Over-the-counter analgesics may not contribute to acute liver decompensation or worsen existing decompensation in patients with cirrhosis, Dr. Sakib Karim Khalid and his colleagues reported.
These hepatotoxic agents—specifically, acetaminophen and NSAIDS such as aspirin, ibuprofen, naproxen, and sulindac—have been suspected of causing acute hepatic decompensation or of worsening the condition of an already decompensated patient with cirrhosis, but prospective data are lacking.
Dr. Khalid of Yale University, New Haven, Conn., and his associates performed a case-control study in which 91 consecutive cirrhosis patients hospitalized for acute hepatic decompensation were compared with two groups of control subjects to determine whether use of over-the-counter analgesics during the preceding 30 days could account for the decompensation.
The study was supported in part by Ortho-McNeil Pharmaceuticals Inc.
Acute hepatic decompensation was characterized by variceal hemorrhage, new or worsening ascites, encephalopathy, jaundice, spontaneous bacterial peritonitis, spontaneous bacteremia, or renal dysfunction, they said (Clin. Gastroenterol. Hepatol. 2009 Apr 24. [doi:10.1016/j.cgh.2009.04.015
One control group comprised 153 cirrhosis patients who were not hospitalized; the other comprised 89 patients without cirrhosis who were hospitalized for reasons unrelated to liver failure.
The researchers expected to find that patients with acute hepatic decompensation had taken more OTC analgesics than either control group, but “our results actually show that a lower proportion of patients with cirrhosis use OTC analgesics in general, and that an even lower proportion… had used them in the preceding month,” they wrote.
Only 32 cirrhosis patients with acute liver failure (35%) reported using any OTC analgesics during the preceding 30 days, compared with 80 cirrhotic controls (52%) and 62 noncirrhotic controls (70%). In particular, acetaminophen “was used by only one-fifth of the cirrhotic cases,” was used at daily doses that were equivalent to those used by cirrhotic control subjects, and was never used at a dose that exceeded the therapeutic dose of 4 g/day.
These results suggest that OTC analgesics “do not contribute to acute hepatic decompensation in cirrhosis,” Dr. Khalid and his colleagues wrote.
Specifically, “acetaminophen at a maximal daily dose of 3 g/day (for up to 2 days) or at a daily dose of 1 g/day (for up to 25 days) does not appear to be associated with acute hepatic decompensation,” they said.
No financial conflicts other than the study sponsorship were reported.