Thyroiditis

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Chapter 560 Thyroiditis

Lymphocytic Thyroiditis (Hashimoto Thyroiditis, Autoimmune Thyroiditis)

Lymphocytic thyroiditis is the most common cause of thyroid disease in children and adolescents and accounts for many of the enlarged thyroids formerly designated “adolescent” or “simple” goiter. It is also the most common cause of acquired hypothyroidism, with or without goiter.

One to 2% of younger school-aged children and 4-6% of adolescents have positive antithyroid antibodies as evidence of autoimmune thyroid disease.

Etiology

This typical organ-specific autoimmune disease is characterized histologically by lymphocytic infiltration of the thyroid. Early in the course of the disease, there may be hyperplasia only; this is followed by infiltration of lymphocytes and plasma cells between the follicles and by atrophy of the follicles. Lymphoid follicle formation with germinal centers is almost always present; the degree of atrophy and fibrosis of the follicles varies from mild to moderate.

Intrathyroidal lymphocyte subsets differ from those in blood. About 60% of infiltrating lymphoid cells are T cells, and about 30% express B-cell markers; the T-cell population is represented by helper (CD4+) and cytotoxic (CD8+) cells. The participation of cellular events in the pathogenesis is clear. Certain HLA haplotypes (HLA-DR4, HLA-DR5) are associated with an increased risk of goiter and thyroiditis, and others (HLA-DR3) are associated with the atrophic variant of thyroiditis.

A variety of different thyroid antigen autoantibodies are also involved. Thyroid antiperoxidase antibodies (TPOAbs; formerly called antimicrosomal antibodies) and antithyroglobulin antibodies are demonstrable in the sera of 90% of children with lymphocytic thyroiditis and in many patients with Graves disease. TPOAbs inhibit enzyme activity and stimulate natural killer cell cytotoxicity. Antithyroglobulin antibodies do not appear to play a role in the autoimmune destruction of the gland. Thyrotropin receptor–blocking antibodies are often present, especially in patients with hypothyroidism, and it is now believed that they are related to the development of hypothyroidism and thyroid atrophy in patients with autoimmune thyroiditis. Antibodies to pendrin, an apical protein on thyroid follicular cells, have been demonstrated in 80% of children with autoimmune thyroiditis.

Clinical Manifestations

The disorder is 2-4 times more common in girls than in boys. It can occur during the first 3 yr of life but becomes sharply more common after 6 yr of age and reaches a peak incidence during adolescence. The most common clinical manifestations are goiter and growth retardation. The goiter can appear insidiously and may be small or large. In most patients, the thyroid is diffusely enlarged, firm, and nontender. In about 30% of patients, the gland is lobular and can seem to be nodular. Most of the affected children are clinically euthyroid and asymptomatic; some may have symptoms of pressure in the neck, including difficulty swallowing and shortness of breath. Some children have clinical signs of hypothyroidism, but others who appear clinically euthyroid have laboratory evidence of hypothyroidism. A few children have manifestations suggesting hyperthyroidism, such as nervousness, irritability, increased sweating, and hyperactivity, but results of laboratory studies are not necessarily those of hyperthyroidism. Occasionally, the disorder coexists with Graves disease. Ophthalmopathy can occur in lymphocytic thyroiditis in the absence of Graves disease.

The clinical course is variable. The goiter might become smaller or might disappear spontaneously, or it might persist unchanged for years while the patient remains euthyroid. Most children who are euthyroid at presentation remain euthyroid, although a percentage of patients acquire hypothyroidism gradually within months or years. In children who initially have mild or subclinical hypothyroidism (elevated serum TSH, normal free T4 level), over several years about 50% revert to euthyroidism, about 50% continue to have subclinical hypothyroidism, and a few develop overt hypothyroidism. Thyroiditis is the cause of most cases of nongoitrous (atrophic) hypothyroidism.

Familial clusters of lymphocytic thyroiditis are common; the incidence in siblings or parents of affected children may be as high as 25%. Autoantibodies to thyroglobulin and thyroid peroxidase in these families appear to be inherited in an autosomal dominant fashion, with reduced penetrance in males. The concurrence within families of patients with lymphocytic thyroiditis, “idiopathic” hypothyroidism, and Graves disease provides cogent evidence for a basic relationship among these 3 conditions.

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