Exacerbation of Thyroid Autoimmunity by Interferon .ALPHA. Treatment in Patients with Chronic Viral Hepatitis: Our Studies and Review of the Literature.

Nagayama, Yuji; Ohta, Kazuhiro; Tsuruta, Masako; Takeshita, Akira; Kimura, Hironori; Hamasaki, Koji; Ashizawa, Kiyoto; Nakata, Keisuke; Yokoyama, Naokata; Nagataki, Shigenobu

doi:10.1507/endocrj.41.565

Cited by 45 publications

(16 citation statements)

References 45 publications

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“…Weobserved that 4 of these 1 1 patients developed subclinical hypothyroidism, of whomPatient 1 had low fT4 and autoantibody levels, and Patients 4, 5 and 10 exhibited TSH elevation. In Hashimoto thyroiditis such as that in Patient 1, IFN-induced thyroid dysfunction occurs usually in association with the elevation of anti-thyroid autoantibody titer, suggesting that IFN exacerbates autoimmunity in the thyroid (10). While most previous reports have focused mainly on the presence of autoantibodies, our observations revealed a high incidence of thyroid dysfunction in the TSHelevation group prior to IFN therapy.…”

Section: Discussionmentioning

confidence: 44%

Incidence and Characteristics of Thyroid Dysfunction Following Interferon Therapy in Patients with Chronic Hepatitis C.

et al. 1998

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Thyroid functions were analyzed before, during and after interferon (IFN) therapy in patients with chronic hepatitis C. According to the results of routine thyroid function tests and measurements of the levels of anti-thyroid autoantibody prior to the therapy, patients were divided into 2 groups; Group A (19 patients) had at least one abnormal finding related to the thyroid, and Group B (40 patients) did not show any abnormality. Five patients (26% ) in Group A and 4 (10%) in Group B showed thyroid dysfunctions which were very clearly reflected by thyrotropin (TSH) measurements. Interestingly, the time of peak TSH elevation in Group A (mean ± SD, 4.3 ±0.8 months) was significantly earlier than that in Group B (6.8 ± 0.8). Most patients in Group B were diagnosed as having destructive thyroiditis. These findings may suggest that the pathogenesis of IFN-induced thyroid dysfunction consists not only of exacerbation ofpre-existing thyroid autoimmunity but also of de novo destructive changes even in the intact thyroid before IFN therapy. (Internal Medicine 37: 246-252, 1998)

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Section: Discussionmentioning

confidence: 44%

Incidence and Characteristics of Thyroid Dysfunction Following Interferon Therapy in Patients with Chronic Hepatitis C.

et al. 1998

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“…Among these, hypothyroidism (62%) seems to be the most frequent, followed by silent thyroiditis (16%) and Graves' disease (11%) [13].…”

Section: Discussionmentioning

confidence: 99%

Graves' Hyperthyroidism Showing Transient Hypothyroidism during Interferon Therapy for Chronic Hepatitis Type C

et al. 2005

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Abstract. We report a patient with Graves' disease in whom thyroid function was changed from initial hyperthyroidism to transient hypothyroidism and back to hyperthyroidism during interferon (IFN) therapy. A 43-year-old man was admitted to our hospital to receive IFN treatment for chronic active hepatitis (type C) in June 1998. His thyroid function was normal and testing for thyroid gland antibodies (TSH binding inhibitor immunoglobulins; TBII, anti-thyroglobulin antibodies; TgAb and anti-thyroid peroxidase antibodies; TPOAb) was negative before IFN therapy. The patient had neither history of thyroid disease nor any particular family history. He developed hyperthyroidism four months after its initiation of IFN therapy. When he was hyperthyroid, TBII, the activity of thyroid-stimulating antibodies (TSAb) and thyroid stimulation-blocking antibodies (TSBAb) were 40.2% (normal range, -15~+15.0%), 1201% (normal range, £180%) and 52.0% (normal range, £45.6%), respectively. Thyroid 99m Tc(technetium)-uptake ratio (Tc-UTR) was 1.07% (normal range, 0.5-3.0%). He transiently developed hypothyroidism in December 1998 and recurrent hyperthyroidism in February 1999. When he was hypothyroid, TBII, TSAb and TSBAb were 74.3%, 769% and 95.9%, respectively. To investigate the mechanism of his fluctuating thyroid status, we serially assessed the serum levels of cytokines (TNF-a, IFN-g, IL-1b, IL-2, IL-4) and the soluble form of ICAM-1 (sICAM-1) as well as the activities of two types of TSH receptor antibodies (TRAb), TSAb and TSBAb, before and after IFN therapy. There were no characteristic changes of cytokines or sICAM-1 during the follow-up period. The transient hypothyroid state may be explained by two possible mechanisms: one may be due to the shift in the balance between the stimulating and blocking types of TRAb, and the other may be due to the complication of destructive thyroiditis that developed during IFN therapy.

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“…Recently, Taniguchi et al [5] and Nagayama et al [8] reported that IFN-a did not induce significant changes in thyroid function in patients with chronic viral hepatitis but no prior history of thyroid dysfunction.…”

Section: Discussionmentioning

confidence: 99%

“…Although most patients who have developed thyroid dysfunction after IFN therapy have had preexisting autoimmune thyroid diseases, IFN therapy, especially IFN-a, also induced thyroid dysfunction in some patients without preexisting thyroid abnormalities [3,[6][7][8]. In addition to IFNinduced autoimmune phenomena, recent in vitro studies [9,10] demonstrated that both IFN-a and IFN-f3 have direct inhibitory effects on thyrocytes, but there are few reports on direct inhibition of IFN-6 on thyroid function in clinical studies.…”

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confidence: 99%

Effect of Interferon-Beta on Thyroid Function in Patients of Chronic Hepatitis C without Preexisting Autoimmune Thyroid Disease.

et al. 1996

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Abstract. The effect of interferon-beta (IFN-fl) on thyroid function was studied in patients with chronic hepatitis who had no preexisting thyroid disease. Eleven patients (9 males and 2 females) aged 20 to 65 years, with a mean age of 47.7 ± 13.5 years, were treated with 6 million units of IFN-fl intravenously every day for 8 weeks. During IFN-13 administration (4th to 8th week of treatment), both serum free thyroxine (FT4) and free triiodothyronine (FT3) concentrations decreased significantly (P<0.0005 and P<0.05, respectively): FT4, 1.37 ± 0.17 to 1.09 ± 0.12 ng/dl, and FT3, 3.71 ± 0.45 to 3.28 ± 0.34 pg/ml. On the other hand, serum TSH increased significantly from a baseline of 1.70 ± 0.82 to 3.34 ± 1.98 jiU/ml during IFN-13 administration (P<0.005). Four to eight weeks after cessation of treatment, the mean serum FT4 concentration was similar to that during IFN-f administration (1.04 ± 0.14 ng/dl), but mean serum FT3 and TSH concentrations returned to pre-treatment levels (FT3, 3.57 ± 0.42 pg/ml and TSH, 1.60 ± 0.84 ,uU/ml). Both reverse T3 and thyroglobulin were essentially unchanged. Tests for anti-thyroglobulin and anti-microsomal antibodies were negative in all the patients. These results indicate that IFN-f3 may inhibit thyroid function in patients without preexisting thyroid disease irrespective of humoral immune responses.

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Exacerbation of Thyroid Autoimmunity by Interferon .ALPHA. Treatment in Patients with Chronic Viral Hepatitis: Our Studies and Review of the Literature.

Cited by 45 publications

References 45 publications

Incidence and Characteristics of Thyroid Dysfunction Following Interferon Therapy in Patients with Chronic Hepatitis C.

Incidence and Characteristics of Thyroid Dysfunction Following Interferon Therapy in Patients with Chronic Hepatitis C.

Graves' Hyperthyroidism Showing Transient Hypothyroidism during Interferon Therapy for Chronic Hepatitis Type C

Effect of Interferon-Beta on Thyroid Function in Patients of Chronic Hepatitis C without Preexisting Autoimmune Thyroid Disease.

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