[Thyroid dysfunctions in patients with viral hepatitis treated with interferon-alpha].

BM Központi Kórház és Intézményei, Izotóp Osztály, Budapest.
Orvosi Hetilap 07/2004; 145(23):1211-6.
Source: PubMed

ABSTRACT Many studies have explored that thyroid dysfunctions can be induced by cytokine therapy. Most observations were collected in connection with the treatment of viral hepatitis with interferon-alpha.
Frequency and types of thyroid dysfunction developed during and after recombinant interferon-alpha treatment were studied in 138 patients with viral hepatitis C or B. Therapy lasted 12 months or more, subjects having thyroid dysfunction at the start of therapy were excluded from the study. Thyroid parameters (TSH, FT4, FT3 and anti-TPO) were controlled every third month. In patients in whom thyroid dysfunction occurred the measurements were repeated monthly and other tests were also performed (anti-Tg, IL-6, TSH receptor antibody, thyroid scan and 99mTc-pertechnetate uptake).
Thyroid function disturbances were found in 30 (21.7%) patients, 12 of them (8.7%) showed persistent hypothyroidism. Hyperthyroidism was transitory in all cases. The clinical course of thyroid dysfunction might be monophasic (hyper- or hypothyroidism), biphasic (hyperthyroidism followed by hypofunction) or triphasic. Immune and non-immune forms can be clearly distinguished.
Every fifth patient with chronic hepatitis showed thyroid dysfunction during interferon-alpha therapy, it is necessary therefore to control the hormonal status and the thyroid antibody titer. Treated patients have to be informed in advance that as a "side effect" persistent hypothyroidism may develop.

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    ABSTRACT: Objective. To determine the association of thyroid dysfunction with the severity of the disease and response to treatment in patients of chronic hepatitis C. Design. Cohort study. Patients. One hundred and sixty seven noncirrhotic chronic hepatitis C patients were grouped into treatment group (n = 107) and control group (n = 60). Measurements. Baseline S. ALT and S. AST by IFCC and S. TSH, S. free T4, and S.T3 level were measured by chemiluminescence method. The severity of the disease was measured by Knodell histopathological index (HPI) on liver biopsy. Study group patients underwent 24-weeks IFN and ribavirin therapy and thyroid functions were determined at weeks 0, 12, and 24. Response to therapy was determined by PCR-HCV test. Results. 20 treated patients (18.69%) developed thyroid dysfunction with relative risk (RR) of 11.25 and attributable risk (AR) of 91%. Females were at higher risk. Hypothyroidism was common than hyperthyroidism. There was no significant association between thyroid dysfunction and severity of the disease (P = 0.81) and response to therapy (P = 0.79). Conclusion. Interferon-alpha and ribavirin therapy induces thyroid dysfunction in chronic hepatitis C patients. There is no association between severity of disease and response to therapy with interferon-induced thyroid dysfunction.
    Hepatitis research and treatment 01/2012; 2012:864315.
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    Hepatitis research and treatment 2090-1372 - Hindawi Publishing Corporation. 01/2012;
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    ABSTRACT: OBJECTIVE: To investigate the prevalence of thyroid dysfunction (TD) and immunoglobulin G (IgG) subclasses of thyroid autoantibodies (TAs), and to determine the predictive factors of TD in chronic hepatitis C (CHC) patients. DESIGN: Three hundred and twelve (312) untreated hepatitis C virus-infected patients without a history of TD or treatment with thyroid hormones were enrolled in a cross-sectional study. Clinical and biological factors were statistically analyzed to determine the correlation between TD and this patient population. RESULTS: The incidence of TD was 12.5% in CHC patients. Clinical hypothyroidism (5.8%) and subclinical hypothyroidism (3.8%) were more frequent than clinical hyperthyroidism (1.6%) and subclinical hyperthyroidism (1.3%). The percentage of TAs positive patients was significantly higher in people >60 than in those <=60 (31.9% vs 18.6%; P=0.042). Positive thyroid peroxidase antibody (TPOAb) was more frequent and ALT levels were lower in patients who displayed TD (TPOAb: 62.1% vs 10.8%, P=0.000; ALT: 43.5IU/L vs 51IU/L, P=0.046). The positive percentage of TPOAb IgG2 subclass in TD group was significantly higher than that of patients without TD (66.7% vs 16.7%, P=0.005). Multiple logistic regression analysis indicated that only TPOAb IgG2 subclass positivity was an independent risk factor for TD in CHC patients (odds ratio=8; 95% confidence interval: 1.225-52.246; P=0.030). CONCLUSIONS: TPOAb IgG2 subclass positivity is a risk factor for TD in CHC patients before antiviral treatment. IgG2 subclass of TPOAb might play an important role in the presence of TD in CHC patients.
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