Abstract
Thyroid involvement is a common condition that can be recorded during the natural course of different systemic rheumatic diseases, including the mixed cryoglobulinemia (MC) syndrome or cryoglobulinemic vasculitis. MC is triggered by hepatitis C virus (HCV) chronic infection in the majority of cases; it represents the prototype of autoimmune-lymphoproliferative disorders complicating a significant proportion of patients with chronic HCV infection. HCV is both hepato- and lymphotropic virus responsible for a great number of autoimmune/lymphoproliferative and/or neoplastic disorders. The complex of HCV-related hepatic and extrahepatic manifestations, including MC and thyroid involvement, may be termed “HCV syndrome.” Here, we describe the prevalence and clinico-serological characteristics of thyroid involvement, mainly autoimmune thyroiditis and papillary thyroid cancer, in patients with HCV syndrome with or without cryoglobulinemic vasculitis.
Highlights
Autoimmune thyroiditis (AT) includes a group of thyroid diseases whose etiopathogenesis is characterized by chronic inflammatory response self-directed against thyroid gland [1,2,3]
Hypothyroidism was associated with higher cryocrit and with the presence of other autoantibody positivity, as well as with longer mixed cryoglobulinemia (MC) duration, presence of proteinuria, or active hepatitis [19]. These findings showed that AT patients exhibited more pronounced autoimmune phenomena and severity of MC, which represents the prototype of autoimmunity in hepatitis C virus (HCV) patients [7]
Considering this latter manifestation, an important contribute to understand the mechanisms involved in the pathogenesis of thyroid disorders was given by Blackard et al [24], who demonstrated that HCV may infect a human thyroid cell line (ML1), which presents the membrane expression of the important HCV receptor CD81
Summary
Autoimmune thyroiditis (AT) includes a group of thyroid diseases whose etiopathogenesis is characterized by chronic inflammatory response self-directed against thyroid gland [1,2,3]. Presence of AT in the course of autoimmune systemic diseases, including mixed cryoglobulinemia (MC), is very frequent. Mixed cryoglobulinemia is a small-vessel vasculitis due to vessel deposition of cryo- and noncryoprecipitable IgG–IgM immune complexes (ICs) and complement, which represent the main pathogenetic mechanism of disease manifestations, such as palpable purpura of the legs, skin ulcers, peripheral polyneuropathy, or glomerulonephritis; arthralgias, fatigue, sicca syndrome are frequently associated [4,5,6,7]. The abnormal production of ICs is determined by B cell clone proliferation triggered by hepatitis C virus (HCV) in a small proportion of infected patients (Figure 1, left). The proposed “HCV syndrome” encompasses the complex of both hepatic and extrahepatic disorders [(7); Figure 1, right] among which the MC, called cryoglobulinemic vasculitis, is the pathophysiological and clinical prototype [8]. AT may be frequently found in HCV patients, with or without MC syndrome, suggesting an etiopathogenetic role of the virus in a subset of predisposed subjects [9,10,11,12]
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