Otomycosis can usually be diagnosed by clinical examination and often occurs in the setting of persistent otorrhea. Complications are not uncommon but usually resolve with application of appropriate topical antifungal agents. Eradication of disease is more difficult in the presence of a mastoid cavity.
ACC of the EAC often recurs many years after definitive treatment. Although our sample size was too small to make definitive conclusions, we recommend aggressive local therapy with lateral temporal bone resection and adjuvant postoperative radiotherapy. In addition to successful local therapy, early diagnosis may be the only other effective means of preventing distant metastases.
The risk association between tobacco and alcohol use with squamous cell carcinoma of the head and neck (SCCHN) is well recognized. However, clearly not all individuals who smoke or drink develop SCCHN. Individual genetic susceptibility differences in carcinogen-metabolizing enzyme function, mutagen sensitivity, apoptosis, and chromosomal aberrations either alone or in combination have been theorized to modify the risk of SCCHN. Nearly all carcinogens and procarcinogens require activation by metabolizing enzymes. Similarly, detoxifying enzymes exist and deactivate carcinogens as well as their intermediate by-products. Together these enzymes are termed xenobiotic-metabolizing enzymes; genetic polymorphisms of these enzymes can modify an individual's response to carcinogens and hence the carcinogenic potential of such exposures. In this review, we explore the available evidence in recent literature regarding the risk association between SCCHN and various xenobiotic-metabolizing enzymes, including cytochrome P450s, glutathione S-transferases, N-acetyltransferases, NAD(P)H:quinone oxidoreductase 1, alcohol dehydrogenase, and aldehyde dehydrogenase.
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