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Adiponectin levels among patients with chronic hepatitis B and C infections and in response to IFN‐α therapy
Author(s) -
Lu JinYing,
Chuang LeeMing,
Yang WeiShiung,
Tai TongYuan,
Lai MingYang,
Chen PeiJer,
Kao JiaHorng,
Lee ChaZe,
Lee HsuanShu
Publication year - 2005
Publication title -
liver international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.873
H-Index - 110
eISSN - 1478-3231
pISSN - 1478-3223
DOI - 10.1111/j.1478-3231.2005.1007.x
Subject(s) - medicine , adiponectin , chronic hepatitis , hepatitis c , hepatitis b , immunology , gastroenterology , obesity , insulin resistance , virus
Aims: The study was designed to survey the change of adiponectin levels before and after interferon‐α (IFN‐α) therapy in patients with chronic hepatitis B and C infections. Methods: Twenty‐one biopsy‐proved patients with chronic hepatitis B (10 cases) and hepatitis C (11 cases) were given IFN‐α for a total of 24 weeks. Fasting plasma glucose, insulin and adiponectin levels were obtained before and 12 weeks after completion of IFN‐α therapy. Insulin suppression test was conducted before and within 1 week after IFN‐α therapy. Results: The change of adiponectin levels differed significantly between responders (eight cases) and non‐responders (13 cases) to IFN‐α treatment (−4.8±2.2 vs. 0.5±1.0 μg/ml, P =0.03). After adjusting for age, gender and change in body mass index, the study found the change of adiponectin levels still significantly related to the response to IFN‐α ( P =0.04). When hepatitis B virus (HBV) and hepatitis C virus (HCV)‐infected patients were separately analyzed, the adiponectin levels reported a trend to decrease in HCV responders (11.9±3.2 vs. 10.8±3.0 μg/ml, P =0.02, n =4) and HBV responders (17.7±4.1 vs. 9.2±1.0 μg/ml, P =0.10, n =4). In addition, a significant decrease of steady‐state plasma glucose in insulin suppression test was noted in responders (13.6±1.8–11.7±1.2 mmol/l, P =0.03), but not in non‐responders (12.3±1.1–11.0±1.0 mmol/l, P =0.20), after IFN‐α therapy. Conclusions: IFN‐α resulted in a decrease of serum adiponectin levels but an improvement of insulin resistance in responders to the treatment. The result contradicts previous concept of the relationship between insulin resistance and adiponectin levels. Whether and how the augmented immune response, which was supposed to result from the disappearance or the profound down‐regulation of the virus or viral antigens in responders to IFN‐α treatment, contributes to the lowering of adiponectin levels needs to be further investigated.