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Graves’ disease is caused due to an overactive thyroid gland commonly due to an autoimmune condition.
The thyroid gland here is the target tissue that is attacked by the body’s own defence cells – the B and T lymphocytes. These cells produce antibodies against the thyroid proteins and receptors that stimulate the gland to secrete increased amounts of the thyroid hormones like thyroxine (T4) and triiodothyronine (T3).
Diagnosis of Graves’ disease may be made by estimating the various biochemical and hormonal patterns in blood as well as by laboratory investigations.
Diagnosis of Graves’ disease may involve family history, physical examination, blood examination and so forth. 1-6
History of similar conditions may be found in the family since there seems to be a genetic link between Graves’ disease causation. Often the patient or his or her family members may have other autoimmune disorders like type 1 diabetes mellitus, rheumatoid arthritis or pernicious anemia
Patient is more often than not a female between ages 20 to 40. This is the most common age that is affected. Women are five to ten times more likely to get Graves’ disease than men.
Physical examination shows characteristic signs of hyperthyroidism, ophthalmopathy or eye affliction and skin conditions associated with hyperthyroidism.
Blood examination shows that there is a low Thyroid Stimulating Hormone (TSH) level. This hormone normally stimulates the thyroid to produce thyroid hormones. In addition, normally when the thyroid gland secretes the hormones, the levels of TSH subside to reduce further stimulation of the thyroid gland.
A low or suppressed TSH must be accompanied by a high level of free thyroxine (FT4) level to confirm hyperthyroidism. In around 10% individuals there may be an increased total or free T3 level along with a normal FT4 and suppressed TSH level. This latter condition is called “T3 toxicosis.”
Blood may be assessed to measure the levels of TSH receptor antibody. Since Graves’ disease is an autoimmune disease, the B and T lymphocytes are found to secrete antibodies against the TSH receptor.
When activated by binding of these antibodies this receptor stimulates the thyroid gland to produce T3 and T4. Thus a high level of TSH receptor antibody helps to confirm Graves’ disease
Other antibodies like those to thyroglobulin and thyroid peroxidase may be present in blood but these are not diagnostic of Graves’ disease.
Confirmation of Graves’ disease is made by an increased 24-hour radioiodine uptake (RAIU). Here the patient is given radioactive iodine preparations and subjected to special scans.
The scans reveal areas of the thyroid gland that are most active and produce maximum T3 and T4. The scans may also reveal thyroid cancers, tumors or nodules. The high uptake areas are termed “hot” and the low uptake areas are termed “cold”.
An ultrasonography is recommended in some individuals. This helps in detection of cycts, tumors and nodules of the thyroid gland.
If a nodule or cyst is detected the next step is usually a fine-needle aspiration biopsy to confirm if there is cancer.
In patients with Graves’ ophthalmopathy or eye condition a CT or MRI scanning of the eye balls shows swelling of the eye muscles and excess fat deposits behind the eyeballs.
Patients with a diffuse, patchy uptake with some hot and some cold spots over the thyroid along with elevated, circulating TSH receptor antibody have a confirmed diagnosis of Graves’ disease.
Elderly patients with Graves’ disease may also have lower radioiodine uptake since there may be previous presence of a multinodular goitre.
Routine blood test shows anemia and a low white blood cell count and low platelets. There may be a higher level of lymphocytes and monocytes in some patients.
Routine blood biochemistry shows:
The liver function tests may be deranged if there are drugs that are causing liver toxicity along with clinical features of hyperthyroidism.
While diagnosis Graves’ disease other conditions that may have similar symptoms should be ruled out. These include: