Implications of prognostic variables in the assessment of autoimmunity in hepatitis C patients receiving interferon therapy.
Systematic administration of interferon-alpha (INF-alpha) is considered as the backbone of HCV therapy since 1991. Interferon (IFN) therapy can cause vasculitis, glomerulonephritis, cryoglobulinemia and certain other autoimmune diseases such as sialoadentitis, lichen planus and thyroiditis. Related to the factors of interferons, extensively studied gland is thyroid gland. A strong association was observed between thyroid disease and HCV patient when they were exposed to IFN therapy. Vitamin D, malondialdehyde (MDA), thyroid hormones and auto antibodies were biochemically assessed from the venous blood of seventy five HCV patients and fifty healthy controls. The results of all parameters were analyzed by independent sample t-test. The results of the study demonstrated a clear picture that the levels of vitamin D decreased as compared to control but increases in case of MDA. The levels of antibody titer represent that thyroglobulin-antibody (TGAb) thyroid peroxidase-antibody (TPOAb) as well as thyroid stimulating hormone receptor-antibody (TSHRAb) were raised in the patients suffering from HCV with thyroid dysfunction as compared to control. Similarly, the levels of thyroid hormones were also elevated in the HCV patients. Antibodies generated against thyroidal enzymes leads to impaired function of these enzymes thus causing decreased synthesis of thyroid hormones. As exogenous INF triggers the release of cytokines that mediate the recruitment of immune cells with increased production of inflammatory markers lead to production of lytic granules which have direct toxic action on thyroid cells and ultimately increased lipid peroxidation of thyrocytes. The results of the present study clearly demonstrated that the decreased levels of vitamin D in HCV patients receiving IFN therapy were responsible to induce autoimmunity against thyroid gland and adjutant therapy may be helpful to alleviate the possible thyroid disorders.
University College of Medicine and Dentistry (UCMD), the University of Lahore, Lahore, Pakistan.
Mahwish
M
Arooj
Institute of Molecular Biology and Biotechnology (IMBB), the University of Lahore, Lahore, Pakistan.
Arif
A
Malik
Institute of Molecular Biology and Biotechnology (IMBB), the University of Lahore, Lahore, Pakistan.
Abdul
A
Basit
Center for Research in Molecular Medicine (CRiMM), the University of Lahore, Lahore, Pakistan.
Mahmood
M
Husain Qazi
Department of Biotechnology, Balochistan University of Information Technology, Engineering and Management Sciences (BUITEMS), Quetta, Pakistan.
Muhammad
M
Asif
King Fahd Medical Research Center (KFMRC), King Abdulaziz University, Jeddah, Saudi Arabia.
Mohammad
M
Sarwar Jamal
King Fahd Medical Research Center (KFMRC), King Abdulaziz University, Jeddah, Saudi Arabia;; Department of Molecular Genetics and Enzymology, Division of Human Genetics and Genome Research, National Research Centre, El-Buhouth St., P.O. 12622, Dokki, Giza, Egypt (Affiliation ID 60014618).
Maged
M
Mostafa Mahmoud
Department of Molecular Genetics and Enzymology, Division of Human Genetics and Genome Research, National Research Centre, El-Buhouth St., P.O. 12622, Dokki, Giza, Egypt (Affiliation ID 60014618).
Hani
H
Choudhry
Center of Excellence in Genomic Medicine Research (CEGMR), King Abdulaziz University, Jeddah, Saudi Arabia.
Peter
P
Natesan Pushparaj
Center of Excellence in Genomic Medicine Research (CEGMR), King Abdulaziz University, Jeddah, Saudi Arabia.; Institute of Molecular Biology and Biotechnology (IMBB), the University of Lahore, Lahore, Pakistan.
Mahmood
M
Rasool
Hepatitis C virus; Interferon alpha; Interleukin-6; Tumor necrosis factor alpha; Vitamin-D