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|Title:||Hepatotoxicity associated with piroxicam therapy|
|Authors:||omar rashid sadeq|
Non-steroidal anti-inflammatory drugs
|Publisher:||Journal of Pharmacy Research|
|Abstract:||Background: The purpose of this study is to estimate the hepatic risk associated with the use of piroxicam, in patients suffering from primary form of osteoarthritis (OA). Materials and Methods: We investigated 32 patients with primary form of OA, and the patients were divided into 2 categories according to stages of OA (II and III stages) and medicated orally by 10 and 20 mg/d piroxicam, respectively, in a period of 2 months and patients’ follow-up for 6 months. Complete blood count and hepatic tests including bilirubin, alanine aminotransferase, and aspartate transaminase were done before, during, and after treatment, in both categories to determine the onset of possible hepatotoxic effect of piroxicam. Ultrasonography and liver biopsy were also provided only for certain patients of II category, in whom hepatotoxicity has occurred due to piroxicam management. Results: Orally prescribed piroxicam, 10 and 20 mg/d in both categories, is a good medicament for the management of OA with a small average percentage of ulcerogenicity (19%). Piroxicam was expected to decrease nocturnal pain and spasticity of OA in the II category. Piroxicam 10 mg/d produces no hepatotoxic effect in the first category but on the other hand (piroxicam 20 m/d) causes a mixed hepatocellular-cholestatic reversible injury in about 75% of OA patients in the second category, predominantly in female gender, at the end of the 8th week of treatment. The hepatic injury is unknown but strongly believed to be idiosyncratic. Conclusion: Piroxicam therapy should be evaluated clinically and laboratory in the first 3–12 weeks to decrease its possible hepatotoxic effect.|
|Appears in Collections:||Faculty & Staff Scientific Research publications|
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