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COMPARATIVE STUDY
JOURNAL ARTICLE
RESEARCH SUPPORT, N.I.H., EXTRAMURAL
RESEARCH SUPPORT, NON-U.S. GOV'T
Use of over-the-counter analgesics is not associated with acute decompensation in patients with cirrhosis.
Clinical Gastroenterology and Hepatology 2009 September
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.
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.
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