Wright Tara M, Vandenberg Amy M
Department of Psychiatry and Behavioral Sciences, Medical University of South Carolina, Charleston, SC 29425, USA.
Ann Pharmacother. 2007 Sep;41(9):1518-23. doi: 10.1345/aph.1K145. Epub 2007 Jul 31.
To describe a case of a patient who developed drug-induced cholestasis after being on risperidone maintenance therapy for 8 years.
A 30-year-old male with schizoaffective disorder, bipolar type, and insulin-dependent diabetes mellitus had been stable on risperidone 6 mg at night for 8 years. His other medications included lithium 900 mg twice daily and enalapril 5 mg daily, as well as regular insulin and NPH insulin as needed. The patient developed cholestasis that resolved once risperidone was discontinued. Over the next 11 months, he tolerated trials of ziprasidone and olanzapine. When quetiapine was initiated, the patient developed signs and symptoms of cholestasis within 3 weeks after starting this medication. The signs and symptoms of cholestasis resolved with removal of quetiapine. The Naranjo probability scale indicated that these atypical antipsychotics (risperidone and quetiapine) were the probable cause of cholestasis in this patient.
It is well known that atypical antipsychotics can cause isolated asymptomatic increases in aminotransferase levels. Liver injury, both the hepatic and cholestatic type, has been described previously, although the incidence with atypical antipsychotics is rare.
To our knowledge, this is the first case of cholestasis that developed after years of treatment and reappeared with another antipsychotic agent. Given that liver failure, of either the hepatic or cholestatic type, is a relatively rare phenomenon with atypical antipsychotics, it seems that the most reasonable approach to manage this risk is through education. By educating patients on early warning signs of hepatotoxicity, this rare but potentially fatal consequence could be detected early to allow appropriate intervention.
描述一例在接受利培酮维持治疗8年后发生药物性胆汁淤积的患者。
一名30岁男性,患有双相型分裂情感障碍和胰岛素依赖型糖尿病,每晚服用6毫克利培酮,病情稳定8年。他的其他药物包括每日两次服用900毫克锂盐、每日服用5毫克依那普利,以及根据需要使用的正规胰岛素和中效胰岛素。患者出现胆汁淤积,停用利培酮后病情缓解。在接下来的11个月里,他耐受了齐拉西酮和奥氮平的试验。当开始使用喹硫平时,患者在开始使用这种药物后3周内出现了胆汁淤积的体征和症状。停用喹硫平后,胆汁淤积的体征和症状消失。Naranjo概率量表表明,这些非典型抗精神病药物(利培酮和喹硫平)可能是该患者胆汁淤积的原因。
众所周知,非典型抗精神病药物可导致转氨酶水平孤立性无症状升高。先前已有肝损伤(包括肝细胞型和胆汁淤积型)的描述,尽管非典型抗精神病药物引起肝损伤的发生率较低。
据我们所知,这是首例在多年治疗后出现胆汁淤积并在换用另一种抗精神病药物后再次出现的病例。鉴于肝细胞型或胆汁淤积型肝衰竭在非典型抗精神病药物中是相对罕见的现象,似乎管理这种风险的最合理方法是通过教育。通过对患者进行肝毒性早期预警信号的教育,可以早期发现这种罕见但可能致命的后果,以便进行适当干预。