Di Domenicantonio A, Politti U, Marchi S, De Bortoli N, Giuggioli D, Antonelli A, Ferri C
Dipartimenti di Medicina Clinica e Sperimentale, Università di Pisa, Italia.
Dipartimenti di Ricerca Traslazionale e delle Nuove Tecnologie in Medicina e Chirurgia, Università di Pisa, Italia.
Clin Ter. 2014;165(5):e376-81. doi: 10.7417/T.2014.1768.
Frequently, patients with hepatitis C virus (HCV) chronic infection have high levels of serum anti-thyroperoxidase and/or anti-thyroglobulin autoantibodies, ultrasonographical signs of chronic autoimmune thyroiditis, and subclinical hypothyroidism, in female gender, vs healthy controls, or hepatitis B virus infected patients. In patients with "HCV-associated mixed cryoglobulinemia" (MC+HCV), a higher prevalence of autoimmune thyroid disorders was shown not only compared to controls, but also compared to HCV patients without cryoglobulinemia. Patients with MC+HCV or with HCV chronic infection, show an higher prevalence of papillary thyroid cancer than in controls, in particular in patients with autoimmune thyroiditis. Patients with HCV chronic infection, or with MC+HCV, in presence of autoimmune thyroiditis, show higher serum levels of T-helper (Th)1 (C-X-C motif) ligand 10 (CXCL10) chemokine than patients without thyroiditis. Probably, HCV thyroid infection acts by upregulating CXCL10 gene expression and secretion in thyrocytes recruiting Th1 lymphocytes, that secrete interferon-gamma and tumor necrosis factor-alpha. These cytokines might induce a further CXCL10 secretion by thyrocytes, thus perpetuating the immune cascade, that may lead into the appearance of autoimmune thyroid disorders in genetically predisposed subjects. A careful monitoring of thyroid function and nodules are recommanded in HCV patients.
通常,丙型肝炎病毒(HCV)慢性感染患者血清抗甲状腺过氧化物酶和/或抗甲状腺球蛋白自身抗体水平较高,有慢性自身免疫性甲状腺炎的超声征象以及亚临床甲状腺功能减退,女性患者与健康对照或乙型肝炎病毒感染患者相比更为明显。在“HCV相关混合性冷球蛋白血症”(MC + HCV)患者中,自身免疫性甲状腺疾病的患病率不仅高于对照组,而且高于无冷球蛋白血症的HCV患者。MC + HCV患者或HCV慢性感染患者的甲状腺乳头状癌患病率高于对照组,尤其是患有自身免疫性甲状腺炎的患者。HCV慢性感染患者或MC + HCV患者,在存在自身免疫性甲状腺炎的情况下,血清辅助性T细胞(Th)1(C-X-C基序)配体10(CXCL10)趋化因子水平高于无甲状腺炎的患者。可能是HCV甲状腺感染通过上调甲状腺细胞中CXCL10基因的表达和分泌,招募分泌干扰素-γ和肿瘤坏死因子-α的Th1淋巴细胞。这些细胞因子可能会诱导甲状腺细胞进一步分泌CXCL10,从而使免疫级联反应持续存在,这可能会导致遗传易感性个体出现自身免疫性甲状腺疾病。建议对HCV患者的甲状腺功能和结节进行仔细监测。