Hepatotoxicity medical therapy

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Medical Therapy

Clinical Assessment

Algorithm for suspected drug induced hepatic toxicity

This remains a major challenge in clinical practice due to lack of reliable markers.[1] Many other conditions lead to similar clinical as well as pathological picture. To diagnose hepatotoxicity, a causal relationship between the use of the toxin or drug and subsequent liver damage has to be established, but might be difficult, especially when idiosyncratic reaction is suspected.[2] Simultaneous use of multiple drugs may add to the complexity. As in acetaminophen toxicity, well established dose dependent pharmacological hepatotoxicity is easier to spot. Several clinical scales such as CIOMS/RUCAM scale and Maria and Victorino criteria have been proposed to establish causal relationship between offending drug and liver damage. CIOMS/RUCAM scale involves a scoring system which categorizes the suspicion into "definite or highly probable" (score > 8), “probable” (score 6-8), “possible” (score 3-5), “unlikely” (score 1-2) and “excluded” (score ≤ 0). In clinical practice physicians put more emphasis on the presence or absence of similarity between the biochemical profile of the patient and known biochemical profile of the suspected toxicity ( e.g. cholestatic damage in amoxycillin-clauvonic acid ).[1]


In most cases liver function will return to normality if offending drug is stopped early. However in acetamenophen toxicity initial insult can be fatal. In most instances supportive treatment is all that is required. However in fulminant hepatic failure from drug induced hepatotoxicity may require liver transplantation. In the past glucocorticoides in allergic features and ursodeoxycholic acid in cholestatic pictures had been used, but there is no good evidence to support their effectiveness.

An elevation in serum bilirubin level of more that 2 times ULN with associated transaminase rise is an ominous sign. This indicates severe hepatotoxicity and is likely to lead to mortality in 10% to 15% of patients, especially if the offending drug is not stopped (Hy's Law).[3][4] This is due to the fact that it requires significant damage to the liver to impair bilirubin excretion, hence minor impairment (in the absence of biliary obstruction or Gilbert syndrome) would not lead to jaundice. Other poor predictors of outcome are old age, female sex, high AST.[5][6]


  1. 1.0 1.1 Andrade RJ, Robles M, Fernández-Castañer A, López-Ortega S, López-Vega MC, Lucena MI (2007). "Assessment of drug-induced hepatotoxicity in clinical practice: a challenge for gastroenterologists". World J. Gastroenterol. 13 (3): 329–40. PMID 17230599.
  2. Arundel C, Lewis JH (2007). "Drug-induced liver disease in 2006". Curr. Opin. Gastroenterol. 23 (3): 244–54. doi:10.1097/MOG.0b013e3280b17dfb. PMID 17414839.
  3. Reuben A (2004). "Hy's law". Hepatology. 39 (2): 574–8. doi:10.1002/hep.20081. PMID 14768020.
  4. Arora N, Goldhaber SZ (2006). "Anticoagulants and transaminase elevation". Circulation. 113 (15): e698–702. doi:10.1161/CIRCULATIONAHA.105.603100. PMID 16618822.
  5. Andrade RJ, Lucena MI, Kaplowitz N; et al. (2006). "Outcome of acute idiosyncratic drug-induced liver injury: Long-term follow-up in a hepatotoxicity registry". Hepatology. 44 (6): 1581–8. doi:10.1002/hep.21424. PMID 17133470.
  6. Björnsson E, Olsson R (2005). "Outcome and prognostic markers in severe drug-induced liver disease". Hepatology. 42 (2): 481–9. doi:10.1002/hep.20800. PMID 16025496.

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