Association of CYP2C9∗3 and CYP2C8∗3 Non-Functional Alleles with Ibuprofen-Induced Upper Gastrointestinal Toxicity in a Saudi Patient.

IF 0.8 Q3 MEDICINE, GENERAL & INTERNAL
Amina M Bagher
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引用次数: 2

Abstract

Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) widely used to alleviate pain and inflammation. Although it is generally considered safe, common adverse drug reactions of ibuprofen include stomach pain, nausea, and heartburn. It can also cause gastrointestinal (GI) bleeding, especially in individuals with a history of GI ulcers or bleeding disorders. Ibuprofen is predominantly metabolized by the cytochrome P450 (CYP) enzymes CYP2C9 and CYP2C8. Individuals carrying the CYP2C93 or CYP2C83 non-functional alleles have reduced enzyme activities resulting in elevated ibuprofen plasma concentrations and half-life. We presented a case of a 31-year-old Saudi female patient with a history of rheumatoid arthritis (RA) who had taken ibuprofen at 600 mg twice daily for eight weeks. The patient presented to the emergency department with symptoms including nausea, vomiting, severe abdominal pain, and black tarry stools. An emergency esophagogastroduodenoscopy was performed on the patient, which revealed a deep bleeding ulcer measuring 1 × 1 cm in the antrum of the stomach. Laboratory investigations indicated anemia (hemoglobin: 7.21 g/dL and hematocrit: 22.40 g/dl). The patient received intravenous proton pump inhibitors and a packed red blood cell transfusion. Genetic analysis revealed that the patient was a carrier of CYP2C93 and CYP2C83 variant alleles, indicating that the patient is a poor metabolizer for both enzymes. The patient's symptoms improved over the subsequent days, and she was discharged with instructions to avoid NSAIDs. This is the first reported Saudi patient homozygous for CYP2C93 and CYP2C83 variant alleles, which led to ibuprofen-induced upper GI toxicity. This case demonstrates the importance of contemplating CYP2C9 and CYP2C8 genetic variations when administrating NSAIDs like ibuprofen. Careful assessment of the risks and benefits of NSAID therapy in each patient and consideration of alternative pain management strategies must be conducted when appropriate.

Abstract Image

CYP2C9∗3和CYP2C8∗3非功能等位基因与布洛芬诱导的沙特患者上胃肠道毒性的关系。
布洛芬是一种非甾体抗炎药(NSAID),广泛用于减轻疼痛和炎症。尽管布洛芬通常被认为是安全的,但常见的不良药物反应包括胃痛、恶心和胃灼热。它还可以引起胃肠道出血,特别是有胃肠道溃疡或出血性疾病史的个体。布洛芬主要由细胞色素P450 (CYP)酶CYP2C9和CYP2C8代谢。携带CYP2C9 * 3或CYP2C8 * 3非功能等位基因的个体酶活性降低,导致布洛芬血药浓度和半衰期升高。我们报告了一例31岁的沙特女性患者,有类风湿关节炎(RA)病史,服用布洛芬600毫克,每日两次,持续8周。患者以恶心、呕吐、剧烈腹痛和黑焦油样便等症状就诊于急诊科。对患者进行了紧急食管胃十二指肠镜检查,发现胃窦处有1 × 1 cm的深出血溃疡。实验室检查显示贫血(血红蛋白:7.21 g/dL,红细胞压积:22.40 g/dL)。患者接受静脉注射质子泵抑制剂和填充红细胞输注。遗传分析显示患者是CYP2C9∗3和CYP2C8∗3变异等位基因的携带者,表明患者是两种酶的不良代谢者。在随后的几天里,病人的症状有所改善,她出院时被告知要避免使用非甾体抗炎药。这是首次报道的沙特患者CYP2C9∗3和CYP2C8∗3变异等位基因纯合,导致布洛芬诱导的上消化道毒性。本病例表明,在给药布洛芬等非甾体抗炎药时,考虑CYP2C9和CYP2C8基因变异的重要性。在适当的时候,必须仔细评估每位患者使用非甾体抗炎药治疗的风险和益处,并考虑其他疼痛管理策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Case Reports in Medicine
Case Reports in Medicine MEDICINE, GENERAL & INTERNAL-
CiteScore
1.70
自引率
0.00%
发文量
53
审稿时长
13 weeks
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