The long-term histological and virological outcomes of spontaneous circulating hepatitis C virus (HCV) clearance were studied in chronic liver disease. Between 1979 and 1984, three patients underwent laparoscopy for chronic non-A, non-B liver disease, and two were found to have cirrhosis and one wit
Spontaneous clearance of chronic hepatitis C after liver transplantation: Are hepatitis C virus–specific T cell responses the clue?
✍ Scribed by P. V. Suneetha; Ingmar Mederacke; Albert Heim; Murat Bastürk; Markus Cornberg; Christian P. Strassburg; Michael P. Manns; Heiner Wedemeyer
- Publisher
- John Wiley and Sons
- Year
- 2008
- Tongue
- English
- Weight
- 103 KB
- Volume
- 14
- Category
- Article
- ISSN
- 1527-6465
- DOI
- 10.1002/lt.21559
No coin nor oath required. For personal study only.
✦ Synopsis
et al., 1 published in the January issue of Liver Transplantation, describing 2 cases of spontaneously cleared hepatitis C virus (HCV) infection in human immunodeficiency virus-coinfected patients early after liver transplantation. The cause for HCV clearance in those cases remained unclear. We recently also saw a 69year-old female patient who was cured of HCV more than 10 years after liver transplantation without any specific antiviral therapy. We believe that the occurrence of a strong and multispecific HCV-specific T cell response contributed to the resolution of HCV infection in this case.
Liver cirrhosis was diagnosed for the first time in 1984. At that time, alcohol abuse was considered the probable cause of liver disease as there were no other obvious reasons for liver cirrhosis in the medical history. The patient developed insulin-dependent type 2 diabetes mellitus in 1991. She underwent orthotopic liver transplantation in 1992 and received an organ from a donor negative for anti-HCV antibody. The initial immunosuppression consisted of cyclosporine, methylprednisolone, and anti-interleukin-2 receptor antibodies for the first 12 postoperative days. 2 In 1993, a liver biopsy revealed acute rejection, and subsequently, methylprednisolone bolus therapy was given. Thereafter, azathioprine was added to the immunosuppressive therapy, but it was stopped in 2003 because of pancytopenia. After that, the patient received cyclosporine monotherapy. No other episodes of acute rejection occurred. In 2004, a transjugular intrahepatic portosystemic shunt had to be placed because of portal hypertension and recurrent gastrointestinal bleeding episodes. Since September 2006, the patient has required hemodialysis because of terminal renal insufficiency due to immunosuppressive drug toxicity and diabetic nephropathy.
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