Autoimmune thyroiditis includes a spectrum of diseases that are distinguished for their clinical course, the degree of thyroid dysfunction, and the changes of thyroid size. All these variants recognize an immune- mediated pathogenesis and usually present with high titres of circulating antithyroid antibodies. As in most organ- specific autoimmune reactions, the aetiology of autoimmune thyroiditis is still unknown but is somehow linked to genetic and environmental factors, and is influenced by the gender and the age.
Chronic Thyroiditis
Chronic thyroiditis is the most common among the autoimmune thyroiditis. Historically, two clinical variants of the disease are de scribed. A goitrous variant (Hashimoto’s thyroiditis), characterized by heavy lymphocytic infiltration and thyroid enlargement, and an atrophic variant (primary myxoedema) with progressive fibrosis and reduction of thyroid size. In clinical practice, a clear distinction between the two forms is not always possible. In the initial stage of the disease the two variants commonly do not present distinctive features. Moreover, atrophy may be a destructive end result of goitrous thyroiditis with the thyroid gland showing near complete replacement with fibrosis. When overt hypothyroidism has occurred, thyroid volume shows a unimodal distribution, with thyroid atrophy and goitre being extremes within the distribution. Overall, these observations suggest that the two variants do not represent separate disorders.
Thyroid failure usually develops very slowly and, as thyroid function fades, the resulting increase in serum thyroid- stimulating hormone (TSH) limits the decline in thyroid secretion. Thus overt hypothyroidism is commonly preceded by a variable period of time in which elevated TSH is the only hormonal abnormality (subclinical hypothyroidism). The transition from euthyroidism to hypothyroidism may pass unrecognized and initial symptoms may be attributed to ageing, menopause, or other chronic concomitant diseases. Thus, it is not uncommon that chronic thyroiditis is diagnosed when clinical manifestations of thyroid failure become severe or complications of hypothyroidism have occurred. The circumstances leading to early diagnosis of the disease include family history for autoimmune thyroid diseases, appearance of goitre, blood testing for screening of autoimmune diseases in patients with polyglandular autoimmunity, routine diagnostic protocols for patients with menstrual dysfunction, or hyperlipidaemia.
Occasionally hypothyroidism may be due to TSH- receptor blocking antibodies preventing thyroid cell stimulation by TSH. TSH- receptor blocking antibodies are more frequent in atrophic thyroiditis than in goitrous thyroiditis. Hypothyroidism may be reversible if the TSH- receptor blocking antibody titre declines and enough thyroid tissue remains for thyroid hormone synthesis. Graves’ hyperthyroidism may develop in hypothyroid patients with chronic thyroiditis because of a change in the nature of TSH- receptor antibodies from blocking to stimulating.
In some instances, the disease may be preceded by a transient phase of thyrotoxicosis (hashitoxicosis) due to the discharge of pre formed thyroid hormones, as a result of an unusually intense inflammatory process. The gland is tender and sometimes painful, resembling subacute thyroiditis. Hypothyroidism usually develops in a short time and may be permanent, especially in patients with elevated thyroid peroxidase antibody.
Features of thyroid- associated ophthalmopathy may occur in patients with chronic thyroiditis and hypothyroidism. This condition is termed ‘hypothyroid Graves’ disease’ and may be the endstage of Graves’ disease after spontaneous remission of hyperthyroidism or may represent a distinct entity with pathogenetic mechanisms common to Graves’ disease, involving thyroid- stimulating antibody.
Focal thyroiditis is characterized by spotty collections of mono nuclear cells within thyroid tissue, and minimal changes in follicular epithelium or stromal fibrosis. Most patients with focal thyroiditis are euthyroid and only 10– 20% have subclinical hypothyroidism. The disease may be suspected at ultrasound examination in patients with circulating thyroid autoantibodies, or may be a histological occurrence in surgical or autopsy specimens. In the presence of circulating thyroid autoantibodies, focal thyroiditis may represent the earliest stage of chronic autoimmune thyroiditis, whereas the clinical significance of non- specific isolated lymphocytic infiltration in patients without circulating autoantibodies has still to be clarified.
Juvenile thyroiditis (autoimmune thyroiditis in childhood and adolescence) is described as a separate entity because follicular oxyphilia is usually mild or absent, goitre is soft, and thyroid anti body titres are not as high as in adults. Fine- needle aspiration biopsy is sometimes required to establish the diagnosis. Spontaneous resolution is relatively common, but hypothyroidism may develop during the course of the disease.
Postpartum Thyroiditis
Pregnancy is known to influence the clinical course of various auto immune disorders, including autoimmune thyroid disease. Typically, amelioration during pregnancy is followed by aggravation after de livery. This phenomenon is thought to depend on the physiological need of inhibiting maternal immune reactions that might cause rejection of the fetus. Thus, thyroid peroxidase antibodies, thyroglobulin antibodies, and TSH- receptor antibody titres decrease or may even disappear during pregnancy. Following delivery, a rebound of auto immune processes occurs and may result in destructive thyroiditis with release of preformed thyroid hormones and transient thyrotoxicosis, followed by a transient hypothyroid phase. Persistent hypo thyroidism may develop in a minority of women. This clinical entity is named postpartum thyroiditis and occurs in 5– 9% of unselected postpartum women.
Graves’ Disease Spontaneous hypothyroidism may develop during the course of Graves’ disease whenever destructive processes of thyroiditis pre dominate over thyroid- stimulating events (burnt out Graves’ dis ease). This may occur after long- term remission of hyperthyroidism associated with disappearance of TSH- receptor stimulating anti bodies, or following prolonged therapy with antithyroid drugs. TSH- receptor blocking antibodies may also appear and neutralize TSH- receptor stimulating antibodies, leading to hypothyroidism.
