Captopril and the Liver

Bellary, S.V.; Isaacs, Peter; Scott, Allison

doi:10.1016/s0140-6736(89)92134-x

Cited by 15 publications

(6 citation statements)

References 7 publications

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“…The incidence is low and may not be dose-related. Findings as fever [19], urticarial rash [1] and eosinophilia [19] have been reported. It is, however, difficult to explain the long duration of drug administration before hepatoxicity occurred.…”

Section: Mechanism For Ace-inhibitor Associated Hepatotoxicitymentioning

confidence: 99%

“…After the first report of hepatotoxicity following treatment with captopril [27] there have been several additional reports with captopril [1,6,10,18,19,21,24,28] as well as with enalapril [12,15,17,20,26] and other ACE inhibitors [4,13]. Most of the patients in these reports were receiving other medication concurrently, though these medications are not commonly associated with hepatotoxicity.…”

Section: Angiotensin-converting-enzyme (Ace) Inhibitors and Hepatotoxmentioning

confidence: 99%

“…One patient died due to a perforated duodenal ulcer while liver function was improving [13]. Another died due to progressive liver failure after captopril intake [1]. Duration of treatment varied from 1 week to 12 months.…”

Section: Angiotensin-converting-enzyme (Ace) Inhibitors and Hepatotoxmentioning

confidence: 99%

“…Duration of treatment varied from 1 week to 12 months. In 1 case hepatotoxicity developed 6 weeks after increasing the captopril dose from 25 to 50 mg. Before that the drug had been well tolerated for 2 years [1].…”

Section: Angiotensin-converting-enzyme (Ace) Inhibitors and Hepatotoxmentioning

confidence: 99%

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Acute Liver Failure due to Enalapril

Jeserich

Ihling²,

Allgaier³

et al. 2000

Herz

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This report presents a 46-year-old man who was treated for hypertension with the angiotensin-converting-enzyme (ACE) inhibitor enalapril. After 3 years of continuous treatment he presented with jaundice and progressive liver failure that continued despite withdrawal of the medication. The patient was taking no other medication. All known causes of acute liver failure could be excluded indicating a drug-induced liver damage after long-term treatment with enalapril. Analysis of liver biopsies revealed a pathomorphological pattern comparable to than observed in severe halothane hepatitis. Serological studies including T-cell stimulation with enalapril and a broad spectrum of tests for autoimmunity including autoantibodies against calreticulin, the major Ca2+ and Zn2+ binding protein of the endoplasmic reticulum and suggested to be involved in the pathogenesis of halothane hepatitis were negative. Thus, the mechanism of enalapril-induced liver injury remains obscure. Liver failure progressed and finally led to orthotopic liver transplantation. To our knowledge, this is the longest duration of chronic treatment with an ACE inhibitor before liver failure occurred. In addition, liver failure progressed despite withdrawal of the medication. It is concluded that even after long-term treatment with an ACE inhibitor liver failure may be induced. Therefore, regular monitoring of liver enzymes should be considered.

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Section: Mechanism For Ace-inhibitor Associated Hepatotoxicitymentioning

confidence: 99%

Section: Angiotensin-converting-enzyme (Ace) Inhibitors and Hepatotoxmentioning

confidence: 99%

Section: Angiotensin-converting-enzyme (Ace) Inhibitors and Hepatotoxmentioning

confidence: 99%

Section: Angiotensin-converting-enzyme (Ace) Inhibitors and Hepatotoxmentioning

confidence: 99%

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Acute Liver Failure due to Enalapril

Jeserich

Ihling²,

Allgaier³

et al. 2000

Herz

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“…104,105 Since the less frequent adverse effects of ACE inhibitors have either very low incidence rates (i.e. 0.1% to 0.2% for angioedema 106,107 and <0.01% for hepatotoxicity 108,109 ) or no clinically serious consequence (i.e. skin rash or dysgeusia), they were not further reviewed or analyzed in this study.…”

Section: Major Adverse Side-effectsmentioning

confidence: 99%

The comparative treatment effectiveness and safety of tissue versus non-tissue ace inhibitors among the elderly after acute myocardial infarction

Fang¹

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Angiotensin Converting Enzyme (ACE) inhibitors are one of the recommended prevention therapy for patients with acute myocardial infarction (AMI) in the clinical guidelines. Two types (tissue and non-tissue) of ACE inhibitors are available with huge cost difference but the comparative treatment benefit and risk between them are unclear. The objective of this study was to investigate the comparative treatment effectiveness and safety between tissue and non-tissue ACE inhibitors among elderly patients after AMI. This is a retrospective cohort study with intention-to-treatment design using Medicare service claims files from 2007 to 2009 with Medicare beneficiaries 65 years or older after the index AMI hospitalization and who survived to discharge between January 1 2008 to December 31 2008 and received ACE inhibitors (N=34,679). Risk adjustment and instrumental variable (IV) analyses were used to investigate comparative treatment effectiveness including AMI, stroke, heart failure requiring hospitalization, all-cause mortality and a composite of the endpoints during the follow-up and the comparative treatment safety-a composite of hyperkalemia and acute renal failure requiring hospitalization during the follow-up. Both the risk adjustment and IV analyses showed no significant differences between tissue and non-tissue ACE inhibitors for the investigated outcomes of the comparative treatment effectiveness and safety in the study cohort. However, subgroup analyses from the IV models showed that tissue ACE inhibitors as compared to nontissue ACE inhibitors increased the hazard risk by approximately 30% to 60% (p < 0.05) for heart failure requiring hospitalization among the patients with heart failure and 3.

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