LARSON AM,POLSONJ,FONTANA RJ,et al.Acetaminophen-induced acute liver failure: results of a United States multicenter,prospective study[J].Hepatology,2005,42(6): 1364-1372.
Severe acetaminophen hepatotoxicity frequently leads to acute liver failure (ALF). We determined the incidence, risk factors, and outcomes of acetaminophen- induced ALF at 22 tertiary care centers in the United States. Detailed prospective data were gathered on 662 consecutive patients over a 6- year period fulfilling standard criteria for ALF (coagulopathy and encephalopathy), from which 275 (42% )were determined to result from acetaminophen liver injury. The annual percentage of acetaminophen-related ALF rose during the study from 28% in 1998 to 51% in 2003. Median dose ingested was 24 g (equivalent to 48 extra-strength tablets). Unintentional overdoses accounted for 131 (48% ) cases, intentional (suicide attempts) 122 (44% ), and 22 (8% ) were of unknown intent. In the unintentional group, 38% took two or more acetaminophen preparations simultaneously, and 63% used narcotic-containing compounds. Eighty-one percent of unintentional patients reported taking acetaminophen and/or other analgesics for acute or chronic pain syndromes. Overall, 178 subjects (65% ) survived, 74 (27% ) died without transplantation, and 23 subjects (8% ) underwent liver transplantation; 71% were alive at 3 weeks. Transplant free survival rate and rate of liver transplantation were similar between intentional and unintentional groups. In conclusion, acetaminophen hepatotoxicity far exceeds other causes of acute liver failure in the United States. Susceptible patients have concomitant depression, chronic pain, alcohol or narcotic use, and/or take several preparations simultaneously. Education of patients, physicians, and pharmacies to limit high-risk use settings is recommended.
LOH CS,PONAMPALAMR.Nephrotoxicity associated with acute paracetamol overdose:a case report and review of the literature[J].Hongkong J Emerg Med,2006,13(2):105-110.
OZKAYAO,GENCG,BEKK.A case of acetaminophen (paracetamol) causing renal failure without liver damage in a child and review of literature[J].Ren Fail,2010,32(9):1125-1127.
Acetaminophen (paracetamol) is a widely used drug and known as a safety antipyretic and analgesic drug in childhood. Acetaminophen-associated liver damage is more recognized than kidney damage. Nephrotoxicity and hepatotoxicity can be seen together after acetaminophen overdose, but renal damage without liver damage is a rarely seen entity in all age groups being reported more rarely in childhood. We present here a 16-year-old girl with renal failure without liver damage because of acetaminophen toxicity and a review of literature for pathophysiological mechanisms, clinical course, treatment, and outcome.
BOUTISK,SHANNONM.Nephrotoxicity after acute severe acetaminophen poisoning in adolescents[J].J Toxicol Clin Toxicol,2001,39(5):441-445.
OBJECTIVE: To determine the rate of acetaminophen related nephrotoxicity in adolescents who present after acute severe acetaminophen intoxication and to identify potential predictors of this outcome. STUDY DESIGN: Retrospective analysis of consecutive patients between the ages of 12 and 18 years who were admitted at a tertiary care children's hospital for treatment of acute severe acetaminophen intoxication with N-acetylcysteine. The main outcome measure was the frequency of acetaminophen-related nephrotoxicity, defined as abnormal blood urea nitrogen (>6.4 mmol/L or > 18 mg/dL) and/or elevated creatinine (97.2 micromol/L or > 1.1 mg/dL) in association with one or both of the following: elevated blood pressure (systolic blood pressure > 140 mm Hg/diastolic blood pressure >85) or abnormal urinalysis (urinalysis with hematuria or proteinuria). Statistical analyses used were measures of central tendency, Student's t-test, Mann-Whitney, and multivariate logistic regression. RESULTS: Fourty-five patients were included. Acetaminophen-related nephrotoxicity occurred in 4 (8.9%) cases. One victim developed severe renal injury in association with elevated hepatic transaminases. Intergroup analyses revealed no statistically significant association between acetaminophen-related nephrotoxicity and amount/kg of acute severe acetaminophen ingested, delay in treatment with N-acetylcysteine, or measures of hepaticfunction. CONCLUSIONS: Acetaminophen-related nephrotoxicity occurred in 8.9% [95% CI: 4.52, 20.48] of children with severe overdose. There are no obvious predictors of this complication of acetaminophen overdose. Because the occurrence of renal injury can not be predicted, serial blood pressure, blood urea nitrogen/creatinine, and urinalysis should be considered an integral part of the management of children with acute, severe acetaminophen intoxication.
BLAKELYP,MCDONALD BR.Acute renal failure due to acetaminophen ingestion: a case report and review of the literature[J].J Am Soc Nephrol,1995,6(1):48-53.
Acetaminophen is the most commonly reported drug overdose in the United States. Acute renal failure occurs in less than 2% of all acetaminophen poisonings and 10% of severely poisoned patients. At the therapeutic dosages, acetaminophen can be toxic to the kidneys in patients who are glutathione depleted (chronic alcohol ingestion, starvation, or fasting) or who take drugs that stimulate the P-450 microsomal oxidase enzymes (anticonvulsants). Acute renal failure due to acetaminophen manifests as acute tubular necrosis (ATN). ATN can occur alone or in combination with hepatic necrosis. The azotemia of acetaminophen toxicity is typically reversible, although it may worsen over 7 to 10 days before the recovery of renal function occurs. In severe overdoses, renal failure coincides with hepatic encephalopathy and dialysis may be required. Recognition of acetaminophen nephropathy requires the following: (1) a thorough drug history, including over-the-counter medications such as Tylenol or Nyquil; (2) knowledge of the risk factors that lessen its margin of safety at therapeutic ingestions, i.e., alcoholism; and (3) consideration of acetaminophen in the differential diagnosis of patients who present with combined hepatic dysfunction and ATN.
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