This chapter assumes a basic knowledge of immunology; readers unfamiliar with this topic can obtain further details about the fundamental processes involved in self/ non- self- discrimination by the immune system elsewhere. The range of thyroid auto immunity is shown in Table 1. The most frequent manifestation is probably the presence of focal thyroiditis, which can be found in around 40% of Caucasian women at autopsy, and is half as frequent in men. Focal thyroiditis is often accompanied by the formation of thyroid antibodies, discussed later, but it is presently unclear whether all examples of focal thyroiditis have a truly autoimmune basis, especially if negative for thyroid anti bodies. Careful longitudinal community studies have shown that individuals with positive thyroid antibodies (and presumably an underlying focal thyroiditis) have an increased risk of developing overt or clinical autoimmune hypothyroidism, which in women might be expected to occur in around 2% per year over a 20- year follow- up period. In men, the risk is threefold greater. Individuals who have a sustained elevated thyroid- stimulating hormone (TSH) but normal free thyroxine (fT4) levels, a state termed subclinical hypothyroidism, have a similar risk of progression to clinical hypothyroidism, and it may be assumed that these patients initially had focal autoimmune thyroiditis which progressed, albeit without the autoimmune response giving rise to detectable thyroid antibodies. When individuals have both subclinical hypothyroidism and positive thyroid antibodies, the relative risk of progression to clinical hypothyroidism is substantially increased, especially for men. Juvenile thyroiditis may be self- limiting.

Table1. The range of thyroid autoimmunity

Postpartum thyroiditis, discussed in detail in Chapter 9.5, arises from subclinical autoimmune hypothyroidism. The under lying autoimmune process is enhanced 3– 6 months postpartum, for reasons which remain obscure, and at this point biochemically or clinically evident thyroid dysfunction occurs, only to remit months later as the postpartum exacerbation subsides. The occurrence of permanent clinical hypothyroidism over sub sequent years in 10– 20% of women presumably results from a continued and worsening autoimmune injury, as found in any type of subclinical hypothyroidism. Like postpartum thyroiditis, silent (or painless) thyroiditis causes a transient disturbance of thyroid function, most often presenting with mild destructive thyrotoxicosis followed by hypothyroidism, and indeed in the early literature, postpartum and silent thyroiditis were not distinguished. Excess iodide is an inciting factor in some cases, and others are due to inadvertent exposure to thyroid hormone (e.g. thyroid tissue contamination of meat products), but in most cases the condition seems to be a spontaneous exacerbation of an underlying autoimmune process and goitre, permanent hypothyroidism, or thyroid antibodies are present in half of such individuals several years after presentation.

The term ‘Hashimoto’s thyroiditis’ is strictly a histological definition, with the features as described next. Clinically, patients present with a painless, lymphocytic goitre of variable size, with or without hypothyroidism, hence the alternative name, goitrous thyroiditis. Thyroid antibodies are strongly positive in almost all cases. Primary myxoedema, or atrophic thyroiditis, presents with clinical hypothyroidism, because the thyroid has usually been severely damaged by the autoimmune process, as the name implies. It seems that there is usually a continuum from one to the other, with fibrosis and follicular destruction gradually dominating in a previously lymphocytic goitre.

At first sight, Graves’ disease appears as a distinct autoimmune disorder, characterized by the presence of stimulating antibodies against the TSH receptor, but it is now clear that such antibodies can also occur in occasional patients with autoimmune hypothyroidism, in whom their effects are masked by a more dominant autoimmune process leading to hypothyroidism. Moreover, up to 20% of Graves’ patients treated successfully with antithyroid drugs develop spontaneous hypothyroidism over the subsequent 20 years, most likely due to supervening destructive auto immunity. In some unusual incidences with patients, fluctuation between hyper- and hypothyroidism occurs over weeks or months, and alterations in the relative levels of TSH- receptor antibodies with stimulating and blocking capabilities may explain this phenomenon. The term ‘Hashitoxicosis’ is used to describe occasional patients with clinical Graves’ disease but a histological picture of Hashimoto’s thyroiditis, again demonstrating the close relationship between these disorders, and their sharing of common pathogen etic features.

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مواضيع ذات صلة

Factors Determining Susceptibility of Autoimmune Thyroid Disease

Pathological Features of Autoimmune Thyroid Disease

Autoimmune lymphoproliferative syndrome

Severe Congenital Neutropenia

Autoimmune type 1 diabetes and immune checkpoint inhibitors

Autoimmune diabetes in adults

Genetic aetiology to initiate islet autoimmunity

Islet autoantibodies as biomarkers

Natural history and staging type 1 diabetes

Treatment of Rheumatoid Arthritis

Juvenile Idiopathic Arthritis

Diagnostic Evaluation of Rheumatoid Arthritis