Chapter 21: Autoimmune diseases, Hashimoto’s Thyroiditis, Grave’s disease
There are 1-2% of populations in the UK and the USA has thyroid diseases.
Thyroid autoantibodies are frequently detected in healthy individuals, particularly in women.
More than 2% of elderly people have autoimmune thyroid disease.
The thyroid produces thyroxin and it is needed for body growth and metabolism.
It is also called autoimmune thyroiditis.
A chronic disease characterized by enlargement (goiter) and dense chronic lymphocytic infiltrate in the thyroid tissue and there is hypothyroidism.
The peak is in middle age.
Four times more common in females and in general population approximately 0.5%.
Signs and Symptoms
- In the beginning, the patient may be euthyroid, but with the passage of time patient will have a loss of thyroid tissue and hypothyroidism.
- The patient will have fatigue, cold intolerance, dryness of skin, anorexia, weight gain, and menstrual disturbance, huskiness of voice, mental slowing, and abnormal reflexes.
- There is a week association with HLA. In the UK, HLA DR5 has three times the relative risk.
- There is a loss of colloid in the follicles.
- In early stages, occasional fibrosis, lymphocytic and plasma cells infiltrate is seen.
- In the florid form, lymphocytes are present in follicles and with the presence of germinal centers.
- In the lymphoid aggregate 20% macrophages are seen, while 30% B-L or plasma cells and remainder T-L (with a ratio of CD4: CD8 = up to 4: 1).
Etiology and Pathogenesis
There is an autoimmune phenomenon.
- There are autoantibodies against thyroglobulin.
- Autoantibodies against thyroid peroxidase are found in high titers. This is the enzyme involved in the iodination of thyroglobulin.
- Other autoantibodies are against the thyroid-stimulating hormone receptor.
- There is evidence of T-lymphocytic mediated cytotoxic reaction, involving thyroid antigen. Specific T-Lymphocytes are present but are limited.
The mechanism of injury may be due to :
- Type two hypersensitivity reaction (lysis).
- Cell-mediated reaction.
- TSH level is raised.
- The T4T3 level is low.
Grave‘s disease is characterized clinically by hyperthyroidism and goiter.
Peak age is the third and fourth decades and approximately 0.1-0.5% in the general population.
Male: Female ratio is 1:7.
- Grave’s disease is due to the presence of autoantibodies that stimulate the glandular function resulting in hyperthyroidism.
- Autoantibodies (IgG type) that compete for TSH for binding to TSH-receptor now called TSH receptor autoantibody. This autoantibody blocks the site of the TSH receptor, blocks TSH action, and stimulates the cell through TSH-receptor.
- HLA-DR3 people have a relatively increased risk of four times.
- – Monozygotic twin has disease in 50%.
- – Stress has frequently been blamed as a precipitating factor.
Signs and Symptoms
The patient will have typical clinical features like:
- Palpitation, tachycardia, arrhythmias.
- Heat intolerance.
- Increased appetite.
- weight loss, weakness.
- Proximal myopathy, tremors.
- Pretibial myxedema and thyroid acropachy.
- Elevated T4 & T3.
- Low TSH.
- There is an increase in size and increased vascularity.
- There are hyperplasia and hypertrophy of the gland.
- Lymphocytic infiltrate is less than Hashimoto’s thyroiditis.
- Lymphocytic infiltrate predominantly consists of T-lymphocytes with a ratio of CD4: CD8 = 2:1.
- B-lymphocytes are much less common, approximately 10% of the infiltrate.
- Isotope scan shows diffuse uptake.
- Autoantibodies including those to the TSH-receptor are not used widely for diagnosis.