The Effect of Hydroxychloroquine Treatment in Hashimoto's Thyroiditis

Hashimoto's thyroiditis is an autoimmune thyroid disease, and when the disease progresses, thyroid function finally declined to hypothyroidism.

There was no medical treatment recommended for patients with Hashimoto's thyroiditis, but currently at euthyroid state. Levothyroxine replacement therapy starts if patients become hypothyroid state.

Hashimoto's thyroiditis is a T-cell mediated autoimmune thyroid disease. The major auto-antigens include thyroid peroxidase (TPO) and thyroglobulin. Anti-TPO antibodies induce antibody-dependent cell-mediated cytotoxicity (ADCC) and cause destruction of thyroid tissues.

Antimalarial agents like hydroxychloroquine have several pharmacologic effects which may be involved in the treatment of rheumatic diseases, but the role of each is not known. These include interaction with sulphydryl groups, interference with enzyme activity (including phospholipase, nicotinamide adenine dinucleotide hydrogen-cytochrome C reductase, cholinesterase, proteases and hydrolases), DNA binding, stabilisation of lysosome membranes, inhibition of prostaglandin formation, inhibition of polymorphonuclear cell chemotaxis and phagocytosis.

This study is to investigate the treatment effect of hydroxychloroquine on autoantibodies and disease progression of Hashimoto's thyroiditis.

Inclusion criteria

• Hashimoto's thyroiditis
• Euthyroid state (free T4 and thyroid-stimulating hormone level within normal limit)
• Never receive immunomodulators or immunosuppressants

Exclusion criteria

• Planned pregnant or already pregnant women
• Renal insufficiency
• Hepatic insufficiency
• Anemia
• Agranulocytosis
• Thrombocytopenia
• Glucose-6-phosphate dehydrogenase deficiency
• Porphyria cutaneous tarda
• Allergy to 4-aminoquinolone