Hashimoto's thyroiditis

Definition and importance in old age. Hashimoto's thyroiditis is chronic autoimmune (lymphocytic) thyroiditis — the classic organ-specific autoimmune disease, in which lymphocytic infiltration and antibody-mediated destruction of thyroid follicular cells produce progressive gland failure. The most frequent cause of hypothyroidism in old age is autoimmune thyroiditis, followed by earlier thyroid surgery or radiation therapy for previous thyrotoxicosis.

Why it is commoner with ageing — the immunological basis. With ageing there is a decrease in T-suppressor lymphocytes and an increase in autoantibodies. Since many endocrine disorders are autoimmune, these changes amplify the possibility of an older person developing hypoendocrine disease in old age, and there is an increased likelihood of developing autoimmune polyglandular failure syndromes. A caution the textbook adds: ageing is frequently associated with an increased prevalence of thyroid autoantibodies, which may be an expression of age-associated diseases rather than a consequence of the ageing process itself — so a positive antibody in an 80-year-old is not automatically clinically significant.

Pathology. Diffuse lymphocytic and plasma cell infiltration with germinal centre formation, Hürthle (Askanazy) cell change of follicular epithelium, follicular atrophy and fibrosis. Two clinical forms: the goitrous variant with a firm, bosselated, painless gland, and the atrophic variant — commoner in the elderly — with a small, impalpable gland. Antibodies are directed against thyroid peroxidase (anti-TPO, the most sensitive) and thyroglobulin; blocking TSH-receptor antibodies contribute to the atrophic form.

Clinical spectrum. May be euthyroid with goitre or antibodies alone, subclinically hypothyroid, or overtly hypothyroid. An early transient thyrotoxic phase — "Hashitoxicosis" — occurs from destructive hormone release. In older people the presentation is atypical and insidious: memory loss, lethargy, constipation, cold intolerance, fatigue, congestive heart failure, depression and weight gain, all often attributed to old age or other causes. Lack of these symptoms does not rule out hypothyroidism, so a high index of suspicion is needed. Associated laboratory findings include a raised creatine phosphokinase and a normocytic normochromic anaemia which responds to thyroid hormone replacement; there is an increased incidence of pernicious anaemia, though iron deficiency remains the most common anaemia associated with hypothyroidism.

Diagnosis and prognostic value of antibodies. An elevated serum TSH level should be confirmed and supplemented with measurements of serum thyroxine (T4) and with thyroid antibodies. Ultrasound shows a hypoechoic, heterogeneous gland with increased vascularity — useful but not required. In subclinical disease, antithyroid antibodies are useful for improving the prognosis of progression to overt hypothyroidism, but they may not change the management of the patient: progression is generally around 5% per year and greater in those with goitre or thyroid antibodies, or both.

Associations, complications and treatment. Associations: other autoimmune disease — pernicious anaemia, vitiligo, Addison's disease, type 1 diabetes, coeliac disease, rheumatoid arthritis, Sjögren's syndrome — as part of autoimmune polyglandular failure. Complications: overt hypothyroidism and, rarely, myxoedema coma; compressive symptoms from a large goitre; encephalopathy associated with autoimmune thyroiditis (Hashimoto's encephalopathy), a steroid-responsive cause of subacute confusion, seizures and myoclonus that is a genuinely reversible dementia mimic in the elderly; and the important association with primary thyroid lymphoma — lymphoma of the thyroid and undifferentiated cancers occur with increasing frequency in the elderly, so a rapidly enlarging gland in known Hashimoto's demands urgent biopsy. Treatment: levothyroxine for overt disease, started at 25–50 µg daily and increased slowly every six to eight weeks, at a lower maintenance dose than in younger people; no immunosuppression is indicated; euthyroid antibody-positive patients need surveillance only, with annual TSH.

Two current themes are worth a sentence each. (a) Immune checkpoint inhibitor–induced thyroiditis is now a common iatrogenic cause of autoimmune thyroid destruction, and older adults receive an increasing share of immunotherapy: it typically produces a transient thyrotoxic phase within the first weeks followed by permanent hypothyroidism, is managed with levothyroxine without stopping the immunotherapy, and requires thyroid function monitoring before each cycle — it is the modern differential for new autoimmune hypothyroidism in an older cancer patient. (b) Selenium supplementation, long promoted to lower anti-TPO titres, has not been shown to alter progression to overt hypothyroidism or improve quality of life and is not recommended. The wider position — reinforced by the TRUST trial and current guidance — is that antibody positivity in an older adult justifies surveillance, not treatment: it refines the prognosis without changing management until TSH crosses the treatment threshold.