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• W1991058840 abstract "Autoimmune thyroid diseases are complex conditions caused by an interaction between genetic and environmental factors (1Tomer Y Davies T.F Searching for the autoimmune thyroid disease susceptibility genes From gene mapping to gene function.Endocrin Rev. 2003; 24: 694-717Crossref PubMed Scopus (310) Google Scholar). Because identical twin concordance for autoimmune thyroid diseases is only 30% to 50% (2Brix T.H Kyvik K.O Hegedus L A population-based study of chronic autoimmune hypothyroidism in Danish twins.J Clin Endocrinol Metab. 2000; 85: 536-539Crossref PubMed Scopus (205) Google Scholar, 3Ringold D.A Nicoloff J.T Kesler M Davis H Hamilton A Mack T Further evidence for a strong genetic influence on the development of autoimmune thyroid disease the California twin study.Thyroid. 2002; 12: 647-653Crossref PubMed Scopus (76) Google Scholar), external, nongenetic factors must play a role in thyroid autoimmunity. Indeed, the role of environmental factors has been the focus of increasing attention. One attractive environmental factor that could trigger autoimmune thyroid diseases in susceptible individuals is infection, and there is a large literature on the subject (4Tomer Y Davies T.F Infection, thyroid disease and autoimmunity.Endocr .Rev. 1993; 14: 107-120PubMed Google Scholar). Antibodies to the bacterium Yersinia enterocolitica, for example, have been reported to be increased in both Graves disease and Hashimoto thyroiditis, and Yersinia release proteins may stimulate proliferation of peripheral blood mononuclear cells and intrathyroidal lymphocytes in patients with Graves disease (5Arscott P Rosen E.D Koenig R.J Kaplan M.M et al.Immunoreactivity to Yersinia enterocolitica antigens in patients with autoimmune thyroid disease.J Clin Endocrinol Metab. 1992; 75: 295-300Crossref PubMed Scopus (18) Google Scholar). A saturable binding site for thyroid stimulating hormone (TSH) has been found on Y. enterocolitica(6Weiss M Ingbar S.H Winblad S Kasper D.L Demonstration of a saturable binding site for thyrotropin in Yersinia enterocolitica.Science. 1983; 219: 1331-1333Crossref PubMed Scopus (107) Google Scholar). Similarly, endogenous and exogenous retroviruses have been implicated in the development of autoimmune thyroid diseases (7Tomer Y Villanueva R Infection and autoimmune thyroid diseases.in: Rose N.R Shoenfeld Y Infections and Autoimmunity. Elsevier, Amsterdam2004: 517-532Google Scholar). Yet another infectious agent that has been gaining interest as a potential trigger of thyroid autoimmunity in susceptible individuals is the hepatitis C virus (HCV).The association of autoimmune thyroid diseases, more specifically Hashimoto thyroiditis, with hepatitis C has been widely studied. However, the data for hepatitis C as a possible factor for the development of autoimmune thyroid diseases have thus far been mixed. Several studies of interferon-naive patients with hepatitis C have not found a significant correlation between HCV infection and the presence of thyroid antibodies (8Loviselli A Oppo A Velluzzi F et al.Independent expression of serological markers of thyroid autoimmunity and hepatitis C virus infection in the general population results of a community-based study in north-western Sardinia.J Endocrinol Invest. 1999; 22: 660-665PubMed Google Scholar, 9Metcalfe R.A Ball G Kudesia G Weetman A.P Failure to find an association between hepatitis C virus and thyroid autoimmunity.Thyroid. 1997; 7: 421-424Crossref PubMed Scopus (52) Google Scholar, 10Boadas J Rodriguez-Espinosa J Enriquez J et al.Prevalence of thyroid autoantibodies is not increased in blood donors with hepatitis C virus infection.J Hepatol. 1995; 22: 611-615Abstract Full Text PDF PubMed Scopus (71) Google Scholar), whereas other studies found elevated levels of thyroid antibodies in up to 42% of patients with HCV infection (11Tran A Quaranta J.F Benzaken S et al.High prevalence of thyroid autoantibodies in a prospective series of patients with chronic hepatitis C before interferon therapy.Hepatology. 1993; 18: 253-257Crossref PubMed Scopus (256) Google Scholar, 12Gann-Carrie N Medini A Coderc E et al.Latent autoimmune thyroiditis in untreated patients with HCV chronic hepatitis A case control study.J Autoimmun. 2000; 14: 189-193Crossref PubMed Scopus (70) Google Scholar, 13Fernandez-Soto L Gonzalez A Escobar-Jimenez F et al.Increased risk of autoimmune thyroid disease in hepatitis C vs hepatitis B before, during and after discontinuing interferon therapy.Arch Intern Med. 1998; 158: 1445-1448Crossref PubMed Scopus (180) Google Scholar, 14Preziati D La Rosa L Covini G et al.Autoimmunity and thyroid function in patients with chronic active hepatitis treated with recombinant interferon alpha-2a.Eur J Endocrinol. 1995; 132: 587-593Crossref PubMed Scopus (219) Google Scholar). Differences in confounding factors, such as genetic background and iodine intake of the populations studied, have been suggested as possible causes for these disparate findings. Some studies have also shown that patients with hepatitis C who developed positive thyroid antibodies or Hashimoto thyroiditis were more likely to be older and female (11Tran A Quaranta J.F Benzaken S et al.High prevalence of thyroid autoantibodies in a prospective series of patients with chronic hepatitis C before interferon therapy.Hepatology. 1993; 18: 253-257Crossref PubMed Scopus (256) Google Scholar, 12Gann-Carrie N Medini A Coderc E et al.Latent autoimmune thyroiditis in untreated patients with HCV chronic hepatitis A case control study.J Autoimmun. 2000; 14: 189-193Crossref PubMed Scopus (70) Google Scholar, 13Fernandez-Soto L Gonzalez A Escobar-Jimenez F et al.Increased risk of autoimmune thyroid disease in hepatitis C vs hepatitis B before, during and after discontinuing interferon therapy.Arch Intern Med. 1998; 158: 1445-1448Crossref PubMed Scopus (180) Google Scholar). Additionally, there are unconfirmed reports of an increased prevalence of HCV antibodies in patients with Hashimoto thyroiditis, suggesting that the disease could be induced by HCV infection (14Preziati D La Rosa L Covini G et al.Autoimmunity and thyroid function in patients with chronic active hepatitis treated with recombinant interferon alpha-2a.Eur J Endocrinol. 1995; 132: 587-593Crossref PubMed Scopus (219) Google Scholar, 15Duclos-Vallee J.C Johanet C Trinchet J.C et al.High prevalence of serum antibodies to hepatitis C virus in patients with Hashimoto's thyroiditis.BMJ. 1994; 309: 846-847Crossref PubMed Scopus (38) Google Scholar, 16Tran A Quaranta J.F Beusnel C et al.Hepatitis C virus and Hashimoto's thyroiditis.Eur J Med. 1992; 1: 116-118PubMed Google Scholar). One possible explanation for these inconsistent results is that HCV may trigger thyroid autoimmunity only in a subset of patients. Up to now, however, studies have not stratified patients with hepatitis C and controls by genetic and environmental risk factors (Table). It is possible that HCV interacts with one or more of these risk factors to trigger the development of autoimmune thyroid diseases, thus, only studies that stratify by these risk factors may reveal a consistent association.TablePossible Risk Factors for Autoimmune Thyroid Disease in HCV PatientsA. Genetic and Constitutional Factors:HLA-DR3CTLA-4Female sexAgeFamily history or autoimmune thyroid diseasePregnancyB. External Factors:Dietary iodineOther infectious agents (HIV? retroviruses?)Interferon alphaStressSmokingCTLA = cytotoxic T lymphocyte antigen; HIV = human immunodeficiency virus; HLA = human leukocyte antigen. Open table in a new tab In this issue of The American Journal of Medicine, another piece in the puzzle has been added to the growing literature on the association between hepatitis C and thyroid autoimmunity. Antonelli and coworkers (17Antonelli A, Ferri C, Pampana A, et al. Thyroid disorders in chronic hepatitis C. Am J Med. 2004;117:10–13Google Scholar) report that thyroid autoimmunity––both autoimmune hypothyroidism and the presence of thyroid antibodies––cosegregated with hepatitis C infection independently of cirrhosis, liver carcinoma, treatment with interferon, or intake of iodine. Antonelli et al studied four groups: 630 interferon-naive patients who had hepatitis C and were free of cirrhosis or hepatocarcinoma; 389 sex- and age-matched subjects from an iodine-sufficient region; 268 people >50 years old from an iodine-deficient region; and 86 patients who were >40 years old and who had hepatitis B virus–related chronic liver disease. They measured TSH, free T4, free T3 and thyroid antibodies (both antithyroglobulin and antithyroid peroxidase antibodies) in all groups. Circulating TSH levels were significantly higher and free T4 and free T3 levels were significantly lower in the patients with hepatitis C compared with the other three groups. They also found that clinical hypothyroidism was significantly more frequent in patients with hepatitis C compared with the other three control groups. Similarly, markers for thyroid autoimmunity, (i.e., the presence of thyroid autoantibodies [both thyroglobulin antibodies and antithyroid peroxidase antibodies]), were higher in the patients with hepatitis C. However, the frequency of hyperthyroidism was similar for all groups.The authors should be commended for controlling their study for two major confounding factors: intake of iodine and therapy with interferon. Controlling for these factors makes the association more valid, and it is hoped that futures studies will also control for these factors as well as additional potential confounding factors. The findings of Antonelli et al are different than those of Loviselli and coworkers, who surveyed the population of two villages in Sardinia, Italy in which hepatitis C is endemic and the prevalence of autoimmune disease is elevated (8Loviselli A Oppo A Velluzzi F et al.Independent expression of serological markers of thyroid autoimmunity and hepatitis C virus infection in the general population results of a community-based study in north-western Sardinia.J Endocrinol Invest. 1999; 22: 660-665PubMed Google Scholar). They calculated standardized prevalence rates for both antibodies to hepatitis C and antibodies to antithyroid peroxidase. The standardized prevalence rates for both antibodies were no different than those expected under the assumption of unrelated events. Using antithyroid peroxidase antibody–positive subjects and antithyroid peroxidase antibody–negative controls in a case-control study, no association could be found between hepatitis C and antithyroid peroxidase antibodies (8Loviselli A Oppo A Velluzzi F et al.Independent expression of serological markers of thyroid autoimmunity and hepatitis C virus infection in the general population results of a community-based study in north-western Sardinia.J Endocrinol Invest. 1999; 22: 660-665PubMed Google Scholar). It is still unclear why the findings of the two studies are disparate, but it may be due to differences in additional risk factors (Table) that may increase the tendency for HCV-induced autoimmune thyroid diseases.By what mechanisms can an infectious agent such as HCV induce autoimmunity? Potential mechanisms include viral-induced changes in self-antigen expression, molecular mimicry, alterations in the idiotypic network, formation of heat shock proteins, and induction of major histocompatibility complex antigens on nonimmune cells (4Tomer Y Davies T.F Infection, thyroid disease and autoimmunity.Endocr .Rev. 1993; 14: 107-120PubMed Google Scholar). It is possible that infectious agents induce thyroid autoimmunity in genetically susceptible individuals by interacting with genetic risk factors (1Tomer Y Davies T.F Searching for the autoimmune thyroid disease susceptibility genes From gene mapping to gene function.Endocrin Rev. 2003; 24: 694-717Crossref PubMed Scopus (310) Google Scholar); however, the biologic mechanisms of these interactions are not known.Infectious agents most likely play a role in triggering several autoimmune conditions. Until recently, studies examining a possible association of HCV with autoimmune thyroid diseases had mixed results that may have been due, in part, to the possibility that HCV increases thyroid autoimmunity only in certain subsets of patients with hepatitis C. Additional studies of subsets of patients with HCV are needed to identify whether certain patients are at highest risk for developing thyroid autoimmunity. Autoimmune thyroid diseases are complex conditions caused by an interaction between genetic and environmental factors (1Tomer Y Davies T.F Searching for the autoimmune thyroid disease susceptibility genes From gene mapping to gene function.Endocrin Rev. 2003; 24: 694-717Crossref PubMed Scopus (310) Google Scholar). Because identical twin concordance for autoimmune thyroid diseases is only 30% to 50% (2Brix T.H Kyvik K.O Hegedus L A population-based study of chronic autoimmune hypothyroidism in Danish twins.J Clin Endocrinol Metab. 2000; 85: 536-539Crossref PubMed Scopus (205) Google Scholar, 3Ringold D.A Nicoloff J.T Kesler M Davis H Hamilton A Mack T Further evidence for a strong genetic influence on the development of autoimmune thyroid disease the California twin study.Thyroid. 2002; 12: 647-653Crossref PubMed Scopus (76) Google Scholar), external, nongenetic factors must play a role in thyroid autoimmunity. Indeed, the role of environmental factors has been the focus of increasing attention. One attractive environmental factor that could trigger autoimmune thyroid diseases in susceptible individuals is infection, and there is a large literature on the subject (4Tomer Y Davies T.F Infection, thyroid disease and autoimmunity.Endocr .Rev. 1993; 14: 107-120PubMed Google Scholar). Antibodies to the bacterium Yersinia enterocolitica, for example, have been reported to be increased in both Graves disease and Hashimoto thyroiditis, and Yersinia release proteins may stimulate proliferation of peripheral blood mononuclear cells and intrathyroidal lymphocytes in patients with Graves disease (5Arscott P Rosen E.D Koenig R.J Kaplan M.M et al.Immunoreactivity to Yersinia enterocolitica antigens in patients with autoimmune thyroid disease.J Clin Endocrinol Metab. 1992; 75: 295-300Crossref PubMed Scopus (18) Google Scholar). A saturable binding site for thyroid stimulating hormone (TSH) has been found on Y. enterocolitica(6Weiss M Ingbar S.H Winblad S Kasper D.L Demonstration of a saturable binding site for thyrotropin in Yersinia enterocolitica.Science. 1983; 219: 1331-1333Crossref PubMed Scopus (107) Google Scholar). Similarly, endogenous and exogenous retroviruses have been implicated in the development of autoimmune thyroid diseases (7Tomer Y Villanueva R Infection and autoimmune thyroid diseases.in: Rose N.R Shoenfeld Y Infections and Autoimmunity. Elsevier, Amsterdam2004: 517-532Google Scholar). Yet another infectious agent that has been gaining interest as a potential trigger of thyroid autoimmunity in susceptible individuals is the hepatitis C virus (HCV). The association of autoimmune thyroid diseases, more specifically Hashimoto thyroiditis, with hepatitis C has been widely studied. However, the data for hepatitis C as a possible factor for the development of autoimmune thyroid diseases have thus far been mixed. Several studies of interferon-naive patients with hepatitis C have not found a significant correlation between HCV infection and the presence of thyroid antibodies (8Loviselli A Oppo A Velluzzi F et al.Independent expression of serological markers of thyroid autoimmunity and hepatitis C virus infection in the general population results of a community-based study in north-western Sardinia.J Endocrinol Invest. 1999; 22: 660-665PubMed Google Scholar, 9Metcalfe R.A Ball G Kudesia G Weetman A.P Failure to find an association between hepatitis C virus and thyroid autoimmunity.Thyroid. 1997; 7: 421-424Crossref PubMed Scopus (52) Google Scholar, 10Boadas J Rodriguez-Espinosa J Enriquez J et al.Prevalence of thyroid autoantibodies is not increased in blood donors with hepatitis C virus infection.J Hepatol. 1995; 22: 611-615Abstract Full Text PDF PubMed Scopus (71) Google Scholar), whereas other studies found elevated levels of thyroid antibodies in up to 42% of patients with HCV infection (11Tran A Quaranta J.F Benzaken S et al.High prevalence of thyroid autoantibodies in a prospective series of patients with chronic hepatitis C before interferon therapy.Hepatology. 1993; 18: 253-257Crossref PubMed Scopus (256) Google Scholar, 12Gann-Carrie N Medini A Coderc E et al.Latent autoimmune thyroiditis in untreated patients with HCV chronic hepatitis A case control study.J Autoimmun. 2000; 14: 189-193Crossref PubMed Scopus (70) Google Scholar, 13Fernandez-Soto L Gonzalez A Escobar-Jimenez F et al.Increased risk of autoimmune thyroid disease in hepatitis C vs hepatitis B before, during and after discontinuing interferon therapy.Arch Intern Med. 1998; 158: 1445-1448Crossref PubMed Scopus (180) Google Scholar, 14Preziati D La Rosa L Covini G et al.Autoimmunity and thyroid function in patients with chronic active hepatitis treated with recombinant interferon alpha-2a.Eur J Endocrinol. 1995; 132: 587-593Crossref PubMed Scopus (219) Google Scholar). Differences in confounding factors, such as genetic background and iodine intake of the populations studied, have been suggested as possible causes for these disparate findings. Some studies have also shown that patients with hepatitis C who developed positive thyroid antibodies or Hashimoto thyroiditis were more likely to be older and female (11Tran A Quaranta J.F Benzaken S et al.High prevalence of thyroid autoantibodies in a prospective series of patients with chronic hepatitis C before interferon therapy.Hepatology. 1993; 18: 253-257Crossref PubMed Scopus (256) Google Scholar, 12Gann-Carrie N Medini A Coderc E et al.Latent autoimmune thyroiditis in untreated patients with HCV chronic hepatitis A case control study.J Autoimmun. 2000; 14: 189-193Crossref PubMed Scopus (70) Google Scholar, 13Fernandez-Soto L Gonzalez A Escobar-Jimenez F et al.Increased risk of autoimmune thyroid disease in hepatitis C vs hepatitis B before, during and after discontinuing interferon therapy.Arch Intern Med. 1998; 158: 1445-1448Crossref PubMed Scopus (180) Google Scholar). Additionally, there are unconfirmed reports of an increased prevalence of HCV antibodies in patients with Hashimoto thyroiditis, suggesting that the disease could be induced by HCV infection (14Preziati D La Rosa L Covini G et al.Autoimmunity and thyroid function in patients with chronic active hepatitis treated with recombinant interferon alpha-2a.Eur J Endocrinol. 1995; 132: 587-593Crossref PubMed Scopus (219) Google Scholar, 15Duclos-Vallee J.C Johanet C Trinchet J.C et al.High prevalence of serum antibodies to hepatitis C virus in patients with Hashimoto's thyroiditis.BMJ. 1994; 309: 846-847Crossref PubMed Scopus (38) Google Scholar, 16Tran A Quaranta J.F Beusnel C et al.Hepatitis C virus and Hashimoto's thyroiditis.Eur J Med. 1992; 1: 116-118PubMed Google Scholar). One possible explanation for these inconsistent results is that HCV may trigger thyroid autoimmunity only in a subset of patients. Up to now, however, studies have not stratified patients with hepatitis C and controls by genetic and environmental risk factors (Table). It is possible that HCV interacts with one or more of these risk factors to trigger the development of autoimmune thyroid diseases, thus, only studies that stratify by these risk factors may reveal a consistent association. CTLA = cytotoxic T lymphocyte antigen; HIV = human immunodeficiency virus; HLA = human leukocyte antigen. In this issue of The American Journal of Medicine, another piece in the puzzle has been added to the growing literature on the association between hepatitis C and thyroid autoimmunity. Antonelli and coworkers (17Antonelli A, Ferri C, Pampana A, et al. Thyroid disorders in chronic hepatitis C. Am J Med. 2004;117:10–13Google Scholar) report that thyroid autoimmunity––both autoimmune hypothyroidism and the presence of thyroid antibodies––cosegregated with hepatitis C infection independently of cirrhosis, liver carcinoma, treatment with interferon, or intake of iodine. Antonelli et al studied four groups: 630 interferon-naive patients who had hepatitis C and were free of cirrhosis or hepatocarcinoma; 389 sex- and age-matched subjects from an iodine-sufficient region; 268 people >50 years old from an iodine-deficient region; and 86 patients who were >40 years old and who had hepatitis B virus–related chronic liver disease. They measured TSH, free T4, free T3 and thyroid antibodies (both antithyroglobulin and antithyroid peroxidase antibodies) in all groups. Circulating TSH levels were significantly higher and free T4 and free T3 levels were significantly lower in the patients with hepatitis C compared with the other three groups. They also found that clinical hypothyroidism was significantly more frequent in patients with hepatitis C compared with the other three control groups. Similarly, markers for thyroid autoimmunity, (i.e., the presence of thyroid autoantibodies [both thyroglobulin antibodies and antithyroid peroxidase antibodies]), were higher in the patients with hepatitis C. However, the frequency of hyperthyroidism was similar for all groups. The authors should be commended for controlling their study for two major confounding factors: intake of iodine and therapy with interferon. Controlling for these factors makes the association more valid, and it is hoped that futures studies will also control for these factors as well as additional potential confounding factors. The findings of Antonelli et al are different than those of Loviselli and coworkers, who surveyed the population of two villages in Sardinia, Italy in which hepatitis C is endemic and the prevalence of autoimmune disease is elevated (8Loviselli A Oppo A Velluzzi F et al.Independent expression of serological markers of thyroid autoimmunity and hepatitis C virus infection in the general population results of a community-based study in north-western Sardinia.J Endocrinol Invest. 1999; 22: 660-665PubMed Google Scholar). They calculated standardized prevalence rates for both antibodies to hepatitis C and antibodies to antithyroid peroxidase. The standardized prevalence rates for both antibodies were no different than those expected under the assumption of unrelated events. Using antithyroid peroxidase antibody–positive subjects and antithyroid peroxidase antibody–negative controls in a case-control study, no association could be found between hepatitis C and antithyroid peroxidase antibodies (8Loviselli A Oppo A Velluzzi F et al.Independent expression of serological markers of thyroid autoimmunity and hepatitis C virus infection in the general population results of a community-based study in north-western Sardinia.J Endocrinol Invest. 1999; 22: 660-665PubMed Google Scholar). It is still unclear why the findings of the two studies are disparate, but it may be due to differences in additional risk factors (Table) that may increase the tendency for HCV-induced autoimmune thyroid diseases. By what mechanisms can an infectious agent such as HCV induce autoimmunity? Potential mechanisms include viral-induced changes in self-antigen expression, molecular mimicry, alterations in the idiotypic network, formation of heat shock proteins, and induction of major histocompatibility complex antigens on nonimmune cells (4Tomer Y Davies T.F Infection, thyroid disease and autoimmunity.Endocr .Rev. 1993; 14: 107-120PubMed Google Scholar). It is possible that infectious agents induce thyroid autoimmunity in genetically susceptible individuals by interacting with genetic risk factors (1Tomer Y Davies T.F Searching for the autoimmune thyroid disease susceptibility genes From gene mapping to gene function.Endocrin Rev. 2003; 24: 694-717Crossref PubMed Scopus (310) Google Scholar); however, the biologic mechanisms of these interactions are not known. Infectious agents most likely play a role in triggering several autoimmune conditions. Until recently, studies examining a possible association of HCV with autoimmune thyroid diseases had mixed results that may have been due, in part, to the possibility that HCV increases thyroid autoimmunity only in certain subsets of patients with hepatitis C. Additional studies of subsets of patients with HCV are needed to identify whether certain patients are at highest risk for developing thyroid autoimmunity." @default.
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• W1991058840 title "Hepatitis C and thyroid autoimmunity: is there a link?" @default.
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