干扰素α致甲状腺功能异常21例临床分析

目的探讨干扰素α治疗慢性丙型病毒性肝炎(丙肝)时对甲状腺功能的影响及治疗对策。方法对我院2007年6月—2011年6月的309例慢性丙肝患者应用干扰素α治疗过程中出现甲状腺功能异常21例的临床资料进行分析。结果本组甲状腺功能异常发生率6.8%(21/309),21例在应用干扰素α治疗前甲状腺功能均正常,治疗2周~6个月后出现甲状腺功能异常,其中甲状腺功能亢进症(甲亢)11例,甲状腺功能减退症(甲减)7例,亚临床甲减3例。明确诊断后2例甲亢停用干扰素,余继续用药,同时予相应治疗,病情好转出院。随访半年,预后良好。结论干扰素α治疗慢性丙肝可诱发甲状腺功能异常,故治疗过程中应密切监测甲状腺功能,以及时采取处理措施。     

Autoimmunity induced by interferon-alpha therapy for chronic viral hepatitis.

Type I interferons, which are mostly alpha-interferons (either as single agents or in combination with antiviral drugs), are currently the standard therapy for chronic viral hepatitis B, B/D, and C. Side-effects are not uncommon and include exacerbation of pre-existing autoimmune disorders or the de novo induction of autoimmunity. These adverse effects are attributed to the immunomodulatory properties of type I interferons, and should be distinguished from autoimmunity associated with chronic viral hepatitis in which interferon treatment may indeed be beneficial. The major autoimmune side-effects of interferon therapy for chronic viral hepatitis are thyroid or liver disease. Therefore, screening for thyroid antibodies and auto-antibodies indicative of autoimmune hepatitis both before, during, and after interferon therapy is strongly recommended. The presence of high concentrations of thyroid auto-antibodies or antibodies associated with autoimmune hepatitis can be contraindicative to interferon therapy. However, treatment is not contraindicated in viral hepatitis (in particular chronic hepatitis C) associated with autoimmune phenomena--including low-titer thyroid antibodies or other non-organ specific auto-antibodies. If interferon-induced autoimmunity occurs, the necessity of therapy has to be balanced carefully against the risks of autoimmune disease. Further research is needed to identify the factors which determine susceptibility to interferon-associated autoimmunity in individual patients.     

Autoimmunity against pancreatic islets and other tissues before and after interferon-alpha therapy in patients with hepatitis C virus chronic infection

OBJECTIVE: The aim of the study was to investigate the prevalence of clinical and latent autoimmune diseases in Italian patients with hepatitis C virus (HCV) chronic infection before and after treatment with interferon-alpha (IFN-alpha). RESEARCH DESIGN AND METHODS: The evidence of clinical autoimmune disease and the presence of autoantibodies were assessed in 70 patients with HCV chronic infection. Autoantibodies to islet cell (ICA), glucagon-producing cells (GCA), parietal cell (PCA), adrenal cortex (ACA), adrenal medulla (AdMA), nuclei (ANA), liver-kidney microsomal (LKM-Ab), mitochondrial, and smooth muscle (SMA) were tested using the classic indirect immunofluorescence technique. Autoantibodies to GAD (GADAb), second islet cell autoantigen (IA2-Ab), and insulin (IAA) were tested by radioimmunoassay and thyroid microsomal autoantibodies (TMHA) and thyroglobulin autoantibodies (TGHA) were assessed by hemoagglutination test. RESULTS: None of the 70 patients studied showed evidence of clinical disease before treatment with IFN-alpha. However, 1 (1.4%) patient was positive for ICA, 2 (2.8%) were positive for GCA, 2 (2.8%) for GADAb, 5 (7.1%) for PCA, 2 (2.8%) for ANA, 3 (3.7%) for SMA, 4 (5.7%) for TMHA, and 2 (2.8%) for TGHA. These frequencies were not significantly different when compared with healthy control subjects. There were 29 (41%) patients who were positive for IAA at low titers compared with 2% of the control subjects (significantly different P < 0.0001). ICA titers of one patient positive for ICA/GADAb increased during the IFN-alpha therapy, and the patient developed type 1 diabetes 5 months after the beginning of treatment. IAA levels did not change during the course of treatment, and none of the IAA+ patients developed diabetes. Thyroid autoantibody titers increased in 3 of the 4 initially positive patients, with 1 patient becoming positive and 2 thyroid antibody-positive patients developing overt hypothyroidism during IFN-alpha treatment. PCA titers increased in 1 of 5 positive patients. Antibodies to other autoantigens did not change during the course of treatment. CONCLUSIONS: We have not found an increased frequency of clinical or latent autoimmune diseases in patients with chronic HCV infection. However, this study suggests that screening patients for autoantibodies (in particular, thyroid and pancreas) before and during IFN-alpha therapy may be useful in assessing the risk of patients developing autoimmune disease.     

Present and future therapy for hepatitis C virus

The treatment of hepatitis C virus (HCV) infection has developed enormously over recent years. Early treatment of acute HCV infection with interferon-alpha can prevent chronicity and a significant proportion of patients with chronic HCV can be cured with the current standard therapy consisting of pegylated interferon-alpha and ribavirin. However, the improvement of current treatment regimens and the development of new antiviral drugs will be essential within the next few years. This review focuses on the present and future concepts for treating HCV infection, including prevention of infection, antiviral therapy of acute and chronic HCV and the management of patients after liver transplantation.     

Peginterferon-alpha(2b) and ribavirin

Hepatitis C virus infection is among the leading causes of chronic liver disease in the USA and has a worldwide prevalence of approximately 300 million people. Chronic hepatitis C virus is the most common indication for liver transplantation in the USA. Due to the chronic nature of hepatitis C virus infection, these numbers are expected to grow fourfold in the next decade. Interferon-alpha(2b) monotherapy followed by combination therapy with ribavirin have been used to treat chronic hepatitis C virus with limited success. The development of pegylated interferon-alpha(2b), (Peg-intron, Schering-Plough) instituted the next chapter in hepatitis C virus therapy. The demonstration of its safety and efficacy led to a major trial studying coadministration with ribavirin for compensated chronic hepatitis C virus infection. Pegylated interferon combination therapy has improved efficacy over standard interferon combination therapy without an increase in adverse effects. This article reviews the data regarding pegylated interferon-alpha(2b) with ribavirin therapy. The pharmacokinetics and pharmacodynamics of combination therapy will be presented along with clinical trial data. The efficacy and ease of usage of Pegintron and ribavirin support its use for chronic hepatitis C virus infection.     

Autoantibodies to CD69 in patients with chronic hepatitis type C: a candidate marker for predicting the response to interferon therapy

OBJECTIVE: To understand the autoimmunity associated with chronic hepatitis C (CHC), we investigated autoantibodies (autoAbs) to CD69. METHODS: With this aim, we tested the reactivity of serum samples from patients with CHC and asymptomatic carriers of hepatitis C virus (HCV), as well as from patients with chronic hepatitis B (CHB) and autoimmune hepatitis (AIH), to recombinant CD69 molecules. RESULTS: Frequencies of anti-CD69 autoAbs were 38.7% in CHC, 15.8% in AIH and 12.3% in CHB. None of the tested asymptomatic HCV carriers had autoAbs to CD69. It is important clinically that the presence of anti-CD69 autoAbs was found to be associated with a poor response to interferon-alpha (IFN-alpha) therapy. In the epitope analysis, multiple epitopes were mapped on CD69, indicating antigen-driven production of the autoAbs. CONCLUSION: We evidenced existence of anti-CD69 autoAbs in patients with CHC, and found that the anti-CD69 autoAb may have potential for predicting responses to IFN-alpha therapy.     

Frequency and significance of antibody to hepatitis C virus in severe corticosteroid-treated autoimmune chronic active hepatitis.

To determine the frequency and significance of antibody to hepatitis C virus (anti-HCV) in severe autoimmune chronic active hepatitis, we tested sera from 85 cortico-steroid-treated patients by an enzyme immunoassay. Seropositive patients were assessed for specific antibodies to hepatitis C virus-encoded antigens by recombinant immunoblot assay. The findings in patients with and without anti-HCV were contrasted, and the frequency of seropositivity was compared with that in patients who had other types of chronic liver disease and in normal adults. Only 5 of the 85 patients with autoimmune hepatitis (6%) were seropositive for anti-HCV, and only 2 of these patients were reactive by recombinant immunoblot assay. The frequency of seropositivity in autoimmune hepatitis was not significantly different from that in hepatitis B surface antigen-positive (9%) and cryptogenic (18%) disease, but it was significantly less than that in posttransfusion chronic active hepatitis (6% versus 75%; P less than 0.001). Two patients became seronegative after corticosteroid therapy; both had been nonreactive by recombinant immunoblot assay. Four of the seropositive patients entered remission during corticosteroid therapy, including three whose sera were nonreactive to virus-encoded antigens. We conclude that anti-HCV occurs infrequently in corticosteroid-treated severe autoimmune hepatitis and that antibodies detected by enzyme immunoassay may be nonreactive to hepatitis C virus-encoded antigens. Seropositive patients who are nonreactive by immunoblot assay may still respond to corticosteroid therapy and become seronegative during treatment.     

α干扰素治疗慢性乙型肝炎儿童诱发甲状腺功能紊乱的临床研究

目的探讨α干扰素治疗的慢性乙型肝炎儿童诱发甲状腺功能紊乱的临床特点。方法 2010年1月至2011年12月在解放军第302医院青少年肝病科住院,干扰素α为基础抗病毒治疗并随访的慢性乙型肝炎儿童406例,每24周检查甲状腺功能五项,对随访的结果进行统计分析。结果 (1)本组患儿25.86%出现甲状腺功能紊乱,以亚临床甲状腺功能减退为主(17.98%),6.16%出现甲状腺功能减退症,1.72%为甲状腺功能亢进症;幼儿组(1³岁)患儿未见甲状腺功能亢进症,43岁)患儿未见甲状腺功能亢进症,4⁷岁(7.55%)及87岁(7.55%)及8¹6岁(9.26%)组甲状腺功能减退症的发生率明显高于幼儿组(1.44%)。甲状腺功能减退症患儿中女性(11.11%)的发生率明显高于男性(4.15%)。(2)68%的甲状腺功能减退症患儿、42.86%的甲状腺功能亢进症患儿有临床表现;治疗前过氧化酶抗体(TPOAb)、甲状腺球蛋白抗体(Tg Ab)升高的患儿均进展为甲状腺功能疾病。(3)Logistic结果显示,甲状腺功能亢进症和甲状腺功能减退症的发生与女性及治疗前治疗中出现TPOAb、Tg Ab升高相关。结论α干扰素治疗的慢性乙型肝炎儿童诱发甲状腺功能紊乱以亚临床甲状腺功能减退为主,甲状腺功能亢进症和甲状腺功能减退症的发生与女性及治疗前治疗中出现TPOAb、Tg Ab升高相关。     

Severe exacerbation of asthma: a new side effect of interferon-alpha in patients with asthma and chronic hepatitis C

Interferon-alpha is used by physicians to treat numerous common medical disorders; however, therapy is often limited by side effects. Pulmonary complications, such as interstitial pneumonitis and bronchiolitis obliterans organizing pneumonia, have been described in patients receiving interferon-alpha therapy. Exacerbation of asthma induced by subcutaneous administration of interferon-alpha has not been previously reported. We describe two patients with mild asthma in whom treatment with interferon-alpha for chronic hepatitis C resulted in exacerbation of the underlying asthma. The severe asthmatic symptoms resolved promptly after use of interferon-alpha was discontinued and corticosteroid therapy was initiated. Repeated treatment with interferon-alpha several months later resulted in a rapid, more severe exacerbation of asthma in both patients. Patients undergoing therapy with interferon-alpha, especially those with chronic asthma, should be monitored closely for pulmonary symptoms. If these symptoms develop, patients should be instructed to discontinue use of interferon-alpha and seek medical attention immediately.     

不同方案治疗YMDD变异慢性乙型肝炎的疗效比较

目的:比较慢性乙型肝炎患者出现YMDD变异后不同治疗方法的疗效。方法:选择采用拉米夫定治疗后出现YMDD变异的慢性乙肝患者96例,分为A组36例,继续采用拉米夫定治疗,疗程52周;B组32例,改用α-干扰素治疗,疗程26周;C组28例,改用阿德福韦治疗,疗程52周。结果:B组和C组HBVDNA转阴率分别是43.8%和64.3%,丙氨酸转移酶(ALT)复常率分别为62.5%和71.4%,与A组相比,差异有显著性(P<0.05)。结论:慢性乙型肝炎发生YMDD变异后,继续使用拉米夫定治疗效果不理想。对于YMDD变异的患者,改用阿德福韦或α-干扰素治疗后,疗效比拉米夫定好。     

Graves' disease in interferon-alpha-treated and untreated patients with chronic hepatitis C virus infection.

An association between Graves' disease (GD) and chronic hepatitis C (C-HC) has been observed both in the presence and the absence of recombinant interferon-alpha (rIFN-alpha) treatment. rIFN-alpha-induced GD is characterized by suppressed thyroid-stimulating hormone levels; normal or elevated free triiodothyronine (FT3) and free thyroxine (FT4) values; the presence of thyroid peroxidase antibodies, antithyroglobulin antibodies, and thyroid receptor antibodies; and high iodine thyroid uptake. In contrast, GD developed during C-HC without rIFN-alpha is less clearly defined. In this study, we examined two groups of patients: group A, 28 patients with C-HC treated with rIFN-alpha who developed GD after 1 to 9 months, and group B, 10 patients with C-HC who developed GD without a previous rIFN-alpha treatment. At the time of GD, both groups started methimazole therapy; thyroid function was reevaluated after 3, 6, 9, and 12 months. Group A patients continued IFN. After 12 months, all patients of group A were euthyroid, and 21 of them (75%) had already stopped methimazole treatment, whereas all patients of group B were euthyroid and only 2 (20%) had stopped methimazole. In conclusion, the data show a better course of GD, with a more precocious and significantly higher number of recoveries in patients with rIFN-alpha-induced GD than in rIFN-alpha-unrelated disease. Further studies are needed to establish whether the two types of GD differ not only from a clinical point of view but also because of different underlying pathogenetic mechanisms.     

Pegylated interferon-alpha2b: pharmacokinetics, pharmacodynamics, safety, and preliminary efficacy data. Hepatitis C Intervention Therapy Group

AIMS: The objectives of this study were to assess the safety, pharmacokinetic and pharmacodynamic profiles, and antiviral efficacy of pegylated interferon-alpha2b monotherapy in patients with chronic hepatitis C. METHODS: Fifty-eight patients (38 men, 20 women; age range, 25 to 65 years) with compensated chronic hepatitis C were enrolled in this open-label, randomized, active controlled study. Patients received 0.035 to 2.0 microg/kg pegylated interferon-alpha2b subcutaneously weekly or the active control, interferon-alpha2b 3 million IU subcutaneously three times/week, for 24 weeks. Safety and antiviral efficacy assessments were performed during treatment and in a subsequent 4-week follow-up period. Detailed pharmacokinetic assessments were performed at weeks 1 and 4. RESULTS: Pegylated interferon-alpha2b produced dose-related reductions in white blood cells, neutrophils, and platelets, and dose-related increases in oral temperature, serum neopterin, and serum 2'5'-oligoadenylate synthetase activity, which were qualitatively similar to those produced by nonpegylated interferon-alpha2b. Reported adverse events (flu-like symptoms, asthenia) were qualitatively similar in pegylated interferon-alpha2b- and nonpegylated interferon-alpha2b-treated groups. Dose-related antiviral activity, as measured by loss of detectable serum hepatitis C virus RNA (<100 copies/mL), was noted at the end of treatment and after 4 weeks of follow-up. Both pegylated and nonpegylated interferon-alpha2b were rapidly absorbed, with maximal concentrations occurring approximately 8 to 12 hours after dose administration. Pegylated interferon-alpha2b had sustained maximal serum concentrations for 48 to 72 hours after dose administration, whereas nonpegylated interferon-alpha2b concentrations declined rapidly. Volume of distribution for both compounds was similar (approximately 1 L/kg). Pegylated interferon-alpha2b elimination half-life was approximately 10-fold greater, and mean apparent clearance was one tenth that of nonpegylated interferon-alpha2b. CONCLUSIONS: Pegylated and nonpegylated interferon-alpha2b safety and pharmacodynamic profiles were comparable. Pegylated interferon-alpha2b demonstrated delayed clearance compared with nonpegylated interferon-alpha2b, consistent with once-weekly administration.     

Problems in the treatment of hepatitis C with interferon.

A marked increase in the rate of eradication of hepatitis C virus (HCV) has been achieved by the combination of interferon-alpha2b and ribavirin when compared with interferon-alpha2b alone. However, even with combination therapy, hepatitis persists in more than half of the patients with chronic herpatitis C and progresses to liver cirrhosis and hepatocellular carcinoma with time. What needs to be kept in mind is that, whether by its natural course or by therapy to suppress liver inflammation or by interferon therapy, the rate of development of hepatocellular carcinoma is reduced if ALT is maintained at low levels. Attention should therefore be focused on the development of drugs which enhance the effect of interferon as well as drugs which suppress liver inflammation.     

Depressive disturbances during antiviral therapy in patients with type C hepatitis

The article presents the results of a clinico-psychopathological study of depressive disorder (DD) in 91 patients with chronic C hepatitis and no psychiatric background during combined antiviral therapy (AVT) with interferon-alpha (IFN-alpha) and ribavirin. Depression developed in 39 or 43% of the patients. Moderate or severe depressions (46% and 31%, respectively) prevailed. Clinical features that were different in cases of IFNa-induced depression and endogenous DD were revealed. The severity of depression did not correlate with the severity of the underlying disease, the duration of AVT, and the type of used. The antidepressants and remeron proved to be effective in treatment of IFN-alpha-induced depressions. In all cases, treatment with antidepressants made it possible to carry out complete AVT.     

Complete remission of cryoglobulinemic glomerulonephritis (HCV-positive) after high dose interferon therapy

We report the case of a 64-year old woman with hepatitis C virus infection, mixed cryoglobulinemia type II (IgG + IgM kappa) and cryoglobulinemic glomerulonephritis. The patient was treated with the standard dose of recombinant interferon alpha-2b (3 million units 3 times a week) for one year, resulting in complete clinical remission and undetectable levels of serum hepatitis C virus RNA. AST and ALT normalized and proteinuria decreased from 2.78 to 0.98 g/day. However, a relapse occurred when therapy was stopped. Additional therapy with interferon-alpha (5 million units 3 times a week for 9 months) resulted again in quick and prolonged remission. The clinical course of our patient showed sustained clinical and virologic response after high-dose interferon-alpha treatment confirming the usefulness of interferon alpha in treatment of patients with cryoglobulinemic glomerulonephritis. Our observation is in agreement with others, suggesting that recommended standard dosage and duration of initial treatment with interferon alpha should be re-evaluated. Although our patient had sustained virologic and clinical response after interferon alpha monotherapy, recent studies clearly support combination therapy of interferon alpha and ribavirin for treatment of chronic HCV infections.     

Chronic hepatitis C treatment with pegilated interferon alpha2a and ribavirin in patients with HIV-infection

AIM: To study efficacy and safety of combined therapy of chronic hepatitis C (CHC) with pegilated interferon-alpha2a in combination with ribavirin at early stages of CHC and HIV-infection untreated with highly active antiretroviral therapy (HAART). MATERIAL AND METHODS: An open, nonrandomized, retrospective and prospective trial included 50 patients with subclinical HIV infection (stage 3; n = 47) and the stage of secondary diseases 4A at a remission phase untreated with HAART. The patients were given pegilated interferon-alpha2a and ribavirin for 48 weeks. RESULTS: The above combined treatment was highly effective, comparable to the results achieved in CHC patients without HIV infection. Tolerance was satisfactory. Most frequent side effects were thrombocytopenia, leukopenia and neutropenia. These were not the cause of the patients withdrawal (n = 9; 18%). The treatment was discontinued because of depression and long-term fever. A significant reduction of CD4+ lymphocytes count was observed but clinical manifestations of HIV-infection progress were not reported. CONCLUSION: CHC treatment in HIV-infected patients should be started as early as possible after diagnosis of chronic hepatitis, before symptoms of cirrhosis. In this case probability of achievement of a stable virusological response in CHC patients with HIV-infection is similar to that in CHC patients without HIV infection.     

Subpopulation blood lymphocyte composition in blood of patients with chronic hepatitis C during therapy with interferon

The number of lymphocytes expressing CD3, CD4, CD8, CD16, CD25, and CD19 antigens was studied in patients with chronic hepatitis C before and after 12-week therapy with interferon-alpha (IFN-alpha). The percentage of cells expressing CD4+, CD16+, and CD25+ antigens decreased significantly in untreated patients, while the percentage of CD8+ and CD19+ lymphocytes was increased (p < 0.05) vs. the control. After 3-month therapy with IFN-alpha the counts of CD4+ and CD25+ increased significantly in patients with chronic hepatitis C (p < 0.05 and p < 0.01, respectively) in comparison with the initial values. The treatment led to a significant (p < 0.05) decrease in the number of CD8+ cells in the blood. The number of cells expressing CD19+ decreased, but remained high in comparison with the control. These results indicate that cellular immune response is inadequate in patients with chronic hepatitis C. Time course of subpopulation composition of T lymphocytes during effective treatment with IFN-alpha indicates an important role of T-cellular component of immunity in the antiviral defense mechanisms in chronic HCV infection.     

Hepatitis C

Hepatitis C virus (HCV) infection is a leading cause of chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma worldwide. Here, we briefly review the virology, diagnosis and therapy of hepatitis C. Standard therapy with pegylated interferon-alpha and ribavirin results in a sustained virological response in 40-50% of genotype 1- and in about 80% of genotype 2- or 3-infected patients. Recent progress has allowed the identification of novel antiviral targets and therapeutic strategies. These will likely complement existing therapeutic modalities in the near future.     

The prevalence, clinical features and response to antiviral therapy of patients with chronic hepatitis C who are seropositive for liver-kidney microsome type 1 antibodies

BACKGROUND: Antibodies to liver-kidney microsome type 1 (anti-LKM-1), which are a marker of autoimmune hepatitis, are found in a minority of patients with chronic hepatitis C virus (HCV) infection. Whether interferon/ribavirin therapy is safe and effective in these patients is unclear. AIM: To describe the prevalence, clinical features and response to interferon/ribavirin therapy of anti-LKM-1 seropositive patients with chronic hepatitis C. PATIENTS AND METHODS: All anti-LKM-1 seropositive patients with chronic hepatitis C who between 1997 and 2002 underwent a diagnostic liver biopsy at the Liver Center Maggiore Hospital, Milan, were studied. Serum HCV RNA was tested by in-house PCR with a limit sensitivity of 50 IU/ml. Tissue antibodies were assessed by indirect immunofluorescence on cryostat sections from rat liver, kidney and stomach. Liver biopsies were graded and staged by the Ishak score. Autoimmune hepatitis was defined according to the International Autoimmune Hepatitis Grading (IAHG) score. RESULTS: Forty-eight (1.8%) of 2675 HCV patients circulated anti-LKM-1 (30 females, 55 years of age). Twenty-eight had genotype 2, 18 genotype 1, and two genotype 3. Aminotransferase levels had been high for 23 + 12 years, on average. Using IAHG, autoimmune hepatitis was excluded in 44 patients (92%) and found to be probable in 4 patients (8%). Chronic hepatitis was histologically mild in 34 patients (70%), moderate to severe in 7 patients (15%) and with cirrhosis in 7 patients (15%). A sustained virological response (SVR) was achieved in 20 of the 27 patients who received interferon/ribavirin (13 genotype 2c with 87% SVR, and 7 genotype 1b with 58% SVR). None of the patients had serum aminotransferases, immunoglobulins or anti-LKM-1 levels flaring following therapy. CONCLUSIONS: LKM-1 antibodies rarely occur in patients with chronic hepatitis C and do not predict autoimmune hepatitis, interferon/ribavirin hyporesponsiveness or immune-related reactions to therapy.     

Thyroid dysfunction is associated with the loss of hepatitis B surface antigen in patients with chronic hepatitis B undergoing treatment with α-interferon

ObjectiveTo investigate the influence of thyroid dysfunction on the antiviral efficacy of α-interferon in adult patients with chronic hepatitis B (CHB).MethodsWe performed a retrospective study of 342 patients with CHB who underwent interferon treatment for >12 weeks. Patients with thyroid dysfunction before or during treatment were defined as the thyroid dysfunction group (n = 141) and those with normal thyroid function were defined as the normal thyroid function group (n = 201). The prevalences of hepatitis B virus (HBV) DNA undetectability, low hepatitis B surface antigen (HBsAg) titre (<250 IU/mL), HBsAg loss, and hepatitis B envelope antigen loss were compared.ResultsDuring interferon treatment, 69 of 270 (25.6%) participants with normal thyroid function at baseline developed thyroid dysfunction, whereas 11 of 72 (15.3%) with thyroid dysfunction at baseline regained normal thyroid function. The thyroid dysfunction group had significantly higher prevalences of low HBsAg titre (29.8% vs. 18.9%) and HBV DNA undetectability (66.0% vs. 40.3%). Multivariate logistic regression analysis showed that thyroid dysfunction was associated with HBsAg loss (odds ratio 4.945, 95% confidence interval 1.325–18.462).ConclusionsThese results suggest that thyroid dysfunction is not an absolute contraindication, but is associated with HBsAg loss, in patients with CHB undergoing α-interferon treatment.