A case of nimesulide induced hepatitis.
- Author:
Hee Bok CHAE
1
;
Won Jun CHOI
;
Mun Woo LEE
;
Seon Mee PARK
;
Hye Young KIM
;
Myeong Chan CHO
;
Ro Hyun SUNG
;
Sei Jin YOUN
Author Information
1. Department of Internal Medicine, Chungbuk National University College of Medicine, Cheongju, Korea. hbchae@med.chungbuk.ac.kr
- Publication Type:Case Report
- Keywords:
Abdominal abscess;
Catheterization;
Drainage
- MeSH:
Abdominal Abscess;
Ascites;
Biliary Tract;
Bilirubin;
Biomarkers;
Biopsy;
Catheterization;
Cholestasis;
Dilatation;
Drainage;
Edema;
Epistaxis;
Female;
Fibrosis;
Gastrointestinal Tract;
Hepatitis A Antibodies;
Hepatitis B Surface Antigens;
Hepatitis*;
Humans;
Immunoglobulin G;
Immunoglobulin M;
International Normalized Ratio;
Jaundice;
Liver;
Liver Cirrhosis;
Necrosis;
Prostaglandin-Endoperoxide Synthases;
Prothrombin Time;
Splenomegaly;
Ultrasonography
- From:Korean Journal of Medicine
2000;59(1):114-119
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Nimesulide, highly selective cyclooxygenase inhibitor-2, is a newly developed, non-steroidal anti-inflammatory drug (NSAID) with low toxicity in gastrointestinal tract. But recently, seven cases of nimesulide-induced hepatitis of which types were hepatocellular, hepatocanalicular, and mixed damage were reported. Our case of nimesulide-induced hepatic damage was mixed cholestatic and hepatotoxic hypersensititvity reaction, and her story was as follows. A 70-year female patient's first hepatic event happened in Jaunuary, 1998 after taking nimesulide 200mg daily for 50 days from November 1997, but it was cleared. She was admitted to our unit because of jaundice, edema and ascites in May, 1998 after retrial of nimesulide 150 mg daily for 50 days. Biochemical determinations showed increase of AST (181 IU/L), ALT (110 IU/L), bilirubin (20.3 mg/dL) and albumin (2.3 g/dL). Prothrombin time was also prolonged upto 2.51 INR. But neither viral markers such as anti-HCV, HBsAg, anti-HBc IgM, anti-HAV IgM, anti-CMV, anti-EBV IgG and IgM nor other immunologic markers such as ANA, SMA, and AMA were positive. Ultrasonography showed diffuse hyperechogenicity in liver and mild splenomegaly but no dilatation in biliary tract. Liver biopsy showed portal to portal bridging necrosis with severe hepatocytic cholestasis. Her liver function returned to normal after discontinuation of nimesulide. At 8 months after beginning treatment, she complained of recurrent epistaxis and abdominal distension. At this time, her liver biopsy showed cirrhosis. In conclusion, we considered that this case was nimesulide-induced Liver cirrhosis.