Autoimmune thyroiditis — spontaneous disease models — cat: critical comments

Abstract

The recently described model of spontaneous autoimmune thyroiditis (SAT) in cats displays several features that deserve special attention. First, SAT in cats appears to be under strict genetic control and its transmission suggests a recessive pattern of inheritance. Thyroid failure appears early in life, and, at variance with SAT in rats, results in severe and permanent hypothyroidism. Administration of a diet containing excessive iodine precipitates the disease in genetically susceptible cats, a phenomenon similar to that observed in OS chicken and in autoirnmune-prone BBIw rats. This precipitating effect of excessive iodine in feline SAT could be exploited to elucidate the mechanisms leading to the increased incidence of autoimmune thyroiditis after the introduction of iodine supplementation in iodine-deficient populations. Similar to human autoimmune thyroiditis, both microsomal (presumably TPO) and thyroglobulin antibodies are detectable in serum of hypothyroid cats. The evolution of thyroid lesions from early lymphocytic infiltration to late atrophy and fibrosis is also peculiar, and could resemble the pathologic picture of autoimmune atrophic thyroiditis (AAT) in humans. In this regard, several considerations suggest a potential interest of spontaneous feline hypothyroidism (and possibly hyperthyroidism) in elucidating the pathogenesis of human autoimmune diseases. In view of the forthcoming discussion I will focus the attention on two specific points: the pathogenetic role of TSH-receptor antibodies in thyroid autoimmune diseases and the effect of L-thyroxine therapy on thyroid autoimmunity.A variable but consistent percentage of patients with AAT has circulating TSH-receptor antibodies with blocking activity (TSHBAb) (Chiovato et al., 1990). These blocking antibodies inhibit the biological effect of TSH on thyroid cells and contribute to the development of thyroid failure and atrophy. We do not know whether immunity to the TSH-receptor is involved in the pathogenesis of feline SAT, but the atrophic appearance of the thyroid in hypothyroid cats warrants a search for TSH-BAb Analysis of HLA types in Japanese (moue et al., 1993) and Korean (Cho et al., 1993) patients with AAT indicates that TSHBAb positive patients are genetically similar to Graves' patients, whereas TSH-BAb negative patients are similar to those with classical goitrous Hashimoto's thyroiditis. These observations would imply that immunity to the TSH-receptor plays a preponderant role in a subgroup of patients with thyroid autoimmunc disorders and either hypothyroidism or hyperthyroidism (Chiovato et al., 1994). In this regard it is relevant to recall that, while no spontaneous animal model of Graves' disease has been described so far, the existence of a TSH-receptor antibody with growth promoting activity has been reported in cats with toxic nodular goiter (Brown et al., 1992). In view of the above observations one could speculate whether cats are more prone to TSH-R autoimmunity than any other species apart from humans.In the 80' evidence...