Autoimmune diseases of the thyroid
Autoimmune thyroid diseases are the most common autoimmune disorders and the main thyroid diseases in iodine-sufficient areas. Women are affected 5–10 times more often. Genetic risk (HLA-DR3, CTLA-4) combines with triggers such as iodine excess, pregnancy, smoking and drugs (amiodarone, lithium, interferon-α). The two main forms are opposites: Hashimoto's thyroiditis destroys the gland, Graves' disease stimulates it.
Hashimoto's thyroiditis (chronic lymphocytic thyroiditis)
- Pathogenesis – T-cell-mediated destruction of thyroid follicles (cytotoxic T cells, apoptosis). Histology: lymphocytic infiltrate with germinal centres, Hürthle (oxyphil) cells and fibrosis.
- Antibodies – anti-TPO in more than 90%; anti-thyroglobulin (anti-Tg) less often and less specific
- Clinical course – middle-aged woman, firm, rubbery, painless goitre (or atrophic gland). Slow progression: euthyroid with antibodies → subclinical hypothyroidism (high TSH, normal FT4) → overt hypothyroidism. A short thyrotoxic phase ("hashitoxicosis") can occur early.
- Associations – type 1 diabetes, pernicious anaemia, coeliac disease, vitiligo, Addison's disease
- Diagnosis – high TSH, low FT4, positive anti-TPO; diffusely hypoechoic gland on ultrasound
Treatment: levothyroxine
- Lifelong; full replacement about 1.6 µg/kg/day; start with 25 µg in the elderly and in ischaemic heart disease
- Taken on an empty stomach before breakfast, apart from calcium and iron
- Check TSH 6–8 weeks after each dose change; target TSH within the reference range
- Pregnancy: increase the dose by about 20–30% as soon as pregnancy is confirmed
- If adrenal insufficiency coexists, give hydrocortisone before levothyroxine – otherwise an adrenal crisis can be precipitated
Graves' disease
The most common cause of hyperthyroidism, typically in women aged 20–50. TSH-receptor stimulating antibodies (TRAb/TSI) mimic TSH and drive diffuse hyperplasia, goitre and excess T4 and T3 production.
- Thyrotoxicosis – weight loss, heat intolerance, palpitations or atrial fibrillation, tremor, anxiety, diarrhoea; diffuse soft goitre with a bruit
- Ophthalmopathy (clinically evident in about 25–50%) – orbital fibroblasts produce glycosaminoglycans, fat and extraocular muscles swell → proptosis, lid retraction, periorbital oedema, chemosis, diplopia. Worsened by smoking and radioiodine. Mild: stop smoking, lubricants, selenium; moderate-to-severe active: IV methylprednisolone.
- Pretibial myxoedema – non-pitting, raised "orange-peel" plaques on the shins; uncommon, almost always with eye disease
- Diagnosis – suppressed TSH, high FT4 and/or FT3, positive TRAb; scintigraphy shows diffuse increased uptake
Treatment of Graves' disease
- Beta-blocker (propranolol) for symptoms until euthyroid