Graves’ disease is an autoimmune disease which causes the thyroid to swell and make too much thyroxine.
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Hyper K-Strumin MB 5.08 © Graves’ disease which is followed by a goiter and Graves’ eye ophthalmopathy
Hyper K-Strumin MB 5.08© is available as 1-month dose £23.70 and 3-month dose £48.96 (regulatory therapy).
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Graves’ disease (or Flajani-Basedow-Graves disease)
is an autoimmune disease. It most commonly affects the thyroid, frequently causing it to enlarge to twice its size or more (goiter), become overactive, with related hyperthyroid symptoms such as increased heartbeat, muscle weakness, disturbed sleep, and irritability. It can also affect the eyes, causing bulging eyes (exophthalmos). It affects other systems of the body, including the skin, heart, circulation and nervous system.
It affects up to 2% of the female population, sometimes appears after childbirth, and occurs seven to eight times more often in women than in men. Genetic factors are a major influence accounting for possibly around 80% of the risk Smoking and exposure to second-hand smoke are associated with the eye manifestations, but not the thyroid manifestations.
Diagnosis is usually made on the basis of symptoms, although thyroid hormone tests may be useful, particularly to monitor treatment. It is classified as a type II noncytotoxic hypersensitivity.
Graves’ disease may present clinically with one of these characteristic signs:
- exophthalmos (protuberance of one or both eyes)
- fatigue, weight loss with increased appetite, and other symptoms of hyperthyroidism/thyrotoxicosis
- rapid heart beat
- muscular weakness
Two signs are truly ‘diagnostic’ of Graves’ disease (i.e., not seen in other hyperthyroid conditions): exophthalmos and nonpitting edema (pretibial myxedema). Goitre is an enlarged thyroid gland and is of the diffuse type (i.e.,spread throughout the gland). Diffuse goitre may be seen with other causes of hyperthyroidism, although Graves’ disease is the most common cause of diffuse goitre. A large goitre will be visible to the naked eye, but a small goitre (mild enlargement of the gland) may be detectable only by physical examination. Occasionally, goitre is not clinically detectable, but may be seen only with CT or ultrasound examination of the thyroid.
Another sign of Graves’ disease is hyperthyroidism, i.e., overproduction of the thyroid hormones T3 and T4. Normothyroidism is also seen, and occasionally also hypothyroidism, which may assist in causing goitre (though it is not the cause of the Graves’ disease). Hyperthyroidism in Graves’ disease is confirmed, as with any other cause of hyperthyroidism, by measuring elevated blood levels of free (unbound) T3 and T4.
Other useful laboratory measurements in Graves’ disease include thyroid-stimulating hormone (TSH, usually low in Graves’ disease due to negative feedback from the elevated T3 and T4), and protein-bound iodine (elevated). Thyroid-stimulating antibodies may also be detected serologically.
Biopsy to obtain histiological testing is not normally required but may be obtained if thyroidectomy is performed.
Differentiating two common forms of hyperthyroidism such as Graves’ disease and toxic multinodular goiter is important to determine proper treatment. Measuring TSH-receptor antibodies with the h-TBII assay has been proven efficient and was the most practical approach found in one study