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篇名 氫離子幫浦阻斷劑與腎病之關聯
卷期 30:4
並列篇名 Association between Proton Pump Inhibitors and Renal Disease
作者 張育霖陳進生黃文威
頁次 239-246
關鍵字 氫離子幫浦阻斷劑急性間質性腎炎急性腎損傷慢性腎臟病Proton pump inhibitorAcute interstitial nephritis, AINAcute kidney injury, AKIChronic kidney disease, CKDScopusTSCI
出刊日期 201908
DOI 10.6314/JIMT.201908_30(4).02

中文摘要

氫離子幫浦阻斷劑是醫療上常被使用的藥物。它是一前驅藥物,於胃的壁細胞轉變成活化狀態,不可逆的綁定氫/ 鉀三磷酸腺苷酶(H+-K+ ATPase),即胃的氫離子幫浦,而抑制胃酸分泌。近十幾年,氫離子幫浦阻斷劑在美、法等世界各地用量愈來愈大。它有效控制胃酸相關疾病,但其副作用的疑慮也陸續被提出。雖無大型隨機前瞻型研究,但新近多篇設計良好的回溯型世代及病例研究還指出氫離子幫浦阻斷劑與腎病有關,對急性腎損傷、慢性腎臟病等,風險比為1.1 至4.35。也有研究指出高劑量與長期使用氫離子幫浦阻斷劑和腎病傷害程度有關。雖受限於回溯型研究的未臻完善證據力,但這些研究提醒我們在長期使用氫離子幫浦阻斷劑時應留意病人的腎功能變化。氫離子幫浦阻斷劑可能經由多種機轉包括:急性間質性腎炎、低血鎂症、內皮細胞受損等對腎造成傷害,導致急性腎損傷、慢性腎臟病及末期腎病變。目前無指引列出長期使用氫離子幫浦阻斷劑在腎功能的必要追蹤項目,但我們仍應留意。在無明確適應症或病人症狀已獲改善後,應將氫離子幫浦阻斷劑減量、降階或停止。仍待陸續研究釐清氫離子幫浦阻斷劑與腎病的因果關係,期能更適當調整對應共病的治療與相關追蹤,以利人類健康。

英文摘要

Proton pump inhibitor (PPI) is among the most commonly prescribed medicines. It is a prodrug which are converted to its active form at the parietal cell of stomach. There it binds irreversibly with H+-K+ ATPase, that causes an inhibition of gastric acid secretion. Over past period, the prescription for PPIs was increased much in all world including America and French. Although they treated acid-peptic disorders effectively, studies revealed that PPIs might elevate the risk of rare adverse events. Although lack of large randomized prospective studies, recent several well-designed retrospective cohort studies and case-control studies revealed the relationship between the PPIs and renal diseases: The patients treated with PPIs had elevated risk to acute kidney injury and chronic kidney disease with hazard ratio 1.1-4.5. There were studies detecting a graded association between high-dose and long-duration of PPI exposure and risk of renal outcomes. The power of evidence of these retrospective studies was weak; nevertheless, the studies remind us to pay attention to the possible renal insult in the patients treated with PPIs long. The possible mechanisms for the development of acute kidney injury, chronic kidney disease and end stage renal disease with PPI use include acute interstitial nephritis, hypomagnesemia and endothelial dysfunction. Currently, there is no guideline for the necessary follow up for renal function in long time PPI use. But we should keep it in mind. When the indications for PPI cease or the symptoms of acid-peptic disorders improve, reducing the dose of, shifting to H2 receptor antagonist or stopping PPIs should be considered. With more studied in future to clarify the causality between PPI and renal disease, we will well adjust the treatment according to comorbidities and the necessary follow up to improve the human health.

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