Henkin R I
Taste and Smell Clinic, Center for Molecular Nutrition and Sensory Disorders, Washington, DC 20016.
Drug Saf. 1994 Nov;11(5):318-77. doi: 10.2165/00002018-199411050-00004.
Drugs in every major pharmacological category can impair both taste and smell function and do so more commonly than presently appreciated. Impairment usually affects sensory function at a molecular level, causing 2 major behavioural changes--loss of acuity (i.e. hypogeusia and hyposmia) and/or distortion of function (i.e. dysgeusia and dysosmia). These changes can impair appetite, food intake, cause significant lifestyle changes and may require discontinuation of drug administration. Loss of acuity occurs primarily by drug inactivation of receptor function through inhibition of tastant/odorant receptor: (i) binding; (ii) Gs protein function; (iii) inositol trisphosphate function; (iv) channel (Ca++,Na++) activity; (v) other receptor inhibiting effects; or (vi) some combination of these effects. Distortions occur primarily by a drug inducing abnormal persistence of receptor activity (i.e. normal receptor inactivation does not occur) or through failure to activate: (i) various receptor kinases; (ii) Gi protein function; (iii) cytochrome P450 enzymes; or other effects which usually (iv) turn off receptor function; (v) inactivate tastant/odorant receptor binding; or (vi) some combination of these effects. Termination of drug therapy is commonly associated with termination of taste/smell dysfunction, but occasionally effects persist and require specific therapy to alleviate symptoms. Treatment primarily requires restoration of normal sensory receptor growth, development and/or function. Treatment which restores sensory acuity requires correction of steps initiating receptor and other pathology and includes zinc, theophylline, magnesium and fluoride. Treatment which inhibits sensory distortions requires reactivation of biochemical inhibition at the receptor or inactivation of inappropriate stimulus receptor binding and/or correction of other steps initiating pathology including dopaminergic antagonists, gamma-aminobutyric acid (GABA)-ergic agonists, calcium channel blockers and some orally active local anaesthetic, antiarrhythmic drugs.
每一大类主要药物都可能损害味觉和嗅觉功能,而且这种情况比目前所认识到的更为常见。损害通常在分子水平上影响感觉功能,导致两种主要的行为变化——敏锐度丧失(即味觉减退和嗅觉减退)和/或功能扭曲(即味觉障碍和嗅觉障碍)。这些变化会损害食欲、食物摄入量,导致显著的生活方式改变,并且可能需要停药。敏锐度丧失主要是由于药物通过抑制味觉/嗅觉受体功能而使其失活:(i)结合;(ii)Gs蛋白功能;(iii)肌醇三磷酸功能;(iv)通道(钙离子、钠离子)活性;(v)其他受体抑制作用;或(vi)这些作用的某种组合。功能扭曲主要是由于药物诱导受体活性异常持续(即正常的受体失活未发生)或通过未能激活:(i)各种受体激酶;(ii)Gi蛋白功能;(iii)细胞色素P450酶;或通常(iv)关闭受体功能、(v)使味觉/嗅觉受体结合失活或(vi)这些作用的某种组合的其他作用。药物治疗的终止通常与味觉/嗅觉功能障碍的终止相关,但偶尔效果会持续存在,需要特定治疗来缓解症状。治疗主要需要恢复正常的感觉受体生长、发育和/或功能。恢复感觉敏锐度的治疗需要纠正引发受体及其他病理变化的步骤,包括锌、茶碱、镁和氟化物。抑制感觉扭曲的治疗需要在受体处重新激活生化抑制作用或使不适当的刺激受体结合失活,和/或纠正引发病理变化的其他步骤,包括多巴胺能拮抗剂、γ-氨基丁酸(GABA)能激动剂、钙通道阻滞剂和一些口服活性局部麻醉药、抗心律失常药物。