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Chronic granumolatous disease (CGD) is due to an genetic disolder of phagocytic cells that effects on the phagocytes’ power to have the respiratory burst that needs to kill specific kind of bacteria and fungus. In addition to persistent tissue granuloma formation, this phagocytic insufficiency leads to a syndrome of recurrence potentially deadly bacteria and fangas infections that 1950’s reports descriptions showed a complex comprised of recurrent corruptions, dropsy, Hyper Gamma Globulinemia, biliousness, and lymphadenopathy. Almost the cases are detected in boys before five-years-old and >90％passed away before the age of 10-years-old [1]. This diagnosis typically is determined due to CGD caused by NAPDH oxidase system mutations and a history of unusual, recurring, or persistant infections. with almost all of them detected by the age of sixteen. Milder phenotypes have been indentified as a result of the discovering of this defect. Disease in patient with the milder phenotypes is often milder, and has unusual presentations and can result in delayed symptoms and diagnosis, sometimes even until adulthood 2-3. Our
Chronic granulomatous disease (CGD) is an inherited disorder of phagocytes that affects their ability to undergo the respiratory burst needed to kill certain types of bacteria and fungi. In addition to persistent tissue granuloma formation, this leads to recurrent potentially deadly bacterial and fungal infections.
Early reports in the 1950s described a syndrome comprising recurrent infections, edema, hypergammaglobulinemia, liver disease
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, and lymphadenopathy. Most cases are detected in boys under 5 years old.
Almost all are detected by the age of 16 years
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, and >90% of patients die before the age of 10 years [1]. This diagnosis is usually considered because of a history of unusual, recurrent, or persistent infections. CGD is caused by mutations in the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase system.
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The identification of this defect has allowed the identification of milder phenotypes. These milder phenotypes may result in milder disease, unusual features, and delayed symptoms, which then delays diagnosis, sometimes even until adulthood
[2–3]
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