Hepatic injury related to enalapril

Rosellini, Salvatore Ricca; Costa, Pier Lorenzo; Gaudio, Michele; A, Saragoni; Miglio, F

doi:10.1016/0016-5085(89)90674-4

Cited by 26 publications

(6 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: 99%

“…Most of the patients in these reports were receiving other medication concurrently, though these medications are not commonly associated with hepatotoxicity. 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.…”

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

confidence: 99%

“…In one report the sulfhydryl group of captopril was discussed as causing liver damage [10]. This seems to be less likely because other ACE inhibitors lacking this group as enalapril and lisinopril also caused hepatoxicity [4,12,13,15,17,20,26]. In addition, cross reactivity between captopril and enalapril in evoking hepatotoxicity has been reported [7,22].…”

Section: Mechanism For Ace-inhibitor Associated Hepatotoxicitymentioning

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: 99%

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

confidence: 99%

Section: Mechanism For Ace-inhibitor Associated Hepatotoxicitymentioning

confidence: 99%

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Acute Liver Failure due to Enalapril

Jeserich

Ihling²,

Allgaier³

et al. 2000

Herz

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“…All of the ACE inhibitors have been implicated in hepatic injury including fulminant hepatic failure (123)(124)(125)(126). The reactions are mostly hepatocellular, but cholestatic reactions have also been reported.…”

Section: Pharmacologic Therapymentioning

confidence: 99%

Spectrum of Liver Disease in Type 2 Diabetes and Management of Patients With Diabetes and Liver Disease

et al. 2007

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“…[12][13][14][15] A study undertaken ,with the crustacean test species Thamnocephalus platyurus, to determine the effect levels of 28 selected pharmaceuticals indicates that enalapril has low toxicity up to the concentration of 200 mg L -1 . 16 The literature reported the half maximal effective concentration (EC 50 ) of 374 mg L -1 and EC 50 of 650 mg L -1 of RAN for P. putida and Daphnia magna respectively.…”

mentioning

confidence: 99%

Characterization of enalapril and ranitidine chlorination by-products by liquid chromatography/high-resolution mass spectrometry and their toxicity evaluation

et al. 2017

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Due to its low cost, its capability for disinfection and oxidation, chlorination using gaseous chlorine or hypochlorite salts, has also been commonly applied in water treatment plants for oxidation and disinfection purposes. Little is known about the identity and toxicity of by-products resulting from the chlorination of pharmaceutical micropollutants, such as enalapril (ENA) and ranitidine (RAN). ENA and RAN chlorination by-products were characterized in this study by high-performance liquid chromatography coupled to high-resolution mass spectrometry (HPLC/HRMS) and their toxicity were assessed by MTT assay. Chlorination experiments with ENA and RAN solutions (10 mg L -1 ) indicate degradation efficiencies of 100% for both compounds after only 5 min of exposure to chlorine at concentration of 9.53 mg Cl 2 L -1. On the other hand mineralization rates were lower than 3%, thereby indicating there was accumulation of degradation by-products in all experiments. Mass spectrometric analysis revealed, at all times of reaction after the addition of hypochlorite, the presence of 1-(2-((4-(chlorophenyl)-1-ethoxy-1-oxobutan-2-yl)amino)propanoyl)pyrrolidine-2-carboxylic acid (enalapril by-product) and N-chloro-N-(2-(((chloro-5-((dimethylamino)methyl)furan-2-yl)methyl)sulfinyl)ethyl)-N-methyl-2-nitroethene 1,1-diamine (ranitidine by-product). Despite the formation of oxidized chlorinated by-products in all chlorination assays, the treated solutions were nontoxic to HepG2 cells by the MTT assay. It has been observed that chlorination (10 mg L -1 , 5 min) of ENA and RAN solutions exhibited high degradation efficiencies of the target compounds and low mineralization rates. Based on the mass spectrometry data, the routes for ENA and RAN successive oxidation by chlorine has been proposed.

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Hepatic injury related to enalapril

Cited by 26 publications

References 3 publications

Acute Liver Failure due to Enalapril

Acute Liver Failure due to Enalapril

Spectrum of Liver Disease in Type 2 Diabetes and Management of Patients With Diabetes and Liver Disease

Characterization of enalapril and ranitidine chlorination by-products by liquid chromatography/high-resolution mass spectrometry and their toxicity evaluation

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