Original articles—liver, pancreas, and biliary tract
Use of Over-the-Counter Analgesics Is Not Associated With Acute Decompensation in Patients With Cirrhosis

https://doi.org/10.1016/j.cgh.2009.04.015Get rights and content

Background & Aims

Over-the-counter analgesics have been proposed to lead to decompensation of compensated cirrhosis or to further decompensation of an already decompensated patient. We performed a prospective, case-control study to investigate the effects of analgesics on acute hepatic decompensation.

Methods

Data from consecutive cirrhotic patients hospitalized at 2 tertiary care hospitals for decompensation of cirrhosis (cases, n = 91) were compared with that from consecutive patients with compensated cirrhosis that were followed in the liver clinic (n = 153) and with randomly selected noncirrhotic patients concurrently hospitalized with the cases (n = 89). All patients were given a structured questionnaire to collect information on recent use of acetaminophen, nonsteroidal anti-inflammatory drugs and alcohol.

Results

Only 32 (35%) of the cirrhotic patients used over-the-counter analgesics (19% acetaminophen, 16% nonsteroidal anti-inflammatory drugs), compared with 80 of the cirrhotic controls (52%; 25% acetaminophen, 31% nonsteroidal anti-inflammatory drugs), and 62 (70%) of the noncirrhotic controls. Acetaminophen use did not differ between groups, even for those with recent alcohol use. The doses and days of nonsteroidal anti-inflammatory drug use were higher among cirrhotic patients, compared with controls. Alcohol ingestion was significantly greater among patients with alcoholic cirrhosis, compared with controls.

Conclusions

In patients with cirrhosis, acetaminophen use at doses lower than those recommended is not associated with acute hepatic decompensation, even in patients with recent alcohol ingestion. Nonsteroidal anti-inflammatory drugs might be associated with deleterious effects on cirrhosis. Alcohol ingestion is associated with decompensation in patients with alcoholic cirrhosis.

Section snippets

Study Design

The study was designed as a case-control study in which consecutive unique patients with cirrhosis hospitalized for “acute hepatic decompensation” (cirrhotic cases) between August 2000 and May 2002 were compared with consecutive patients with cirrhosis who had not been hospitalized in the previous 3 months and in the month following enrollment (cirrhotic controls) and with patients without cirrhosis hospitalized at the same time as the cases (noncirrhotic controls). Cases were identified

Patient Characteristics

In the period between August 2000 and May 2002 (end of the study), 333 patients were enrolled: 91 cirrhotic cases, 153 cirrhotic controls, and 89 noncirrhotic controls. Forty-five cases could be matched by age and CTP class to 45 cirrhotic controls.

Table 1 shows the demographic characteristics of patients included in the study. Among cirrhotic cases, alcohol was the most common etiology, while among cirrhotic controls viral hepatitis (hepatitis C or B) was the most common etiology. Liver

Discussion

Decompensated cirrhosis is defined by the development of ascites, variceal hemorrhage, encephalopathy, or jaundice. It is at this stage of cirrhosis that the patient is at risk of dying from liver disease.6 Patients with cirrhosis are usually hospitalized when the first episode of decompensation occurs or when an already decompensated patient deteriorates further. A superimposed acute injury (acute-on-chronic event) can precipitate decompensation in the compensated patient or lead to further

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    This article has an accompanying continuing medical education activity on page 914. Learning Objectives—At the end of this activity the learner should identify the role of acetaminophen use and use of nonsteroidal drugs in promoting decompensation of liver disease in patients with cirrhosis.

    Conflicts of interest The authors disclose no conflicts.

    Funding This project was supported in part by grant from McNeil Pharmaceuticals and the Clinical Core of the Yale Liver Center NIDDK P30-34989.

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