdens.