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对灰黄霉素或酮康唑等抗真菌药的抗药性表现为广泛皮肤真菌感染而服药无效,这种病例中的许多例称之为顽抗性似更适当。皮肤真菌感染顽固不愈可能有以下原因:(1)病人不配合。包括未服药,未服足剂量,过早停药,服药不当如酮康唑与抗酸剂同服等。(2)药物未吸收或虽吸收又从胃肠道丢失。这多半是呕吐、腹泻的结果。(3)药物在肝脏被微粒体酶降解。药物虽被充分吸收,但经肝内微粒体酶降解失活。克霉唑能诱导细胞色素 p-450微粒体氧化酶体系,使克霉唑开始治疗约1周后即全被降解。(4)药物-药物相互反应。某些抗真菌药若与诸如酚巴比妥、华法令、西咪替丁、利福平等药同用,则抗真菌药的分解代谢加快。这是由于上述与抗真菌药伍用的药物能诱导微粒体酶。药物-药物相互反应也发生于外周循环,结果是一种蛋白结
Drug resistance to antifungal agents such as griseofulvin or ketoconazole has been shown to be ineffective in treating a wide range of fungal infections of the skin. Many of these cases are referred to as recalcitrant. Fungal infection of the skin can be stubborn for the following reasons: (1) the patient does not cooperate. Including non-medication, not enough dose, premature withdrawal, improper medication such as ketoconazole with antacids and the like. (2) The drug is not absorbed or absorbed from the gastrointestinal tract though it is absorbed. This is mostly the result of vomiting and diarrhea. (3) The drug is degraded by microsomal enzymes in the liver. Although the drug is fully absorbed, but by the liver microsomal enzyme inactivation. Clotrimazole induces a cytochrome p-450 microsomal oxidase system that degrades clotrimazole about 1 week after treatment is initiated. (4) drug-drug interaction. Some anti-fungal drugs such as phenobarbital, warfarin, cimetidine, rifampin and other drugs with the anti-fungal catabolism accelerated. This is due to the above-mentioned anti-fungal drugs used to induce microsomal enzymes. Drug-drug interactions also occur in the peripheral circulation, the result is a protein knot