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  • Thyrotoxicosis factitia


    Thyrotoxicosis factitia refers to a condition of thyrotoxicosis caused by the ingestion of exogenous thyroid hormone. It can be the result of mistaken ingestion of excess drug, such as levothyroxine, or as a symptom of Munchausen syndrome. It is an uncommon form of hyperthyroidism. Patients present with hyperthyroidism and may be mistaken for Graves’ disease, if TSH receptor positive, or thyroiditis because of absent uptake on a thyroid radionuclide uptake scan due to suppression of thyroid function by exogenous thyroid hormones. Ingestion of thyroid hormone also suppresses thyroglobulin levels helping to differentiate thyrotoxicosis factitia from other causes of hyperthyroidism, in which serum thyroglobulin is elevated. Caution, however, should be exercised in interpreting thyroglobulin results without thyroglobulin antibodies, since thyroglobulin antibodies commonly interfere in thyroglobulin immunoassays causing false positive and negative results which may lead to clinical misdirection. In such cases, increased faecal thyroxine levels in thyrotoxicosis factitia may help differentiate it from other causes of hyperthyroidism.

  • Thyrotoxic periodic paralysis


    Thyrotoxic periodic paralysis (TPP) is a condition featuring attacks of muscle weakness in the presence of hyperthyroidism (overactivity of the thyroid gland). Hypokalemia (a decreased potassium level in the blood) is usually present during attacks. The condition may be life-threatening if weakness of the breathing muscles leads to respiratory failure, or if the low potassium levels lead to cardiac arrhythmias (irregularities in the heart rate). If untreated, it is typically recurrent in nature. The condition has been linked with genetic mutations in genes that code for certain ion channels that transport electrolytes (sodium and potassium) across cell membranes. The main ones are the L-type calcium channel α1-subunit and potassium inward rectifier 2.6; it is therefore classified as a channelopathy. The abnormality in the channel is thought to lead to shifts of potassium into cells, under conditions of high thyroxine (thyroid hormone) levels, usually with an additional precipitant. Treatment of the hypokalemia, followed by correction of the hyperthyroidism, leads to complete resolution of the attacks.

  • Autoimmune thyroiditis


    Autoimmune thyroiditis, (or Chronic Autoimmune thyroiditis), is a chronic disease in which the body interprets the thyroid glands and its hormone products T3, T4 and TSH as threats, therefore producing special antibodies that target the thyroid’s cells, thereby destroying it. It may present with hypothyroidism or hyperthyroidism and with or without a goiter.

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