Skip to main content
PMC home page
Journal of Medical Toxicology logoLink to Journal of Medical Toxicology
. 2010 Apr 21;6(3):294–300. doi: 10.1007/s13181-010-0075-9

Liver Aminotransferases Are Elevated with Rhabdomyolysis in the Absence of Significant Liver Injury

Kathryn Weibrecht 1, Matthew Dayno 2, Chad Darling 2, Steven B Bird 1,✉
PMCID: PMC3550495  PMID: 20407858

Abstract

Rhabdomyolysis is an uncommon finding in the emergency department. However, the clinical implications of rhabdomyolysis are important, with a significant minority of patients developing acute renal failure and multiorgan failure. When present, the cause of elevated aminotransferases in the setting of rhabdomyolysis is often unclear. We sought to determine the incidence of abnormal aminotransferases (defined as aspartate aminotransferase (AST) or alanine aminotransferase (ALT) >40 U/L) in the setting of rhabdomyolysis and how the aminotransferases decrease relative to the creatine phosphokinase (CPK) concentration as rhabdomyolysis resolves. A retrospective chart review of 215 cases of rhabdomyolysis with CPK of ≥1,000 U/L was performed. The incidence of an abnormal AST in the setting of rhabdomyolysis was 93.1% (95% confidence interval, 88.7% to 95.8%). An abnormal ALT was much less common and found in 75.0% (95% confidence interval, 68.7% to 80.2%) of patients with a CPK of ≥1,000 U/L (p < 0.0001). In only one instance was the ALT > 40 U/L while the AST was <40 U/L. Furthermore, AST concentrations (and not ALT) fall in parallel with CPK during the first 6 days of hospitalization for patients with rhabdomyolysis. Aminotransferase abnormalities, particularly AST, are common in the setting of rhabdomyolysis. AST concentrations decrease in parallel to CPK, suggesting skeletal muscle may be a significant source of AST elevation in these patients.

Keywords: Aspartate aminotransferase, Alanine aminotransferase, Rhabdomyolysis

Full Text

The Full Text of this article is available as a PDF (177.7 KB).

References

  • 1.Better OS. The crush syndrome revisited (1940–1990) Nephron. 1990;55(2):97–103. doi: 10.1159/000185934. [DOI] [PubMed] [Google Scholar]
  • 2.Fernandez WG, Hung O, Bruno GR, et al. Factors predictive of acute renal failure and need for hemodialysis among ED patients with rhabdomyolysis. Am J Emerg Med. 2005;23(1):1–7. doi: 10.1016/j.ajem.2004.09.025. [DOI] [PubMed] [Google Scholar]
  • 3.Goldfarb DS, Chung S. The absence of rhabdomyolysis-induced renal failure the World Trade Center collapse. Am J Med. 2002;113:250. doi: 10.1016/S0002-9343(02)01188-9. [DOI] [PubMed] [Google Scholar]
  • 4.Sinert R, Kohl L, Rainone T, et al. Exercise-induced rhabdomyolysis. Ann Emerg Med. 1994;23:1301–1306. doi: 10.1016/S0196-0644(94)70356-6. [DOI] [PubMed] [Google Scholar]
  • 5.Ward MM. Factors predictive of acute renal failure in rhabdomyolysis. Arch Intern Med. 1988;148:1553–1557. doi: 10.1001/archinte.148.7.1553. [DOI] [PubMed] [Google Scholar]
  • 6.Gilbert EH, Lowenstein SR, Koziol-McLain J, et al. Chart reviews in emergency medicine research: where are the methods? Ann Emerg Med. 1996;27(3):305–308. doi: 10.1016/S0196-0644(96)70264-0. [DOI] [PubMed] [Google Scholar]
  • 7.Strassburg CP. Gastrointestinal disorders of the critically ill. Shock liver. Best Pract Res Clin Gastroenterol. 2003;17(3):369–381. doi: 10.1016/S1521-6918(03)00025-8. [DOI] [PubMed] [Google Scholar]
  • 8.Calderon-Margalit R, Mor-Yosef S, Mayer M, et al. An administrative intervention to improve the utilization of laboratory tests within a university hospital. Int J Qual Health Care. 2005;17:243–248. doi: 10.1093/intqhc/mzi025. [DOI] [PubMed] [Google Scholar]
  • 9.Tarpey J, Lawler PG. Iatrogenic anemia? A survey of venesection in patients in the intensive therapy unit. Anaesthesia. 1990;45:396–398. doi: 10.1111/j.1365-2044.1990.tb14785.x. [DOI] [PubMed] [Google Scholar]
  • 10.Kamimoto Y, Horiuchi S, Tanase S, et al. Plasma clearance of intravenously injected aspartate aminotransferase isozymes: evidence for preferential uptake by sinusoidal liver cells. Hepatology. 1985;5(3):367–375. doi: 10.1002/hep.1840050305. [DOI] [PubMed] [Google Scholar]
  • 11.Goessling W, Friedman LS. Increased liver chemistry in an asymptomatic patient. Clin Gastroenterol Hepatol. 2005;3(9):852–858. doi: 10.1016/S1542-3565(05)00416-7. [DOI] [PubMed] [Google Scholar]
  • 12.Schiff ER, Sorrell MF, Maddrey WC, et al. Schiff’s diseases of the liver. Philadelphia: Lippincott Williams & Wilkins; 2006. [Google Scholar]
  • 13.Wakim KG, Fleisher GA. The fate of enzymes in body fluids—an experimental study. II. Disappearance rates of glutamic-oxalacetic transaminase I under various conditions. J Lab Clin Med. 1963;61:86–97. [PubMed] [Google Scholar]
  • 14.Fleisher GA, Wakim KG. The fate of enzymes in body fluids—an experimental study. I. Disappearance rates of glutamic-pyruvic transaminase under various conditions. J Lab Clin Med. 1963;61:76–85. [PubMed] [Google Scholar]
  • 15.Giannini EG, Testa R, Savarino V. Liver enzyme alteration: a guide for clinicians. CMAJ. 2005;172(3):367–379. doi: 10.1503/cmaj.1040752. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 16.Wroblewski F. The clinical significance of alterations in transaminase activities of serum and other body fluids. Adv Clin Chem. 1958;1(2):313–351. doi: 10.1016/S0065-2423(08)60362-5. [DOI] [PubMed] [Google Scholar]
  • 17.Nathwani RA, Pais S, Reynolds TB, et al. Serum alanine aminotransferase in skeletal muscle diseases. Hepatology. 2005;41(2):380–382. doi: 10.1002/hep.20548. [DOI] [PubMed] [Google Scholar]
  • 18.Korones DN, Brown MR, Palis J. “Liver function tests” are not always tests of liver function. Am J Hematol. 2001;66(1):46–48. doi: 10.1002/1096-8652(200101)66:1&#x0003c;46::AID-AJH1007&#x0003e;3.0.CO;2-O. [DOI] [PubMed] [Google Scholar]
  • 19.Huerta-Alardin AL, Varon J, Marik PE. Bench-to-bedside review: rhabdomyolysis—an overview for clinicians. Crit Care. 2005;9:158–169. doi: 10.1186/cc2978. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 20.Brown CV, Rhee P, Chan L, et al. Preventing renal failure in patients with rhabdomyolysis: do bicarbonate and mannitol make a difference? J Trauma. 2004;56:1191–1196. doi: 10.1097/01.TA.0000130761.78627.10. [DOI] [PubMed] [Google Scholar]
  • 21.Pratt D, Kaplan MM. Laborator tests. In: Schiff ER, Sorrell MF, Maddrey WC, editors. Schiff’s Diseases f the Liver. Philadelphia: Lippincott-Raven; 1999. pp. 205–244. [Google Scholar]
  • 22.Pratt D, Kaplan MM. Evaluation of abnormal liver-enzyme results in asymptomatic patients. N Engl J Med. 2000;342:1266–1271. doi: 10.1056/NEJM200004273421707. [DOI] [PubMed] [Google Scholar]
  • 23.Conigrave KM, Davies P, Haber P, et al. Traditional markers of excessive alcohol use. Addiction. 2003;98(2):31–43. doi: 10.1046/j.1359-6357.2003.00581.x. [DOI] [PubMed] [Google Scholar]
  • 24.Cohen JA, Kaplan MM. The SGOP/SGPT ratio—an indicator of alcoholic liver disease. Dig Dis Sci. 1979;24:835–838. doi: 10.1007/BF01324898. [DOI] [PubMed] [Google Scholar]
  • 25.Conigrave KM, Degenhardt LJ, Whitfield JB, et al. CDT, GGT, and AST as markers of alcohol use: the WHO/ISBRA collaborative project. Alcohol Clin Exp Res. 2002;26(3):332–339. [PubMed] [Google Scholar]
  • 26.Casiglia E, Spolaore P, Ginocchio G, et al. Unexpected effects of coffee consumption on liver enzymes. Eur J Epidemiol. 1993;9(3):293–297. doi: 10.1007/BF00146266. [DOI] [PubMed] [Google Scholar]

Articles from Journal of Medical Toxicology are provided here courtesy of Springer

RESOURCES