Reversible primary hypothyroidism with blocking or stimulating type TSH binding inhibitor immunoglobulin following recombinant interferon-alpha therapy in patients with pre-existing thyroid disorders.
OBJECTIVE
Treatment with recombinant interferon-alpha (rIFN-alpha) may induce autoimmunity. We have evaluated the effect of rIFN-alpha on pre-existing thyroid disease with special reference to changes in TSH receptor antibody.


METHODS
Five patients, who had a history of autoimmune thyroid disease diagnosed between 2 and 16 years earlier (three patients had Graves' disease while two had Hashimoto's thyroiditis), were treated with rIFN-alpha for chronic hepatitis C. Before, during and after rIFN-alpha therapy, we determined thyroid function, antithyroid antibody, thyroid echogenicity and the surface phenotype of the peripheral and intrathyroidal lymphocytes.


RESULTS
Four of the patients developed overt hypothyroidism after 4-7 months of rIFN-alpha therapy, and two of them had a preceding history of low-uptake thyrotoxicosis. Recovery of thyroid function was observed in all four patients. Strongly positive blocking type TSH receptor antibody was detected and an increase in the percentage of CD19 positive cells in the intrathyroidal lymphocytes was also observed in three of the patients even though the goitre size increased in two of them. One of the patients became thyrotoxic later when stimulating type TSH receptor antibody became positive. Another patient suffered from reversible hypothyroidism although stimulating type TSH receptor antibody remained strongly positive throughout the clinical course.


CONCLUSIONS
Our data thus indicated a high incidence of an unusual type of reversible hypothyroidism with TSH receptor antibodies in patients with chronic hepatitis C and pre-existing autoimmune thyroid disease after recombinant interferon-alpha therapy through a mechanism involving both the humoral and cellular immune systems.
Chen
F Q
FQ
Second Department of Internal Medicine, Kyushu University, Fukuoka, Japan.
Okamura
K
K
Sato
K
K
Kuroda
T
T
Mizokami
T
T
Fujikawa
M
M
Tsuji
H
H
Okamura
S
S
Fujishima
M
M
D000328:Adult; D018941:Antigens, CD19 / Q000276:immunology; D001323:Autoantibodies / Q000276:immunology*; D005260:Female; D006111:Graves Disease / Q000150:complications / Q000276:immunology*; D006526:Hepatitis C / Q000150:complications / Q000628:therapy; D006801:Humans; D007037:Hypothyroidism / Q000209:etiology / Q000276:immunology*; D018828:Immunoglobulins, Thyroid-Stimulating; D007370:Interferon Type I / Q000627:therapeutic use*; D008214:Lymphocytes / Q000276:immunology; D008297:Male; D008875:Middle Aged; D011989:Receptors, Thyrotropin / Q000276:immunology*; D011994:Recombinant Proteins; D013961:Thyroid Gland / Q000276:immunology; D013967:Thyroiditis, Autoimmune / Q000150:complications / Q000276:immunology*
D018941:Antigens, CD19; D001323:Autoantibodies; D018828:Immunoglobulins, Thyroid-Stimulating; D007370:Interferon Type I; D011989:Receptors, Thyrotropin; D011994:Recombinant Proteins; C094372:thyrotropin-binding inhibitory immunoglobulin