Celecoxib
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Larrey E, et al. Fatal cholestatic hepatitis after a single dose of celecoxib. Clinics and Research in Hepatology and Gastroenterology 43: e82-e85, No. 5, Oct 2019. Available from: URL: http://doi.org/10.1016/j.clinre.2018.10.007 France 803433435
Cholestatic hepatitis and vanishing bile duct syndrome: case report A 74-year-old woman developed fatal cholestatic hepatitis and vanishing bile duct syndrome following treatment with celecoxib for back pain. The woman had a history of lumbar osteoarthritis. On 06 April 2019, she started receiving treatment with celecoxib 200mg for back pain [route not stated]. After 4–5 hours, she felt nauseous, asthenic and experienced abdominal pain. On 08 April, a skin rash (non-pruritic), was observed in both armpits and inguinal regions and then quickly disappeared. She had never used celecoxib in her life and was not taking any other treatment. There was no record of allergy, particularly for sulphonamides. On 10 April 2017, she was hospitalised for acute jaundice. Clinical examination showed sensitivity in the right hypochondrium, acute jaundice and fever. Hepatomegaly, adenomegaly and hepatocellular insufficiency were not observed. The skin rash had disappeared. Blood tests were significant with jaundice and hyperbilirubinaemia and major cholestasis. Also, hepatic cytolysis was noted with elevated liver enzymes. Serology for hepatitis A, B, C, E was negative and a serum immunoglobulin analysis did not reveal any specific antibody. Abdominal CT and magnetic resonance cholangiography revealed distension of the gallbladder with infiltration around the gallbladder and parietal enhancement. A slight dilation was noted in the principal biliary duct; however, the intra-hepatic bile ducts were normal. Endoscopic retrograde cholangiopancreatography noted vacuity of the biliary duct. On day 7 of hospitalisation, progression in her condition was noted with the increase in severity of jaundice, elevated bilirubin and liver enzymes. On the same day, hepatic biopsy showed suppurative cholangitis, periductal fibrosis and atrophy of some biliary ducts. Eosinophils, plasmocytes or fibrous septa were not observed. Based on these findings a diagnosis of cholestatic hepatitis was made. The woman started receiving treatment with ursodeoxycholic acid [ursodesoxycholic acid] 10 mg/kg/day. Transient improvement in cholestasis was noted; however, there was no improvement in jaundice and the pruritus. Subsequently, she started receiving treatment with hydroxyzine and rifampicin, but there was no improvement in pruritus. On day 30, second hepatic biopsy showed total ductopenia with no other specific lesion, which suggested vanishing bile duct syndrome associated with severe pruritus. Therefore, she received few sessions of plasmapheresis, with only partial and transient clinical-biological improvement. She received three sessions of molecular adsorbents recirculation system; however, no improvement noted in pruritus and hyperbilirubinaemia. She was anorexic from the start of the symptoms; however, th
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