title: Malakoplakia. Defect in digestion of phagocytized material due to impaired vacuolar acidification?
abstract: On the basis of light and electron microscopical findings in a case of malakoplakia of urinary bladder, (1) we concur with others that malakoplakia is a hyperplastic accumulation of histiocytes, and that the formation of Michaelis-Gutmann bodies is associated with incomplete digestion of phagocytized cell debris; (2) we hypothesize that digestion within phagolysosomes is impaired because of deficient acidification; and (3) we suggest that the defect in acidification in some cases may be related to treatment with drugs that affect the mechanism of phagocytic vacuolar acidification.
mesh_terms: D002257:Carbonic Anhydrase Inhibitors / Q000494:pharmacology; D003238:Connective Tissue / Q000473:pathology; D003593:Cytoplasm / Q000648:ultrastructure; D004848:Epithelium / Q000473:pathology; D005260:Female; D006644:Histiocytes / Q000473:pathology*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D002479:Inclusion Bodies / Q000648:ultrastructure; D008247:Lysosomes / Q000378:metabolism / Q000648:ultrastructure; D008287:Malacoplakia / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D008875:Middle Aged; D009940:Organoids / Q000648:ultrastructure; D010587:Phagocytosis; D001745:Urinary Bladder Diseases / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D014617:Vacuoles / Q000378:metabolism / Q000648:ultrastructure
chemical_list: D002257:Carbonic Anhydrase Inhibitors