Severe duodenal candidiasis in a patient with IgA deficiency and T cell defects.
Candida albicans was found to repeatedly colonise and invade the duodenal ulcer base in a 45 years old otherwise healthy patient receiving H2 receptor antagonists for a prolonged period. He had no delayed hypersensitivity to Candida skin test, and had T cell deficiency, abnormality in T cell blast transformation, defective macrophage migration inhibition factor (MIF) and IgA hypogammaglobulinemia. When treated with ketoconazole alone his ulcer healed completely. Ulcer scar biopsy and aspirates revealed no Candida and anti candidal antibodies disappeared from his serum. His T cell blastoid transformation, MIF and skin DTH to Candida were restored to normal levels, but IgA levels remained unchanged. Thus H2 receptor antagonists probably caused abnormalities in T helper cells leading to lymphokine unresponsiveness and subsequently loss of cellular immunity to candidal antigen. This combined with prior IgA immunodeficiency resulted into severe invasive candidiasis.
Singh
S
S
Department of Medical Microbiology, Postgraduate Institute of Medical Education and Research, Chandigarh.
Kochhar
R
R
Dutta
U
U
D002177:Candidiasis / Q000188:drug therapy / Q000276:immunology*; D002927:Cimetidine / Q000276:immunology; D004381:Duodenal Ulcer / Q000188:drug therapy / Q000276:immunology*; D004406:Dysgammaglobulinemia / Q000150:complications*; D006801:Humans; D017098:IgA Deficiency; D007108:Immune Tolerance; D008297:Male; D008875:Middle Aged; D011899:Ranitidine / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology
D002927:Cimetidine; D011899:Ranitidine