Methyldopa Liver Damage

Toghill, P J; Smith, Paul; Benton, P; Brown, Rachel C.; Matthews, H.L.

doi:10.1136/bmj.3.5930.545

Cited by 87 publications

(15 citation statements)

References 12 publications

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“…This is generally not the case in drug-induced liver injury hepatitis that is predominantly immune-mediated. For example, druginduced hepatitis due to methyldopa and tienilic acid ceases with drug discontinuation [32].…”

Section: Summary Of Clinical Resultsmentioning

confidence: 99%

Mitochondrial dysfunction and delayed hepatotoxicity: another lesson from troglitazone

Julie

Kende

et al. 2008

Diabetologia

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Section: Summary Of Clinical Resultsmentioning

confidence: 99%

Mitochondrial dysfunction and delayed hepatotoxicity: another lesson from troglitazone

Julie

Kende

et al. 2008

Diabetologia

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“…The patient recovered completely after the drug was withdrawn. Toghill et al [6] also observed cholestasis in some biopsy samples from patients with methyldopa hepatotoxicity. Sataline and Lowell [10] described another case that closely resembles our patient, although ex trahepatic obstruction was not entirely ex cluded.…”

Section: Discussionmentioning

confidence: 95%

“…Rechallenge with the drug was considered as ethically unacceptable because deaths have occurred under similar circumstances [6,8]. Although the patient had received other medications we are not aware of cholestatic hepatitis with any of them.…”

Section: Discussionmentioning

confidence: 99%

“…The usual manifestation of the drug's hepatotoxicity is mild hepatocel lular dysfunction which is hard to distinguish from viral hepatitis, and often resolves de spite continued administration [1], Severe hepatic injury is far less common, and only 85 such cases had been reported up to 1981 [4], This form of liver injury affects predomi nantly women and tends to appear after a rel atively long exposure, the longest period re ported being 11 years. It usually takes the forms of chronic active hepatitis, cirrhosis and/or fatal hepatic necrosis [2,[5][6][7].…”

Section: Discussionmentioning

confidence: 99%

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Cholestatic Liver Injury after Prolonged Exposure to Methyldopa

Moses

Zahger²,

Amir³

1989

Digestion

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We describe a 75-year-old patient who presented with severe cholestatic liver disease. He had been receiving methyldopa, 250 mg daily, for 6 years. An extensive evaluation failed to reveal extrahepatic obstruction or serologic evidence of viral hepatitis. A liver biopsy disclosed marked cholestasis, without hepatitis, and was compatible with a rare form of methyldopa-induced liver injury. Cessation of drug treatment was followed by a slow but complete recovery. Cholestasis is a rare manifestation of methyldopa hepatotoxicity. Although methyldopa-associated liver injury usually appears after about 4 weeks of treatment, a history of a much longer exposure does not exclude this entity.

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“…One of these two cases developed our facility and 30.4% of fulminant hepatic failure of liver injury (histologically characterized by submassive unknown cause. Drugs known to induce fulminant henecrosis) after 10 months of ecarazine therapy, and the patic failure include halothane, 10 tetracycline, 11 acetother developed liver injury (histologically characteraminophen, 3,4 methyldopa, 12,13 isoniazid, 14 monoamine ized by focal necrosis) after 2 years of ecarazine theroxidase inhibitors, 15 sodium vaproate, 16 pirprofen, and apy. In these cases, however, liver injury did not adphosphorus.…”

Section: In All Cases Fulminant Hepatic Failure In These Cases Couldmentioning

confidence: 99%

Fulminant hepatic failure caused by ecarazine hydrochloride (a hydralazine derivative)

et al. 1996

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The cause of fulminant hepatic failure is reported to icant number of cases of this disease are caused by be unknown in more than half the cases in Japan. We suicide attempts with paracetamol. 3,4 In France, it is recently reviewed 23 cases of fulminant hepatic failure often caused by ingestion of poisonous mushrooms. 5,6 that had been treated at our hospital. The cause of dis-According to a nationwide survey of fulminant hepatic ease had been regarded as unknown before this study. failure among Japanese in 1993, the cause was attribIt was found that seven of these patients had been under uted to acute hepatitis A in 16% of all cases, acute ecarazine hydrochloride therapy when they developed hepatitis B in 22%, drug-induced hepatitis in 10%, and fulminant hepatic failure. We examined the reasons why was unexplained in 52%.2 Identification of the cause of fulminant hepatic failure in these seven patients had not unexplained fulminant hepatic failure, which accounts been previously attributed to ecarazine, and found that for more than half of all cases, is essential in selecting it could be explained by the following factors: (1) the time from the start of ecarazine therapy to the onset of optimal therapies and preventing the onset of this dishepatic failure was long; (2) in all cases, hepatic failure ease.developed more than 10 days after the clinical recogni-In the current study, we attempted to identify the tion of hepatitis; and (3) characteristic signs of drug-cause of fulminant hepatic failure, with emphasis on induced hepatic failure such as skin rash and positive the analysis of possible relationships to drug usage, in lymphocytes stimulation test with the drug were absent 23 cases of fulminant hepatic failure of unknown cause. in all cases. Fulminant hepatic failure in these cases could be characterized by: (1) rapid decrease in serum PATIENTS AND METHODS alanine transaminase (ALT) level after discontinuationBetween 1968 and 1994, 114 patients with fulminant heof ecarazine, (2) prolonged jaundice despite discontinuapatic failure were treated at our hospital or its related facilition of ecarazine, (3) high incidence of anti-nuclear antities. Of these cases, 8 were diagnosed as caused by hepatitis body (ANA) (57%), and (4) histological findings of exten-A virus because of immunoglobulin M anti-HA, 37 were diagsive hepatocellular necrosis ranging from bridging nosed as being due to hepatitis B virus because of the presnecrosis to massive necrosis. Of the seven patients, four ence of immunoglobulin M anti-HBc, and 37 were diagnosed died of fulminant hepatic failure. These four patients as being due to drugs because of a history of using drugs had received high doses of ecarazine hydrochloride for (e.g., halothane) that were known to provoke fulminant hepaprolonged periods. Our data suggest that there may be titis and because of positive lymphocytes stimulation test many cases in which the cause of fulminant hepatic failwith the drug. The lymphocyte stimulation test with drug ure or acute hepatitis was not pre...

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Methyldopa Liver Damage

Cited by 87 publications

References 12 publications

Mitochondrial dysfunction and delayed hepatotoxicity: another lesson from troglitazone

Mitochondrial dysfunction and delayed hepatotoxicity: another lesson from troglitazone

Cholestatic Liver Injury after Prolonged Exposure to Methyldopa

Fulminant hepatic failure caused by ecarazine hydrochloride (a hydralazine derivative)

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