Peginterferon-α-2a/peginterferon-α-2b

Reactions 1302 - 22 May 2010 S Peginterferon-α-2a/peginterferon- α-2b Type 1 diabetes mellitus: 2 case reports Two women developed type 1 diabetes mellitus following treatment of chronic hepatitis C virus infection with peginterferon-α-2a and peginterferon-α-2b. A 46-year-old woman was diagnosed with chronic hepatitis C in 2003, and was treated with peginterferon- α-2a, 180µg once weekly, or peginterferon-α-2b, 80–150µg once weekly, plus ribavirin from March 2004 to March 2006. Four weeks after treatment for 48 weeks, the woman developed thirst, which gradually worsened. On admission, her HbA1c levels were high, and ketone bodies were detected in urine, without acidaemia. Autoantibodies titres to glutamic acid decarboxylase (GADAb) were high (42700 IU/mL), and autoantibodies to insulinoma- associated protein 2 were negative. The woman received insulin aspart, and her fasting blood glucose stabilised. HbA1c levels gradually reduced. Withdrawal of insulin was possible one year after onset of diabetes. HOMA-β increased, indicating a recovery of insulin secretion. GADAb titers decreased to 7340 IU/mL four years after the onset of diabetes. A 67-year-old woman was diagnosed with chronic hepatitis C in 2002, and received peginterferon-α-2a, 180µg once weekly, or peginterferon-α-2b, 1.5 µg/kg once weekly, plus ribavirin from January 2005 to April 2006. Treatment was restarted in August 2006. Four months after restarting treatment, the woman developed thirst and general malaise. Hyperglycaemia was detected in January 2007, and the woman received treatment with insulin aspart and NPH insulin. She was hospitalised due to repeated hypoglycaemic attacks. GADAb was positive at 1320 IU/mL. The woman received treatment with insulin aspart and NPH insulin, and had stable preprandial blood glucose levels. Following discharge, she experienced repeated hyperglycaemia and hypoglycaemia, leading to high HbA1c levels, and NPH insulin was replaced with insulin glargine. GADAb titers were temporally reduced to 656 IU/mL, but rose to 1150 IU/mL 17 months after admission. Author comment: Interferon therapy for chronic hepatitis C can increase the risk of developing diabetes mellitus. Yamazaki M, et al. Distinct clinical courses in type 1 diabetes mellitus induced by peg-interferon-alpha treatment for chronic hepatitis C. Internal Medicine 49: 403-407, No. 5, Jan 2010. Available from: URL: http://dx.doi.org/10.2169/ internalmedicine.49.2656 - Japan 803014121 1 Reactions 22 May 2010 No. 1302 0114-9954/10/1302-0001/$14.95 © 2010 Adis Data Information BV. All rights reserved

Upload
truonghuong
Category

Documents
view
212
download
0

Embed Size (px):

Transcript of Peginterferon-α-2a/peginterferon-α-2b

Page 1: Peginterferon-α-2a/peginterferon-α-2b

Reactions 1302 - 22 May 2010

SPeginterferon-α-2a/peginterferon-α-2b

Type 1 diabetes mellitus: 2 case reportsTwo women developed type 1 diabetes mellitus

following treatment of chronic hepatitis C virus infectionwith peginterferon-α-2a and peginterferon-α-2b.

A 46-year-old woman was diagnosed with chronichepatitis C in 2003, and was treated with peginterferon-α-2a, 180µg once weekly, or peginterferon-α-2b,80–150µg once weekly, plus ribavirin from March 2004 toMarch 2006. Four weeks after treatment for 48 weeks, thewoman developed thirst, which gradually worsened. Onadmission, her HbA1c levels were high, and ketone bodieswere detected in urine, without acidaemia. Autoantibodiestitres to glutamic acid decarboxylase (GADAb) were high(42700 IU/mL), and autoantibodies to insulinoma-associated protein 2 were negative. The woman receivedinsulin aspart, and her fasting blood glucose stabilised.HbA1c levels gradually reduced. Withdrawal of insulin waspossible one year after onset of diabetes. HOMA-βincreased, indicating a recovery of insulin secretion.GADAb titers decreased to 7340 IU/mL four years after theonset of diabetes.

A 67-year-old woman was diagnosed with chronichepatitis C in 2002, and received peginterferon-α-2a,180µg once weekly, or peginterferon-α-2b, 1.5 µg/kg onceweekly, plus ribavirin from January 2005 to April 2006.Treatment was restarted in August 2006. Four months afterrestarting treatment, the woman developed thirst andgeneral malaise. Hyperglycaemia was detected in January2007, and the woman received treatment with insulinaspart and NPH insulin. She was hospitalised due torepeated hypoglycaemic attacks. GADAb was positive at1320 IU/mL. The woman received treatment with insulinaspart and NPH insulin, and had stable preprandial bloodglucose levels. Following discharge, she experiencedrepeated hyperglycaemia and hypoglycaemia, leading tohigh HbA1c levels, and NPH insulin was replaced withinsulin glargine. GADAb titers were temporally reduced to656 IU/mL, but rose to 1150 IU/mL 17 months afteradmission.

Author comment: Interferon therapy for chronic hepatitisC can increase the risk of developing diabetes mellitus.Yamazaki M, et al. Distinct clinical courses in type 1 diabetes mellitus induced bypeg-interferon-alpha treatment for chronic hepatitis C. Internal Medicine 49:403-407, No. 5, Jan 2010. Available from: URL: http://dx.doi.org/10.2169/internalmedicine.49.2656 - Japan 803014121