German Medical Science; Düsseldorf, Köln
100 Jahre Phoniatrie in Deutschland;
22. Jahrestagung der Deutschen Gesellschaft für Phoniatrie und Pädaudiologie, 24. Kongress der Union der Europäischen Phoniater;
The ototoxic effects of aminoglycoside antibiotics are well known. A mitochondrial mutation (A1555G) is responsible for a maternally inherited hypersensitivity to aminoglycosides causing an antibiotic-induced ototoxicity with non-syndromic hearing loss.The present study reports on the moleculargenetic findings of the deafness-associated mitochondrial A1555G mutation from a German population of 178 children and their relatives in a cohort of 6500 children collected by the German Registry for Hearing Loss in Children (DZH). The diagnosis is made by including anamnestic factors for non-syndromic hearing loss, hearing impaired mother or further female relatives with non-syndromic hearing impairment. Exclusion criteria were e.g. dysmorphism, prenatal rubella or cytomegaly or treatment with other ototoxic drugs.From our data, aminoglycoside induced hearing loss due to A1555G mutation does not seem to be an important risk factor for communication related hearing impairment in our cohort. The mitochondrial polymorphism A1555G was not found in any of the studied individuals neither in patients nor in the controll-group. The A1555G polymorphism seems to be not very common in Caucasian individuals. Because of the low likelihood for hearing loss due to inherited aminoglycoside hypersensitivity a general routine screening for a mitochondrial A15555G mutation does not need to be recommended.