Captopril-Associated Cholestatic Jaundice

Rahmat, J.

doi:10.7326/0003-4819-102-1-56

Cited by 57 publications

(9 citation statements)

References 11 publications

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“…Increase in creatinine levels with captopril therapy may be due to biological effects, as reported by in previous studies (Siest et al,2001 andRobert, 2010).This study found that the use of captopril in hypertensive patients has resulted in a significant reduction of mean total bilirubin level, which was in accordance with the results of Rahmat et al;(2000) who reported that most hepatic toxicity caused by captopril is mild and transient and the elevation in the serum ALT and AST activities is mild and resolved after discontinuation of the therapy. This mild cellular damage may be attributed to the accumulation of toxic metabolite of the drug within the hepatocytes causing direct injury or indirect injury by immune mediated cellular damage (Bonacini and Miyashita;2002).The elevation in serum ALT activity suggested that captopril may have mild to moderate cholestatic effect on the liver ( Rahmat et al, 2000). Both drugs investigated in the present study caused an increase the level of lipid profile which consistent with result obtained by previous reporters (Maritiz;et al 1995;Ibrahim et al 2010 ) this may be explained by their impact directly on lipid metabolism.…”

Section: Discussion:-supporting

confidence: 91%

Effect of oral Hypertensive agents on Biochemical parameters in Diabetic patients : In vivo study.

Alblihed¹,

Farah²

2016

IJAR

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Objectives:In vivo study was carried out to monitor the effect of antihypertensive drugs (Captopril and Atenolol) on the metabolites and enzymes that are requested for professional diagnosis in diabetic patients. Methods: 30 hypertensive diabetic subjects of type II (18 males and 12 females) with an average age of (55 ±15 years) and average weight (61 ±16.5 kg) were participated in this study. 17 subjects were on Captopril therapy (50mg/daily) and 13 subjects were on Atenolol therapy (50mg/daily). 30 healthy volunteers of comparable age (52 ± 15 years ) and an average weight (85.5±15.5 kg) was used as control sample. Two venous blood samples were collected from each subject, first blood sample was taken before drug therapy and the second blood sample was taken three weeks after drug therapy.

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Section: Discussion:-supporting

confidence: 91%

Effect of oral Hypertensive agents on Biochemical parameters in Diabetic patients : In vivo study.

Alblihed¹,

Farah²

2016

IJAR

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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%

“…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%

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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“…Representatives of this class of drugs (captopril, enalapril, fosinopril) have usually been implicated in causing bland cholestasis or cholestatic hepatitis. 72 Hepatocellular injury [73][74][75][76] has also been described. Duration of treatment has varied from 1 week to 1 year, with a mean of 14 weeks.…”

Section: Angiotensin-converting Enzyme (Ace) Inhibitorsmentioning

confidence: 99%

“…Hallmarks of hypersensitivity such as fever, skin rash, and eosinophilia may be evident. 73 Recovery is usual, but serum alkaline phosphatase may remain abnormal for up to 18 months. 72 Fulminant hepatic failure is a rare complication and has been reported with lisinopril 78 and enalapril.…”

Section: Angiotensin-converting Enzyme (Ace) Inhibitorsmentioning

confidence: 99%

Hepatotoxicity of Commonly Used Drugs: Nonsteroidal Anti-Inflammatory Drugs, Antihypertensives, Antidiabetic Agents, Anticonvulsants, Lipid-Lowering Agents, Psychotropic Drugs

Chitturi¹,

George²

2002

Semin Liver Dis

194

106

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Hepatotoxic adverse drug reactions have contributed to the decline of many promising therapies, even among mainstream medication classes (bromfenac and troglitazone are recent examples). The spectrum of nonsteroidal anti-inflammatory drug-related liver toxicity continues to expand, with reports in children, interactive toxicity in persons with hepatitis C, and recognition of the toxicity of both the preferential and selective cyclooxygenase-2 inhibitors. Of the antihypertensive agents, methyldopa is now rarely prescribed and adverse effects are reported infrequently, whereas cases of liver injury associated with the angiotensin receptor and converting enzyme inhibitors are increasingly reported. Of the antidiabetic agents, acarbose, gliclazide, metformin, and human insulin have been implicated in causing liver injury. To date, the newer thiazolidinediones do not appear to share the hepatotoxic potential of troglitazone, although a few reports of acute hepatitis have accrued. Although liver injury has been associated with the "statins," the frequency of such toxicity is lower than that of the background population and the value of biochemical monitoring remains unproved. Newer concepts in anticonvulsant hepatotoxicity have been the recognition of the reactive metabolite syndrome, delineation of the risk factors for valproic acid toxicity, the potential role of carnitine in preventing valproic acid hepatotoxicity, and the toxicity of second-line antiepileptic drugs. Liver injury associated with newer psychotropic agents, particularly the selective serotonin reuptake inhibitors, is also discussed. The focus of the review is the hepatotoxicity of commonly used drugs with particular reference to recent and novel reports of toxicity. Well-known causes of liver injury such as chlorpromazine, phenytoin, and methyldopa are not discussed.

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Captopril-Associated Cholestatic Jaundice

Cited by 57 publications

References 11 publications

Effect of oral Hypertensive agents on Biochemical parameters in Diabetic patients : In vivo study.

Effect of oral Hypertensive agents on Biochemical parameters in Diabetic patients : In vivo study.

Acute Liver Failure due to Enalapril

Hepatotoxicity of Commonly Used Drugs: Nonsteroidal Anti-Inflammatory Drugs, Antihypertensives, Antidiabetic Agents, Anticonvulsants, Lipid-Lowering Agents, Psychotropic Drugs

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