Thyrotoxicosis is the state produced by excessive thyroid
hormone. It is not necessarily the same thing as hyperthyroidism, as there are a few things that can cause thyrotoxicosis without hyperthyroidism being present – for example – the administration of excessive thyroxine that may be seen when hypothyroidism
- Affects 2-5% of females and 0.2-03% of men.
- The female : male ratio is 5:1.
- Onset usually occurs between the ages of 20 and 40 in cases of Graves disease, but later in life in cases of nodular thyroid disease.
- 99% of cases are caused by intrinsic thyroid disease, and less than 1% caused by pituitary problems.
- Grave’s disease accounts for 60-80% of cases of thyrotoxicosis.
- Nodular thyroid disease accounts for most of the rest (20-40%).
- Rarer causes include:
- Secondary causes:
- TSH secreting pituitary tumour
- Thyroid hormone resistance
- Gonadotrophin-secreting tumours
This is caused by TSH receptor stimulating antibodies. In monozygotic twins, concordance is 20-50% - so there is some genetic factor involved. In dizygotic twins concordance is 5%. The antibodies are detectable in the blood. The exact cause is unknown, however it is interesting to note that E. Coli and other Gram-negative bacteria contain TSH binding sites. Thus, Grave’s disease may result from some sort of initiating event caused by one of these pathogens in a genetically susceptible individual.
Environment triggers include:
- High iodine intake
Smoking is also a major risk factor in thyroid associated opthalmopathy. Grave’s disease is also closely related to other auto-immune diseases such as myasthaenia gravis and pernicious anaemia. The disease follows a relapse and remission pattern. Up to 40% of patients may have only a single episode. Many patients eventually become hypothyroid.
- There is thyroid hypertrophy and hyperplasia.
- The follicles have a very small colloid, and the follicular cells are columnar.
- There is focal and generalised lymphocytic infiltrate
- Lymph node hyperplasia can occur in the spleen, lymph nodes and thymus.
- The above changes are all reversed by antithyroid drugs.
Clinical features of thyrotoxicosis
These vary depending on the age of the patient and severity of the disease. Occasionally, the symptoms may seem paradoxical, for example:
10% of patients may have weight gain
This is due to the increased appetite caused by the condition, and in 10% of cases the increase in appetite exceeds the effects of increased metabolism
There is an acute presentation of thyrotoxicosis known as thyrotoxic storm
(thyrotoxic crisis). In a similar way to myxedema coma
, this often presents as a result of acute illness, and there may not be any previous history of thyrotoxicosis. It has a 20-30% mortality rate. With this there is:
A marked fever (>38.5’) Seizures Vomiting Diarrhoea Jaundice Death will be caused by arrhythmias, heart failure or hyperthermia.
Treatment should be started as soon as possible – and patients should be given propanolol, antithyroid drugs, potassium
iodide (to reduce vascular flow to the gland) and corticosteroids.
General features of thyrotoxicosis
- Hyperactivity, irritability, altered mood
- Heat intolerance, sweating
- Fatigue, weakness
- Weight loss with increased appetite
- Diarrhoea, steatorrhea
- Loss of libido
- Oligomenorrhoea (infrequent periods)
- Menorrhagia (very heavy periods)
- sinus tachycardia
- atrial fibrillation (particularly in elderly)
- fine tremor
- warm, moist skin
- diffuse pigmentation
- palmar erythema
- muscle weakness and wasting
- eyelid retraction