Candida vulvovaginitis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Dima Nimri, M.D. [2]
Overview
Pathophysiology
Pathogenesis
Genetics
Genetic factors could be involved in the pathophysiology of Candida vulvovaginitis. Supporting evidence is that many cases were found to be more common in African-American women, run in families, as well as being associated with ABO-Lewis non-secretor phenotype, a rare blood group. In addition, women with Candida vulvovaginitis were found to have decreased concentrations of mannose-binding lectin (MBL), hence, the variant (MBL) gene is thought to be a contributing factor in the development of Candida vulvovaginitis.[1][2][3]
Gross Pathology
Microscopic Pathology
Associated Conditions
References
- ↑ Liu F, Liao Q, Liu Z (2006). "Mannose-binding lectin and vulvovaginal candidiasis". Int J Gynaecol Obstet. 92 (1): 43–7. doi:10.1016/j.ijgo.2005.08.024. PMID 16256117.
- ↑ Donders GG, Babula O, Bellen G, Linhares IM, Witkin SS (2008). "Mannose-binding lectin gene polymorphism and resistance to therapy in women with recurrent vulvovaginal candidiasis". BJOG. 115 (10): 1225–31. doi:10.1111/j.1471-0528.2008.01830.x. PMID 18715406.
- ↑ Sobel JD (2007). "Vulvovaginal candidosis". Lancet. 369 (9577): 1961–71. doi:10.1016/S0140-6736(07)60917-9. PMID 17560449.