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Effect of interferon therapy on glucose metabolism in children with chronic hepatitis B
Zarife Kuloğlu1, Merih Berberoğlu, Aydan Kansu
1Department of Pediatric Gastroenterology, Ankara University Faculty of Medicine, Turkey.
Insights
Interferon-alpha treatment did not adversely affect glucose metabolism in children with chronic hepatitis B. Children with chronic hepatitis B showed insulin sensitivity, with no significant changes in glucose homeostasis after treatment.
Area of Science:
- Pediatrics
- Hepatology
- Endocrinology
Background:
- Chronic hepatitis B (CHB) affects glucose metabolism.
- Interferon (IFN)-alpha is a treatment for CHB.
- The impact of IFN-alpha on glucose metabolism in pediatric CHB patients is not well understood.
Purpose of the Study:
- To investigate the effect of IFN-alpha treatment on glucose metabolism in children with CHB.
- To assess changes in insulin resistance, beta-cell function, and glucose homeostasis.
- To compare glucose metabolism parameters between CHB patients and healthy controls.
Main Methods:
- Forty children with CHB received IFN-alpha (10 MU/m2) for six months.
- Evaluated oral glucose tolerance, antibodies (anti-insulin, anti-GAD), fasting plasma insulin, C-peptide, HOMA-IR, HOMA-cell, and glucose/insulin ratio.
- Compared pre- and post-treatment values with 42 healthy controls.
Main Results:
- CHB patients exhibited lower fasting plasma glucose and HOMA-IR than controls.
- A correlation was found between liver disease severity and fasting plasma glucose.
- No significant differences in glucose metabolism abnormalities were observed before and after IFN-alpha therapy.
Conclusions:
- Children with CHB demonstrate insulin sensitivity.
- IFN-alpha treatment for CHB in children does not appear to adversely affect glucose homeostasis.
- Potential for beta-cell hypofunction was noted in some CHB patients, persisting after treatment.
Abstract:
The aim of this study was to investigate the effect of interferon (IFN)-alpha treatment on glucose metabolism in children with chronic hepatitis B (CHB). Forty children with CHB received IFN 10 MU/m2 for six months. Oral glucose tolerance test, anti-insulin and anti-glutamic acid decarboxylase (GAD) antibody, fasting plasma C-peptide and insulin (FPI), postprandial insulin, homeostasis model assessment of insulin resistance (HOMA-IR), HOMA-cell, and glucose/insulin ratio (G/I) were measured before and after treatment. The last four parameters were also evaluated in healthy controls (n=42). In patients, fasting plasma glucose (FPG) and HOMA-IR levels were significantly lower than in controls (p = 0.001 and p = 0.020, respectively). There was a strong correlation between degree of liver disease and FPG. Two patients had hyperinsulinemia. HOMA-IR was suppressed in 7 patients enough to indicate increased sensitivity. FPI of 13 patients and HOMA-cell of 9 patients were lower than the minimum level of controls, features compatible with beta-cell hypofunction. Frequency of glucose metabolism abnormalities was not different before and after therapy. After therapy, only 1 patient developed anti-GAD antibody, and FPI of 8 children and HOMA-cell level of 9 children were lower than the minimum level of controls. Hyperinsulinemia was persistent in the same patients. We demonstrated that HBV-infected children had insulin sensitivity; however, no adverse effects of IFN on glucose homeostasis were seen.
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