Hashimoto's Disease

Hashimoto's thyroiditis is named after the first doctor who described the condition, Dr. Hakaru Hashimoto, in 1912. It is part of the spectrum of autoimmune disease. It is the commonest cause of goitrous hypothyroidism in non-iodine deficient areas. However, there is also an atrophic form of autoimmune thyroiditis (Ord's thyroiditis) which is more common in Europe.

In this condition typically there is aggressive destruction of thyroid cells by various cell- and antibody-mediated immune processes (in contrast to the stimulatory effect seen in Graves' disease). It is not yet understood why this occurs.

• Antibodies binding to and blocking the thyroid-stimulating hormone (TSH) receptor have been described and may contribute to further impairment in thyroid function.¹
• The result is inadequate thyroid hormone production and secretion, although, initially both preformed thyroxine (T4) and triiodothyronine (T3) may "leak" into the circulation from damaged cells.
• The goitrous form (rather than atrophic) is associated with HLA-DR5.

• The true incidence of Hashimoto's thyroiditis is unknown, but is approximately the same as Graves' disease - 0.3 - 1.5 cases per 1,000 population per year.² It is probably under-diagnosed and its frequency seems to be increasing.
• The disease is 15 - 20 times as frequent in women as in men.
• It occurs especially during the decades from 30 to 50, but may be seen in any age group, including children.^3,4

• The thyroid gland may enlarge rapidly:
  • Occasionally it is associated with dyspnoea or dysphagia from pressure on structures in the neck, or with mild pain and tenderness.
  • Rarely, pain is persistent and unresponsive to medical treatment and requires medical therapy or surgery.
  • The goitre of Hashimoto's thyroiditis may remain unchanged for decades, but usually it gradually increases in size.
  • Occasionally the course is marked by symptoms of mild thyrotoxicosis, especially during the early phase of the disease.
• Symptoms and signs of hypothyroidism may be present in 20% of patients when first seen, or commonly develop over a period of several years. These may include:
  • Fatigue, constipation, dry skin and weight gain
  • Cold intolerance
  • Slowed movement and loss of energy
  • Decreased sweating
  • Mild nerve deafness
  • Peripheral neuropathy
  • Menstrual irregularities, typically menorrhagia
  • Depression, dementia and memory loss
  • Hair loss from an autoimmune process
• Eventually thyroid atrophy and myxoedema may occur.

Hashimoto thyroiditis is a histological diagnosis. The thyroid gland shows diffuse lymphocytic and plasma cell infiltration with formation of lymphoid follicles from follicular hyperplasia and damage to the follicular basement membrane. Atrophy of the thyroid parenchyma is usually evident. Thyroid autoantibodies may also be seen.

• Thyroid stimulating hormone (TSH) levels; this is a sensitive test of thyroid function. Levels are usually raised in hypothyroidism due to Hashimoto thyroiditis (but also in primary hypothyroidism of any cause).
• Thyroid autoantibodies - anti-TPO and also anti-Tg antibodies. However, 10-15% of patients with Hashimoto thyroiditis may be antibody negative.
• Thyroid ultrasound - usually not necessary in diagnosing Hashimoto thyroiditis, but it is useful to assess thyroid size, echotexture, and, most importantly, in assessing for the presence of thyroid nodules.
• Radioactive iodine uptake and scan is used to classify a nodule as hot or cold. A cold thyroid nodule would indicate a higher risk for malignancy and would need a fine-needle aspiration biopsy.

Other studies are only performed to evaluate complications of primary hypothyroidism when indicated.

Hashimoto's thyroiditis and hypothyroidism are associated with other autoimmune conditions:

• Addison's disease
• Diabetes mellitus
• Hypogonadism
• Hypoparathyroidism
• Pernicious anaemia
• Alopecia areata, totalis, and universalis
• Chronic active hepatitis⁵
• Polymyalgia rheumatica and giant cell arteritis
• Primary biliary cirrhosis
• Rheumatoid arthritis, Sjögren syndrome, Systemic lupus erythematosus
• Systemic sclerosis (scleroderma)
• Vitiligo⁶

Although chronic inflammation, leading to neoplastic transformation, is a well-established clinical phenomenon, the link between Hashimoto’s thyroiditis and thyroid cancer remains controversial.⁷ There have been reports of patients with Hashimoto’s thyroiditis being three times more likely to have thyroid cancer.⁸

Pharmacological

• Thyroid hormone replacement - orally administered levothyroxine sodium, usually for life.
• The dose should be titrated to the individual patient's needs. The aim is to restore a clinically and biochemically euthyroid state.
• Patients who are older than 50 years (and younger patients with cardiac disease) should be started on a low dose of 25 mcg (0.025 mg) per day.⁹ Their clinical and biochemical state is then re-examined in 6-8 weeks.

Surgical

Indications for surgery include:

• A large goitre with obstructive symptoms e.g. dysphagia or stridor
• Presence of a malignant nodule
• Presence of a lymphoma diagnosed on fine-needle aspiration
• Cosmetic reasons for unsightly, large goitres

• Over-replacement with thyroxine causing accelerated bone loss or increased heart rate.
• Myxoedema coma (due to extreme hypothyroidism). Untreated this has a poor prognosis and a high mortality rate (around 60%).

With early diagnosis and levothyroxine replacement therapy, the prognosis is excellent and patients lead a normal life.