atorvastatin/fluvastatin

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Reactions 1285 - 23 Jan 2010 ursodeoxycholic acid and insulin for his hyperglycaemia. Over the following month, his ALP level continued to S Atorvastatin/fluvastatin exceed the upper normal limit by 2- to 3-fold and his total bilirubin peaked at 30 mg/dL. He also received rifampicin Liver injury and autoimmune hepatitis: 2 case for severe pruritus. One month later, his pruritus had reports improved and after a further 2 months his ALT, AST, ALP A 52-year-old woman and a 54-year-old man developed and total bilirubin levels had returned to normal. liver injury after receiving fluvastatin [Lescol] and Metformin was restarted without recurrence of his atorvastatin [Lipitor], respectively, for dyslipidaemia. The hepatitis. woman later developed autoimmune hepatitis after commencing therapy with atorvastatin [Lipitor]. Russo MW, et al. Drug-induced liver injury associated with statins. Seminars in Liver Disease 29: 412-422, No. 4, 2009. Available from: URL: http:// Three months after being diagnosed with type II dx.doi.org/10.1055/s-0029-1240010 - USA 803004497 hyperlipidaemia, the woman started treatment with fluvastatin 20 mg/day; her baseline liver function test results were normal. During week 12 of therapy she experienced anorexia and fatigue. Laboratory investigations revealed increased ALT, AST and ALP levels (850, 880 and 215 U/L, respectively). Fluvastatin was stopped. Testing for autoantibodies was negative as were the results of serological tests for hepatitis A, B and C. Moderate lobular and portal hepatitis was evident on liver biopsy, along with mild portal fibrosis and moderate hepatocytic apoptosis and necrosis. One month later, her anorexia and fatigue had improved and her liver function tests eventually returned to normal. Around 2 years later, the woman started treatment with atorvastatin 20 mg/day for persistent hypercholesterolaemia. She reported fatigue and generalised pruritus within 3 weeks of starting statin therapy and then right upper quadrant pain 8 weeks later; she also experienced extreme fatigue and hypersomnia. Laboratory investigations revealed ALT, AST and ALP levels of 1750, 1800 and 285 U/L, respectively, and total bilirubin and globulin levels of 14 mg/dL and 3.6 g/dL, respectively. Testing was negative for viral hepatitis but positive for antinuclear antibody (1:160) and anti-smooth muscle antibody (1:80). Eight weeks after stopping atorvastatin her ALT, AST and ALP levels remained elevated and her antinuclear and anti-smooth muscle antibody titres were unchanged. A liver biopsy showed marked lobular and interface hepatitis, severe fibrosis and signs indicative of cirrhosis. Chronic acute autoimmune hepatitis precipitated by atorvastatin was suspected. Her symptoms improved following 3 weeks’ therapy with prednisone. Azathioprine was then added and her prednisone dosage was gradually decreased over a 3-month period. After a further 3 months her liver function test results returned to normal, prednisone was tapered off and azathioprine was discontinued 3 months later. However, she experienced a modest rise in her ALT level 2 months later. Prednisone and azathioprine were restarted; after 1 year prednisone was gradually tapered off while azathioprine was continued. Her antinuclear and anti-smooth muscle antibody titres declined to 1:40 and 1:20, respectively. The man started treatment with atorvastatin 10 mg/day for hypercholesterolaemia. He was also receiving metformin for type II diabetes mellitus. Seventy days after starting atorvastatin he experienced a gradual onset of nausea, anorexia and abdominal discomfort. He was then admitted with jaundice. On examination he was febrile with right upper quadrant tenderness and a firm palpable liver. Laboratory investigations revealed markedly elevated ALT, AST and ALP levels (6200, 5500 and 280 U/L, respectively). All drugs were immediately stopped and he received intravenous fluid therapy. Testing for autoantibodies was negative as were the results of tests for hepatitis A, B, C and E, Epstein-Barr virus, cytomegalovirus and herpes simplex. Marked portal inflammation was evident on liver biopsy as well as fibrosis (1+), endotheliitis of portal veins and signs of injury to the epithelium of interlobular bile ducts. He was treated with 1 Reactions 23 Jan 2010 No. 1285 0114-9954/10/1285-0001/$14.95 © 2010 Adis Data Information BV. All rights reserved

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Reactions 1285 - 23 Jan 2010

ursodeoxycholic acid and insulin for his hyperglycaemia.Over the following month, his ALP level continued to SAtorvastatin/fluvastatinexceed the upper normal limit by 2- to 3-fold and his totalbilirubin peaked at 30 mg/dL. He also received rifampicinLiver injury and autoimmune hepatitis: 2 casefor severe pruritus. One month later, his pruritus hadreportsimproved and after a further 2 months his ALT, AST, ALPA 52-year-old woman and a 54-year-old man developedand total bilirubin levels had returned to normal.liver injury after receiving fluvastatin [Lescol] andMetformin was restarted without recurrence of hisatorvastatin [Lipitor], respectively, for dyslipidaemia. Thehepatitis.woman later developed autoimmune hepatitis after

commencing therapy with atorvastatin [Lipitor]. Russo MW, et al. Drug-induced liver injury associated with statins. Seminars inLiver Disease 29: 412-422, No. 4, 2009. Available from: URL: http://Three months after being diagnosed with type IIdx.doi.org/10.1055/s-0029-1240010 - USA 803004497hyperlipidaemia, the woman started treatment with

fluvastatin 20 mg/day; her baseline liver function testresults were normal. During week 12 of therapy sheexperienced anorexia and fatigue. Laboratory investigationsrevealed increased ALT, AST and ALP levels (850, 880 and215 U/L, respectively). Fluvastatin was stopped. Testing forautoantibodies was negative as were the results ofserological tests for hepatitis A, B and C. Moderate lobularand portal hepatitis was evident on liver biopsy, along withmild portal fibrosis and moderate hepatocytic apoptosisand necrosis. One month later, her anorexia and fatiguehad improved and her liver function tests eventuallyreturned to normal.

Around 2 years later, the woman started treatment withatorvastatin 20 mg/day for persistenthypercholesterolaemia. She reported fatigue andgeneralised pruritus within 3 weeks of starting statintherapy and then right upper quadrant pain 8 weeks later;she also experienced extreme fatigue and hypersomnia.Laboratory investigations revealed ALT, AST and ALP levelsof 1750, 1800 and 285 U/L, respectively, and total bilirubinand globulin levels of 14 mg/dL and 3.6 g/dL, respectively.Testing was negative for viral hepatitis but positive forantinuclear antibody (1:160) and anti-smooth muscleantibody (1:80). Eight weeks after stopping atorvastatin herALT, AST and ALP levels remained elevated and herantinuclear and anti-smooth muscle antibody titres wereunchanged. A liver biopsy showed marked lobular andinterface hepatitis, severe fibrosis and signs indicative ofcirrhosis. Chronic acute autoimmune hepatitis precipitatedby atorvastatin was suspected. Her symptoms improvedfollowing 3 weeks’ therapy with prednisone. Azathioprinewas then added and her prednisone dosage was graduallydecreased over a 3-month period. After a further 3 monthsher liver function test results returned to normal,prednisone was tapered off and azathioprine wasdiscontinued 3 months later. However, she experienced amodest rise in her ALT level 2 months later. Prednisone andazathioprine were restarted; after 1 year prednisone wasgradually tapered off while azathioprine was continued.Her antinuclear and anti-smooth muscle antibody titresdeclined to 1:40 and 1:20, respectively.

The man started treatment with atorvastatin 10 mg/dayfor hypercholesterolaemia. He was also receivingmetformin for type II diabetes mellitus. Seventy days afterstarting atorvastatin he experienced a gradual onset ofnausea, anorexia and abdominal discomfort. He was thenadmitted with jaundice. On examination he was febrilewith right upper quadrant tenderness and a firm palpableliver. Laboratory investigations revealed markedly elevatedALT, AST and ALP levels (6200, 5500 and 280 U/L,respectively). All drugs were immediately stopped and hereceived intravenous fluid therapy. Testing forautoantibodies was negative as were the results of tests forhepatitis A, B, C and E, Epstein-Barr virus, cytomegalovirusand herpes simplex. Marked portal inflammation wasevident on liver biopsy as well as fibrosis (1+), endotheliitisof portal veins and signs of injury to the epithelium ofinterlobular bile ducts. He was treated with

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Reactions 23 Jan 2010 No. 12850114-9954/10/1285-0001/$14.95 © 2010 Adis Data Information BV. All rights reserved