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A genetic defect of granulocyte oxidative metabolism in a man with disseminated aspergillosis


, : A genetic defect of granulocyte oxidative metabolism in a man with disseminated aspergillosis. Journal of Laboratory and Clinical Medicine 97(5): 730-738

A 26 yr old man presented with progressive pneumonia; Aspergillus was grown from cultures of lung, cutaneous nodules and urine. His PMN [polymorphonuclear leukocytes] had a poor CL [chemiluminescence] response after exposure to phagocytic stimuli (Staphylococcus aureus, latex, aggregated IgG and IgG-coated latex) (P < 0.01 vs. controls) and soluble stimuli (PMA [phorbol myristate acetate], sodium fluoride and Con A [concanavalin A]) (P < 0.05). His PMN failed to reduce NBT [nitro-blue tetrazolium], oxidize 14C-1 glucose (P < 0.001) or iodinate proteins (P < 0.001) normally, compared with controls, and his PMN killed Candida albicans and S. aureus abnormally (P < 0.05). The patient was anergic; his plasma inhibited responsiveness of his lymphocytes to stimulation with Aspergillus and Candida antigens. His lymphocytes failed to produce the lymphokine LMIF [leukocyte migration inhibition factor] normally. The patient's 10 mo. old daughter was demonstrated to have the same defects of PMN metabolism and function. The findings in this patient were similar to those in CGD [chronic granulomatous disease] but transmission of the defect from father to daughter and the presence of lymphocyte abnormalities make this diagnosis unlikely. Inhalation of Aspergillus by patients with defective PMN oxidative metabolism may be associated with development of significant infection.

US$29.90

PMID: 6783713


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