Autoimmune thyroid diseases and cancer associated with chronic hepatitis C infection

Author(s): Antonelli Alessandro

Typically, patients with chronic Hepatitis C Virus (HCV) infection have elevated serum anti-thyroperoxidase and/or anti-thyroglobulin antibodies, ultrasound evidence of chronic autoimmune thyroiditis, and hypothyroidism. Subclinical thyroid disease in women compared with healthy controls or infected patients with hepatitis B virus. In patients with “HCV-associated mixed hemoglobinopathy” (MC + HCV), a higher incidence of thyroid autoimmune disorders was compared not only with controls but also with HCV patients without cold hemoglobin disease. Patients with CD+HCV or chronic HCV infection have a higher incidence of papillary thyroid cancer than controls, especially in patients with autoimmune thyroiditis. Patients with chronic HCV or CD+HCV infection, in the presence of autoimmune thyroiditis, have elevated serum levels of the chemokine T-helper (Th)1 (C-X-C module) ligand 10 (CXCL10) than, but normal Th2 (C-C module) levels of chemokine ligand 2, than patients without thyroiditis. Thyroid HCV infection may act by upregulating CXCL10 gene expression and secretion in thyroid cells that recruit interferon-γ and tumor necrosis factor-α-secreting Th1 cells. These cytokines are able to induce new CXCL10 secretion by thyroid cells, thereby maintaining the immune cascade, which may lead to the emergence of autoimmune thyroid disorders in susceptible subjects have a genetic disease. Thyroid function should be carefully monitored, especially if nodules are present in HCV patients. Approximately 130 to 170 million people worldwide have been infected with the Hepatitis C Virus (HCV). Hepatocytes represent the primary site of viral replication, and HCV replication is present in extra hepatic tissues and peripheral blood mononuclear cells. In a first study, Tran et al. reported two cases of Hashimoto’s thyroiditis associated with chronic active HCV infection, suggesting that HCV infection may be involved in the onset of AT.