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Thyroid gland - Hypothyroidism

In This Article

Introduction

Hypothyroidism (aka myxoedema)

This is quite common, and easy to treat. As the symptoms can be non-specific, be on the lookout, particularly in women over 40.
The two main causes are:
  • Primary disease of the thyroid - In the developed world, this can often be autoimmune thyroid disease, or due to damage caused by radioiodine that has been used to treat hyperthyroidism.
  • Iodine deficiency
Very occasionally, the disease may be secondary to pituitary or hypothalamic disorders.
The onset of the disease is gradual, and will be associated with a rise in TSH levels – as the body tries to combat decreasing thyroid hormone output.
The point where TSH levels are above normal, but there are no symptoms yet apparent is known as subclinical hypothyroidism. As the damage continues, TSH levels will rise higher, and free T4 levels will fall.
Once levels of TSH are greater than 10u/L then symptoms will usually be apparent.At this stage, we say the patient has overt or clinical hypothyroidism.
 
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Causes

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Primary

  • Congenital
  • Defects in hormone synthesis can be due to: Iodine deficiency, Antithyroid drugs (e.g. lithium, amiodarone, interferon)

Autoimmune – these are by far the largest cause -Infective
Secondary - Hypopituitarism (which produces isolated TSH deficiency)
Post Surgery - Post irradiation Radioactive iodine therapy External neck irradiation
Other - peripheral resistance to thyroid hormone

 
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Epidemiology

  • Prevalence in the UK is about 1% in women, but only 0.1% in men.
  • Lifetime risk is actually higher – about 9% for women and 1% for men.
  • The mean age of diagnosis is about 60.
  • Prevalence of subclinical hypothyroidism is about 7% of women and 3% of men. About 4% of these people will progress to clinical hyperthyroidism annually. 
  • Congenital hypothyroidism is present in about 1 in 4000 babies, and this has lead to screening programs of neonates.
 
Autoimmune hypothyroidism (atrophic hypothyroidism)
Do NOT confuse this with auto-immune hyperthyroisidm (Grave’s disease)!
  • This is the most common type of hypothyroidism.
  • It is the result of T-cell mediated auto-reactive cytotoxicity against follicular cells.
  • Cytotoxicity just means ‘toxic to cells’ – so in this case, it just means that T-cells are toxic to follicular cells – i.e. they kill them! -This condition is 6x more common in females, and incidence increases with age. It is also often associated with other autoimmune diseases such as pernicious anaemia and other endocrine disorders.
  • Aetiology is unclear, but it is thought that the antibodies may block TSH receptors and that this results in the hypothyroidism. As with most auto-immune diseases, the exact causes are complex and unknown, but it will involve a combination of genetic and environmental factors. In some instances, development of this condition has been associated with a high iodine intake. -
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Pathology

There will usually be massive fibrosis, but not much evidence of lymphocytic infiltrate. (This is different to Hashimoto’s thyroiditis, where the infiltrate is much greater). By the time of diagnosis, often there will be few thyroid follicles remaining. o    

 
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Hashimoto’s Thyroiditis

  • This is also an autoimmune disease. It was the first ever autoimmune disease to be recognised as such.
  • In this disease, the thyroid is again attacked by T-cells. The main difference between this and atrophic hypothyroidism, is that atrophic hypothyroidism does not cause goitre.
  • The condition causes an enlarged thyroid (goitre). The enlargement is due to infiltration of the thyroid with lymphocytes, and resultant fibrosis.
  • The thyroid usually becomes firm and rubbery but this is not always the case – it can be anywhere from soft to hard.
  • It is approximately 15x more common in women, and onset occurs usually in middle age (about 50) -Goitre is often associated with hyperthyroidism, but in these circumstances, this is not the case.
  • You will find very high levels of TPO antibody in the blood. TPO (Thyroid peroxidase) is the enzyme that ionises iodine to I+, ready for release into the colloid. Without this enzyme, there will not be enough I+ released into the colloid to produce sufficient amounts of T3 and T4. Patients with this condition will often have TPO levels of > 1000 U/L.
  • Patients with the condition may be hypothyroid or euthyroid (normal thyroid function). If they are euthyroid, you will only detect the condition with TPO tests and neck examination. Both types of the disease can be treated with thyroxine (T4) therapy, and this will usually shrink the goitre. -Initially, the disease will cause toxicity (Hashi-toxicity) – i.e. it will cause a lot of initial damage, and then after this the patient may become hypothyroid or euthyroid.
  • Pathology There will be massive lymphocytic infiltrate into the thyroid, and there will be varying destruction of tissue. Often there will be no colloid. The remaining cells will have an increased concentration of mitochondria. There will be varying degrees of fibrosis. With thyroxine replacement, the goitre will usually disappear
  • Some people believe that Hashimoto’s disease progresses to atrophic hypothyroidism.
 
Autoimmune