Circulating Viral and Thyroid Antibodies in Subacute Thyroiditis1

Abstract
Seventy-one patients with proven subacute (nonsuppurative) thyroiditis have had determinations of antibody to a variety of viruses during the course of their illnesses. While 58 of these showed some circulating viral antibody, in 26 the antibodies did not change in titer through 4-fold dilutions during the course of illness and thus were not considered “significant.” In 32, the antibodies showed “significant” (at least 4-fold) changes in titer during their illnesses, suggesting recent viral infection. The period of rising titers was usually missed since these patients were not generally seen early in their illnesses, and these changes in titers were usually in the direction of declining titers. The virus antibodies included those to influenza, Coxsackie, adenoviruses, ECHO, and mumps viruses. Coxsackie virus antibodies have most commonly correlated with the course of the illness. However, it is possible that these viral antibodies represent only anamnestic responses to the inflammatory thyroid lesion, and do not represent specific viral infections. The data are equally consistent with the view that any one of a variety of viruses could be an etiological factor in the genesis of subacute thyroiditis. Viral cultures were not attempted. The possibility that auto-immunity plays a role in the pathogenesis of subacute thyroiditis has also been studied. Antithyroid antibodies may appear several weeks after the onset of the illness, only to disappear gradually after several months. The titers are usually low or moderate at their height. In the majority of patients, such antibodies do not appear at all during the course of the disease. These observations suggest that antithyroid antibodies occur as a result of tissue injury secondary to the disease, and are not an etiological factor. Recovery is the general rule, although one patient with proven subacute thyroiditis has passed into a state of chronic thyroiditis with myxedema. It could be that subacute thyroiditis represents a thyroid response to any one of at least a small group of viral agents, rather than to a single virus. However, this remains a theory and requires further proof.

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