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Thyroid eye disease

Graves diseaseĀ isĀ a pathology of autoimmune origin characterized by increased thyroid hormone levels. Thyroid stimulating immunoglobulins(TSIs) bind to the thyrotropin receptors and activate them. The excess hormones increase the thyroid gland size and produce characteristic morphology and manifestations as in graves disease.

Clinical features:

Following are some signs and symptoms associated with Graves Disease:

  • Lethargy and weakness
  • Hot clammy skin; increased sweating; increased risk of nail infection; loss of hairs; swelling around the eyes
  • Backache and risk of fractures
  • Involuntary movements, weakness especially in proximal limbs, easily fatigability, periodic paralysis in some cases
  • Increased heart rate, exertional breathlessness, chest tightness, edema
  • Diarrhea due to increased gut motility
  • Lacrimation, foreign body sensation in the eye, photophobia, ocular pain, exophthalmos, double vision and loss of sight
  • Increased thirst and urination
  • Heat intolerance, weight reduction, uncontrolled diabetes
  • amenorrhea, oligomenorrhea, increased breast mass in males, sterility
  • Irritability, apprehensive and depressed mood, disturbed sleep

Initial investigation:

The best initial test for screening Graves disease is the Ultrasensitive Thyrotropin Assay.

Thyroid hormone levels of free T3 and free T4 are done and are usually above reference range although the asymptomatic disease may show these levels to be well within the range but thyrotropin is decreased.

TSIs are usually positive and a confirmatory test for Graves disease.

Other antibodies which are checked include:

  • thyrotropin receptor-blocking antibodies
  • antithyroid peroxidase antibodies
  • antithyroglobulin antibodies
  • anti sodium iodide symporter antibodies

These antibodies shift the diagnosis in favor of Graves.

Regular LFTs are done in patients on Thioamides to check for liver damage.

Regular CBCs are done to check for signs of infection

Underlying pathology:

The pathophysiology of the disease is that B and T lymphocytes attack the following 4 thyroid antigens:

  • thyroglobulin
  • thyroid peroxidase
  • sodium-iodide symporter
  • thyrotropin receptor

Thyrotropin seems to be the chief autoantigen causing hyperthyroidism. The antibody and cell mediated thyroid antigen specific immune reaction are markedly seen. To test this, thyrotropin receptor antibodies were injected in healthy individuals and passively to the fetus in pregnant females. The resulting pathology in both cases confirmed the claim.

Common treatments:

Goal of treatment is symptomatic relief and reduction of excess hormones. Beta adrenergic blockers are given to decrease the sympathetic overactivity while antithyroid drugs and radioactive iodine help reduce hormone production.