Elkady, M., Omar, M., Elbehisy, M., Mohamed, M. (2015). Interplay Between Tumor Necrosis Factor-α, Insulin Resistance and Type 2 Diabetes Mellitus in Chronic Hepatitis C Egyptian Patients Interplay Between Tumor Necrosis Factor-α, Insulin Resistance and Type 2 Diabetes Mellitus in Chronic Hepatitis C Egyptian Patients. Afro-Egyptian Journal of Infectious and Endemic Diseases, 5(4), 246-254. doi: 10.21608/aeji.2015.17845
Mostafa Elkady; Maha Z Omar; Mona M Elbehisy; Mohamed A Mohamed. "Interplay Between Tumor Necrosis Factor-α, Insulin Resistance and Type 2 Diabetes Mellitus in Chronic Hepatitis C Egyptian Patients Interplay Between Tumor Necrosis Factor-α, Insulin Resistance and Type 2 Diabetes Mellitus in Chronic Hepatitis C Egyptian Patients". Afro-Egyptian Journal of Infectious and Endemic Diseases, 5, 4, 2015, 246-254. doi: 10.21608/aeji.2015.17845
Elkady, M., Omar, M., Elbehisy, M., Mohamed, M. (2015). 'Interplay Between Tumor Necrosis Factor-α, Insulin Resistance and Type 2 Diabetes Mellitus in Chronic Hepatitis C Egyptian Patients Interplay Between Tumor Necrosis Factor-α, Insulin Resistance and Type 2 Diabetes Mellitus in Chronic Hepatitis C Egyptian Patients', Afro-Egyptian Journal of Infectious and Endemic Diseases, 5(4), pp. 246-254. doi: 10.21608/aeji.2015.17845
Elkady, M., Omar, M., Elbehisy, M., Mohamed, M. Interplay Between Tumor Necrosis Factor-α, Insulin Resistance and Type 2 Diabetes Mellitus in Chronic Hepatitis C Egyptian Patients Interplay Between Tumor Necrosis Factor-α, Insulin Resistance and Type 2 Diabetes Mellitus in Chronic Hepatitis C Egyptian Patients. Afro-Egyptian Journal of Infectious and Endemic Diseases, 2015; 5(4): 246-254. doi: 10.21608/aeji.2015.17845
Interplay Between Tumor Necrosis Factor-α, Insulin Resistance and Type 2 Diabetes Mellitus in Chronic Hepatitis C Egyptian Patients Interplay Between Tumor Necrosis Factor-α, Insulin Resistance and Type 2 Diabetes Mellitus in Chronic Hepatitis C Egyptian Patients
1Department of Hepatology, Gastroenterology and Infectious Diseases, Benha University,Egypt
2Department of Clinical Pathology, Benha University,Egypt.
3New General Mansoura Hospital , Egypt
Abstract
Background and study aim : Hepatitis C is a disease with significant global impact, it is the most common cause of chronic liver diseases, and in addition it causes insulin resistance (IR) leading to increase the risk of type 2 diabetes mellitus (DM). This current study aimed to assess the relationship between serum tumor necrosis factor-α (TNF-α), insulin resistance (IR) and type 2 DM in patients HCV. Patients and Methods: The study cohort consisted of 91 subjects stratified into 4 groups; Group (I): Included 25 HCV patients without DM, Group (II): Included 25 HCV diabetic patients, Group (III): Included 25 diabetic patients without HCV infectionand group (IV): Included 16 healthy subjects serving as a control group. All patients were subjected to full history taking, thorough clinical examination and estimation of body mass index (BMI). Anti-HCV Ab was detected by the 3rd generation (ELISA) testand was confirmed by PCR. Assessment of fasting plasma insulin level (FBI) and TNF-α were done by ELISA test, while assessment of the insulin resistance was estimated by Homeostatic Model Assessment (HOMA-IR). Results: Higher mean levels of FBS, 2 hr (2HPP) and fasting plasma insulin (FSI) were detected in group II (HCV+DM) compared to other groups with statistically significant differences between all the studied groups (P value <0.001), consequently HCV diabetic patients were found to have significant higher IR than HCV patients without DM, diabetic patients alone and control group (P value <0.001). Furthermore, there was highly statistically significant differences between all studied groups as regard level of TNF-α (P value <0.001) with higher mean level in group I (HCV group). Insignificant difference in level of TNF-α in HCV patients with or without IR (P value =0.072). Insignificant positive correlation between HOMA-IR and TNF-α (P value = 0.63). Conclusion: Chronic HCV patients have significantly elevated fasting plasma insulin level, TNF-α and significant IR and there was insignificant correlation between HOMA-IR and TNF-α.
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