Reversible cholestatic jaundice and hyperamylasaemia associated with captopril treatment.

Zimran, Ari; Abraham, A. S.; Hershko, C

doi:10.1136/bmj.287.6406.1676

Cited by 14 publications

(3 citation statements)

References 3 publications

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“…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: 98%

“…Some of the reported patients were asymptomatic [20,22] but the majority presented with jaundice. In 3 reported cases [7,9,28] the ACE inhibitor was continued despite elevated alkaline phosphatase or transaminases and the patients developed jaundice later on. After withdrawal of the ACE inhibitor in all but 2 cases liver enzyme abnormalities resolved.…”

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

confidence: 98%

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

confidence: 99%

Acute Liver Failure due to Enalapril

Jeserich

Ihling²,

Allgaier³

et al. 2000

Herz

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“…Additionally, as with other agents, hypersensitivity phenomena are associated with the drug's toxic actions (15). Other potential intracellular poisons include novobiocin, rifampin, cholephilic anions, nitrofurantoin, captopril, thiabendazole, and oral hypoglycemic drugs (12,15,58,59). Inhibition of hepatic uptake of organic anions and of their glucuronidation have been proposed as the mechanisms by which novobiocin and rifampin induce cholestasis.…”

Section: Metabolic Poisonsmentioning

confidence: 98%

Cellular Mechanisms of Cholestasis

Oelberg¹,

Lester²

1986

Annu. Rev. Med.

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Concepts regarding the pathogenesis of cholestasis continue to evolve as investigational techniques improve and molecular mechanisms of bile formation are clarified. With the accumulation of information it is becoming increasingly evident that cholestasis results from not one but multiple disturbances in the sequence of events responsible for bile production. In addition to the inhibition of bile flow attributable to initiating events, cholestasis itself may inhibit bile flow by altering the intra- and extracellular environments of liver cells. Many questions about cholestasis remain unanswered, but future directions for research are suggested by the information currently available.

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Adverse Effects of Drugs on the Liver

Jim¹,

Gee²

1992

Applied Therapeutics

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Reversible cholestatic jaundice and hyperamylasaemia associated with captopril treatment.

Cited by 14 publications

References 3 publications

Acute Liver Failure due to Enalapril

Acute Liver Failure due to Enalapril

Cellular Mechanisms of Cholestasis

Adverse Effects of Drugs on the Liver

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