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Thyroid disorders associated with Hepatitis C or interferon based therapies

Sener Barut, �zg�r G�nal* 
Gaziosmanpasa University Faculty of Medicine, Department of Infectious Diseases and Clinical Microbiology, Tokat, Turkey.

*Corresponding author: 
Dr. �zg�r G�nal
Gaziosmanpasa Universitesi T1p Fakultesi, 
Infeksiyon Hastaliklari ve Klinik Mikrobiyoloji 
60100 Tokat, Turkiye
Tel: +90 356 212 9500-1283
Fax: +90 356 2133179
E mail:  HYPERLINK "mailto:ozgurgop@yahoo.com" ozgurgop@yahoo.com








Absract
Several extrahepatic diseases have been associated with chronic HCV infection (i.e. hematologic diseases, renal disease, dermatologic conditions). Chronic HCV infection has also been shown to be associated with increased incidence of clinical and subclinical autoimmune thyroiditis. Moreover, IFN-� therapy of chronic HCV infection is associated with subclinical or clinical thyroiditis in up to 40% of cases. Interferon induced thyroiditis (IIT) can be classified as autoimmune type and non-autoimmune type. Current studies indicate that viral load, viral genotype and therapeutic regimen do not influence development of  IIT in CHC patients thus, development of IIT is not a predictor of SVR. However, evidence suggests that genetic factors, gender, hepatitis C virus infection and positivity of Tab�s may play a role.















Several extrahepatic diseases have been associated with chronic HCV infection.  These include hematologic diseases such as cryoglobulinemia and lymphoma, renal disease, dermatologic conditions such as lichen planus and porphyria cutanea tarda (1). Chronic HCV infection has also been shown to be associated with increased incidence of clinical and subclinical autoimmune thyroiditis (i.e. the presence of thyroid antibodies in euthyroid subjects) (2,3).Two studies are important in this field. One study of Antonelli et al, a large and a well-controlled study, showed  that both hypothyroidism and thyroid autoimmunity were significantly more common in patients with hepatitis C compared to controls [3]. The other study strengthened further the evidence for this association which found that the prevalence of non-autoimmune hypothyroidism, as well as the presence of anti-thyroglobulin antibodies, was higher in untreated children with HCV compared to healthy non-HCV infected controls. Other parameters except active HCV infection were not related to (family history of autoimmune diseases, duration of HCV infection, viral genotype, viral load or liver function) the increased prevalance (4).
In addition to that, all published contolled studies on HCV infection and thyroid autoimmunity were analysed by Antonelli et al who demonstrated a significant increase in the risk of thyroiditis in HCV patients. This implies that, HCV infection is the only infectious agent that is clearly associated with an increased risk for autoimmune thyroiditis (2).
It is possible that HCV induce thyroid autoimmunity in genetically susceptible individuals by interacting with genetic risk factors ; however, the biologic mechanisms of these interactions are not known (6).
According to current medical practice, Interferon-alpha (or pegylated interferon) is fundamental for chronic hepatitis C treatment, in fact, the most common prescription for IFN-alpha (IFNa)  (or pegylated interferon) is hepatitis C (7). 
Moreover, IFN-� therapy of chronic HCV infection is associated with subclinical or clinical thyroiditis in up to 40% of cases and, IFNa is one of the  most important environmental triggers of autoimmune thyroid disesease (AITD) (2).
Interferon induced thyroiditis (IIT) can be classified as autoimmune type and non-autoimmune type (7).



1. Autoimmune IIT
The entire spectrum of autoimmune thyroid diseases (AITD) has been defined with the results of patients receiving IFN-�:Graves  disease (GD), Hashimoto s thyroiditis (HT) and the presence of thyroid antibodies (Tab s) without clinicaldisease (7).
Hashimoto s thyroiditis (HT) is the most common clinical manifestation of autoimmune IIT whereas Grave's disease (GD) is a less common clinical manifestation (Tomer Y 2009). HT develops commonly in patients having positive TAb before they receive IFNa. Besides, HCV patients receiving INFa  may also develop HT as de novo although they did not have positive TAb prior to therapy. These data implies a triggering effect for IFNa in individuals with genetic susceptibility to the development of AITD[2,7 ].
Subclinical AITD may also develop with IFNa therapy. Subclinical AITD manifests by the production of TAb without clinical disease.The incidence of de novo development of TAb is about 10-40% [7,8].
2- Non-autoimmune IIT
Non-autoimmune IIT is also common like autoimmune IIT. It can manifest as destructive thyroiditis, with early thyrotoxicosis and later hypothyroidism, or as non-autoimmune hypothyroidism (). In most cases of destructive thyroiditis, subclinical thyroid dysfunction and spontaneous resolution mainly occurred. The negative TSH-receptor antibodies(TRAb)and low thyroid radioactive iodine uptake  are the base for the diagnosis of destructive thyroiditis in patients receiving interferon therapy (Mandac, Tomer interferon induced).  The destructive form of IIT is theorized as being secondary non-autoimmune thyroid inflammation (7). Thus, this type of thyroiditis is mainly due to direct effect of inteferon on thyroid gland.
Danilovic et al prospectively selected 26 patients with chronic hepatitis C infections to characterize thyroid disturbances induced by interferon-alpha and ribavirin therapy. Of all patients, 54% had no thyroid disorders associated with the interferon-alpha therapyA total of 19% of the subjects had autoimmune interferon-induced thyroiditis characterized by an emerge of antithyroid antibodies or overt hypothyroidism. Additionally, 16% had non-autoimmune thyroiditis, which presents as destructive thyroiditis or subclinical hypothyroidism, and 11% of patients who had antithyroidal antibodies before therapy remained in a state of euthyroidism (9).
In our study published recently, 119 patients with CHC receiving pegylated interferon plus ribavirin were included in the study, de novo incidence of TD was found to be 16.8% (10).  Similarly, in the study by Yan Z et al, at the end of the IFN-�based therapy, 68 patients (11.5%) in the study had developed TD, 58 patients (85.3%) presented with subclinical TD, and only 10 patients (14.7%) developed overt thyroiditis. The thyroid function of 46 patients (67.8%) spontaneously returned to normal in the six months of follow-up and only three patients (4.4%) had persistent overt TD symptoms after the 24 month follow-up period (11). The likelyhood of TD development during the treatment changes between 5.5% and 27.8%  according to different studies (1,10,12,13).
There are various factors that predisposed  patients with HCV toIIT. There is a genetic susceptibility to IIT (2,7). Specifically, the presence of TPO-Ab before treatment was a statisticallysignificant risk factor for developing thyroid disease in patients treated with interferon (8). Similarly, Watanabe et al. showed the incidence of thyroid diseases in patientswith pretreatment TPO-Ab was much higher comparedto patients with negative TPO-Ab levels (60% vs. 3.3) (14). Roti et al. demonstrated that elevated TPO antibodies before IFN� therapy had a positive predictive value of 67% for the development of clinical autoimmune IIT (15). We also found according to logistic regression analysis that anti-TPO positivity was the only significant predictor of thyroid disorder during IFN based therapy of chronic hepatitis C (10). Similarly Yan Z et alperformed a study on 592 Chinese patients who received interferon-� based therapy for CHC,  carried out multivariate stepwise analysis to find out factors associated with thyroid dysfunctionand demonstrated that gender and pretreatment TPOAb were the independent factors related to the incidence of TD(11). Therefore, it is recommended that patients with baselineTab�s should be followed more closely for thyroid dysfunctionwhile on IFN-�therapy (7).
Various risk factors for IIT have been evaluated.  Although Tran et al.,in a recent study, reporteda positive and significant association between thyroid diseaseand viral clearance,our study together with the study of Vezali et al. demonstrated that virologic factors such as early virologc response or sustained viral response(SVR)as well as the type of interferon alpha  were not associated with interferon induced thyroid dysfunction in CHC patients receiving peginterferon plus ribavirin (10,13,16). Vezali and coworkers evaluated 94 CHC patients long term for TD (61 patients treated with pegylated interferon alpha (PEG-IFN-a) plus ribavirin vs 33 untreated patients) in their study. The control group patients remained euthyroid (P < 0.001) and 13 of the treatment group patients experienced (21.3%) TD. 11 of this 13 patients were diagnosed with hypothyroidism and 2 of them with hyperthyroidism that later converted to hypothyroidism. The incidence of TD in women (9 of 13, 69.2%) was higher than the incidence of TD in men (four of 13, 30.8%),however this difference was not significant statistically (P = 0.122). Moreover, 10 patients receiving the therapy (16.4%) developed at least one more autoimmune disease during the treatment course (four psoriasis, two mixed cryoglobulinemia, two rheumatoid arthritis-like syndrome, one lichen planus and one idiopathicthrombocytopenia).Thirteen independent variables potentially associated with TD (sex, age, BMI, HCVgenotype, pretreatment viral load, treatment regimen and duration,total dose of PEG-IFN-a and ribavirin, RVR, EVR, ETR andSVR) were evaluated via multivariate logistic regression analysis.  However TD could not be predicted with any of these.  The only correlation declared by this study was the relationship between TD development and the onset of other autoimmune disorders during combination therapy (P = 0.003;OR, 8.29; 95% CI, 2.09�32.83) (13).
Therefore it can be concluded that viral load, viral genotype and therapeutic regimen do not influence development of  IIT in CHC patients thus, development of IIT is not a predictor of SVR. However, evidence suggests that genetic factors, gender, hepatitis C virus infection and positivity of Tab�s may play a role.

















References:
Andrade LJ, Atta AM, D�Almeida Junior A, Paran� R. Thyroid dysfunction in hepatitis C individuals treated with interferon-alpha and ribavirin � a review. Braz J Infect Dis. 2008;12:144�8.
Tomer Y. Hepatitis C and interferon induced thyroiditis. J Autoimmun. 2010;34:322�6.
Antonelli A, Ferri C, Pampana A, Fallahi P, Nesti C, Pasquini M, et al. Thyroid disorders in chronic hepatitis C. Am J Med 2004;117(1):10e3.
Indolfi G, Stagi S, Bartolini E, Salti R, De Martino M, Azzari C, et al. Thyroid function and anti-thyroid autoantibodies in untreated children with vertically acquired chronic hepatitis C virus infection. Clin Endocrinol (Oxf) 2008;68 (1):117e21
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