Diclofenac hepatitis

Article Abstract:

Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used in the treatment of minor muscle and skeletal disorders, having partially replaced the use of simple analgesics (pain killing drugs) in this regard. As NSAID use has grown, so has concern over the toxic effects that many of these drugs show, including gastrointestinal hemorrhage and kidney impairment. In addition, many NSAIDs show evidence of producing hepatic (liver) damage; in many cases this problem is asymptomatic, hence the true incidence is probably underreported. Hepatitis is a chronic inflammatory condition affecting the liver, caused in some cases by chemical toxicity; instances of hepatitis have been reported following NSAID use. To document the occurrence of liver damage, including hepatitis, following use of the popular NSAID diclofenac, the records of the Australian Adverse Drug Reactions Advisory Committee were examined for the period of 1981 (when marketing of this drug started in Australia) to 1989. Eighty-two reports of liver damage possibly associated with the use of diclofenac were received by the committee during this period; in 26 of these cases (one fatal) diclofenac was the sole suspected cause of liver damage. The average age of the patients was 64 years; 70 percent were female. The most common clinical symptoms of liver damage were jaundice, liver enlargement, lack of appetite, and nausea. The duration of diclofenac treatment prior to the development of liver damage ranged from 6 to 417 days (midpoint 76 days). Blood levels of the liver enzymes aspartate transaminase and alanine transaminase were increased in this group of patients. Recovery started soon after withdrawal of drug treatment, and was paralleled by decreasing blood levels of liver enzymes. Hence, liver damage, although rare, can be induced in a subset of patients by diclofenac treatment, either by direct toxic effects of the drug or its metabolites. (Consumer Summary produced by Reliance Medical Information, Inc.)

Diclofenac, Hepatitis

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Experimental non-steroidal anti-inflammatory drug-induced enteropathy in the rat: similarities to inflammatory bowel disease and effect of thromboxane synthetase inhibitors

Article Abstract:

Nonsteroidal anti-inflammatory drugs (NSAIDs) can cause lesions of the gastrointestinal tract (enteritis) that are characterized by pathological changes similar to those seen in Crohn's disease (an inflammatory condition affecting the small intestine, typified by malabsorption of nutrients, diarrhea, malnutrition, and intestinal bleeding). It is thought that the gastrointestinal lesions in both NSAID-induced enteritis and Crohn's disease represent a common disease process, and that local changes in intestinal permeability are the earliest detectable indicator of this process. An animal model of NSAID-induced enteritis has been established and validated in which chronic administration of the NSAID indomethacin causes increased intestinal permeability and, ultimately, enteritis-like lesions. The administration of glucocorticoids and sulphasalazine, but not the antibiotic tetracycline, prevented the development of lesions when given prior to indomethacin treatment, and partially reversed the lesions when administered afterwards. These effects were mirrored in the results of both indomethacin and preventative treatment on tissue myeloperoxidase activity (a marker of inflammatory cell invasion). To investigate the role of the lipoxygenase/cyclooxygenase pathway in the development of enteritis, two thromboxane synthetase inhibitors (compounds that interfere with that biochemical pathway) were administered. As did glucocorticoids and sulphasalazine, these compounds prevented NSAID-induced enteritis when given prior to treatment, and partially reversed it when given afterwards. It is concluded that thromboxane synthetase inhibitors may be an important therapy for inflammatory intestinal disease conditions in man, and should be evaluated further. (Consumer Summary produced by Reliance Medical Information, Inc.)

Models, Inflammatory bowel diseases, Crohn's disease

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Relation of upper gastrointestinal bleeding to non-steroidal anti-inflammatory drugs and aspirin: a case-control study

Article Abstract:

Several anti-inflammatory, including nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin and other drugs, have been implicated as a cause of upper gastrointestinal bleeding. Although there is extensive anecdotal evidence to support this link, only a very few studies involving a very small number of subjects have been performed with adequate control conditions to draw firm conclusions. To further investigate the relationship between anti-inflammatory drugs (aspirin as well as others) and gastrointestinal (GI) bleeding, a study was carried out with 161 patients (102 men and 59 women) who were being treated for either hematemesis (vomiting blood) or melena (blood in stool), and an age-matched control group of patients who were being treated for non-gastrointestinal maladies. There was significantly more use of both non-aspirin NSAIDs and aspirin in the gastrointestinal treatment group. There were no differences between the groups in the extent to which they used other drugs, including acetaminophen, corticosteroids, tobacco, and alcohol. When patient characteristics were calculated for users and non-users of the various drugs, NSAID users were found to be older, more likely to be female, and to have a higher mortality rate than non-users. Among those patients who were found to be suffering from bleeding peptic ulcer disease, NSAID users were equally likely to have reported previous symptoms of ulcer compared with non-users, and did not have a higher frequency of multiple gastric or duodenal ulcers. The increased risk of developing gastrointestinal bleeding attributable to non-aspirin NSAID use was higher than that attributable to the use of aspirin. (Consumer Summary produced by Reliance Medical Information, Inc.)

Gastrointestinal bleeding, Gastrointestinal hemorrhage, Pain, Pain management, Aspirin

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