Etiology of Thyrotoxicosis

Etiology of Thyrotoxicosis is a clinical illness caused by an excess of circulating free thyroid hormones thyroxine (3, 5, 3′, 5′-tetrapods-L-thyronine, T4) and/or triiodothyronine (3, 5, 3′-triiodo-L-thyronine, T3). It affects about 1-1.5 percent of the world’s population making it a common occurrence. It affects women 5-10 times more frequently than males. Graves’ disease (GD) is responsible for the vast majority of instances (up to 80%), while it can also be caused by other illnesses such as toxic adenoma (TA), and toxic multinodular goiter (TMNG), and thyroiditis of any etiology. Thyrotoxicosis caused by GD is significantly more common than thyrotoxicosis caused by other causes in iodine-deficient regions.

Etiology of Thyrotoxicosis

Thyrotoxicosis appears to be influenced by genetic factors. Multiple family members are frequently affected by autoimmune thyroid diseases, such as Hashimoto’s hypothyroidism and Graves disease.

Hyperthyroidism has been linked to a number of hereditary diseases, particularly autoimmune thyroid disease. Mutations in the GNAS gene cause McCune-Albright syndrome. The stimulatory G-protein alpha subunit, which is a crucial component of numerous signal transduction pathways, is encoded by this gene. Polyostotic fibrous dysplasia, uneven café-au-lait patches, and early puberty are the classic trio seen in patients. Acromegaly, Cushing syndrome, hyperthyroidism, and facial asymmetry are all possible symptoms of the illness.

Mutations in the TSHR gene, which codes for the TSH receptor protein, have been linked to a variety of thyroid diseases. The following are examples of these disorders:

  • Familial gestational hyperthyroidism
  • One type of nonimmune hyperthyroidism
  • Nongoiterous thyrotoxicosis
  • Somatic mutation in a toxic thyroid adenoma

Hyperthyroidism and hypothyroidism, as well as type 1 diabetes and adrenal insufficiency, are all linked to type II autoimmune polyendocrine syndrome. Patients with persistent mucosal candidiasis may also have an immunological deficit.

Patients with human leukocyte antigen (HLA)-DRw3 and HLA-B89 have an increased risk of autoimmune thyroid illness. Graves disease is thought to be an organ-specific HLA-related impairment in suppressor T-cell activity. Similarly, persons with HLA-Bw35 are more likely to develop subacute painful or granulomatous thyroiditis. Thyroid disorders, like other immunological diseases, are more common in women than in males.

Symptoms of Thyrotoxicosis

  • Nervousness
  • Anxiety
  • Perspiration has increased.
  • Intolerance to heat
  • Hyperactivity
  • Palpitations

Treatment of Thyrotoxicosis

Symptom alleviation is part of the treatment for hyperthyroidism and thyrotoxicosis, but hyperthyroidism also necessitates antithyroid medication, radioactive iodine-131 (131I) therapy (the preferred treatment for hyperthyroidism among US thyroid experts), or thyroidectomy. Antithyroid medicines, on the other hand, are ineffective in cases of thyrotoxicosis in which scintigraphy reveals poor iodine-123 (123I) uptake, such as in patients with subacute thyroiditis, because these cases are caused by the release of preformed thyroid hormone.

If a clinician treats enough hyperthyroid patients, he or she will eventually come across a patient who gets agranulocytosis or hepatitis as a result of the antithyroid drugs. It is critical to discuss these side effects with patients prior to starting therapy; as a result, patients should be given written or verbal instructions to cease taking the medicine and seek medical assistance if they develop a high temperature (>100.5°F) or a severe sore throat.

The American Thyroid Association (ATA) and the American Association of Clinical Endocrinologists developed guidelines for the treatment of hyperthyroidism and other forms of thyrotoxicosis.