Thyrotoxicosis

Thyrotoxicosis is a condition in which tissues are exposed to high levels of circulating thyroid hormones. The most common cause of thyrotoxicosis is Hyperthyroidism, ie excessive thyroid function. Usually in practice, the two terms are often confused.

Etiopathogenesis
Hyperthyroidism


 * Graves' disease - the most common cause of hyperthyroidism; antibodies against receptors for TSH (TRAK);
 * Hyperfunctional goiter
 * Hyperfunctional thyroid adenoma - very rare
 * Pituitary adenoma secreting TSH - very rare
 * Increased secretion of hCG - hCG and TSH are glycoprotein hormones and are partly similar, so at higher concentrations there may be cross-reactivity with TSH receptors, eg pregnancy (mostly at the end of the 1st trimester), hCG-producing mole hydatidosis, testicular tumor

Other (not included in hyperthyroidism)


 * Thyroiditis - can cause transient thyrotoxicosis due to the disruption of thyroid follicles by inflammation and the release of stored hormones into the blood. Hypothyroidism usually occurs afterwards. Eg: Hashimoto's thyroiditis, subacute granulomatous thyroiditis, subacute lymphocytic thyroiditis


 * Ovarian goiter - ovarian teratoma, producing thyroid hormones


 * Thyreotoxicosis factitia - overdose of thyroid hormones or preparations with iodine (contrast agents, amiodaron)


 * Neonatal thyrotoxicosis can be caused by transplacental immunoglobulin (TSI) transmission from a mother with Graves' disease.

Clinical picture
It is due to the hypermetabolic state and activation of the sympathetic nervous system


 * warm, increased perfusion of the skin, excessive sweating, heat intolerance
 * weight loss, accelerated growth
 * GIT hypermotility and diarrhea
 * tachycardia, palpitations, systolic hypertension, large pressure amplitude
 * tremor, increased irritability
 * thyroid myopathy - weakness of the proximal muscles of the limbs, up to 50% of patients
 * exophthalmos (staring expression of the eyes) - caused by the increase of connective tissue due to autoimmune stimulation ,
 * diffuse goiter
 * nervousness, motor restlessness, concentration disorders, mood swings
 * Graefe's symptom: looking down does not follow the bulbus cap,
 * Stellwag symptom: decreased blinking frequency,
 * Moebi's sympto m: weakened convergence of bulbs.

Diagnostics

 * Increased T3 and fT4 (the free form of thyroxine, is biologically active and responsible for the tissue effects of the hormone),
 * reduced TSH,
 * antibodies (against TSH-receptors (TRAK, TRAb, rTSH-ab), thyroglobulin, thyroid peroxidase),
 * low serum cholesterol
 * Ultrasound of the thyroid gland: volume determination, adenoma diagnosis (+ scintigraphy),
 * bone age.

Diferencial diagnosis

 * Sepsis
 * malignant hyperthermia
 * transfusion reaction
 * adrenal crisis

Treatment

 * 1) Inicial:
 * 2) *thyrostatics (block T3 and T4 synthesis) - HVLP (Thyrozole), carbimazole or propylthiouraci
 * 3) *beta-blockers (hyperkinetic circulation)
 * 4) Definitive:
 * 5) *long-term treatment with thyrostatics
 * 6) *(sub)total thyroidectomy (after repeated relapses after discontinuation of thyrostatics)
 * 7) *radioiodulation of the thyroid gland by radioiodine ( surgical treatment preferred in the USA)

After TTE (total thyroidectomy) or destruction of the gland by radioactive iodine, the patient usually gradually switches to hypothyroidism with a lifelong need for levothyroxine replacement therapy.

Neonatal hyperthyroidoism

 * a rare life-threatening disorder
 * etiology: transplacental transmission of maternal antibodies against the TSH receptor (TRAb, rTSH-ab) or unrecognized Graves-Basedow-type thyrotoxicosis,
 * clinical picture in the fetus: intrauterine growth retardation, fetal tachycardia, acceleration of bone maturation, goiter, exophthalmos,
 * clinical picture in untreated newborn: metabolic disruption, heart failure,
 * therapy: conservative antithyroid treatment, gradual discontinuation within 2-3 months (maternal antibodies disappear from the circulation).

Related articles

 * Graves Basedow disease
 * Hypothyroidism
 * Examination and function of the thyroid gland

Used literature

 * HAVRÁNEK, Jiří: Tyreotoxická krize.
 * KUMAR, Vinay. Robbins basic pathology. 8. vydání. Philadelphia : Saunders/Elsevier, 2007.  ISBN 978-0-8089-2366-4.


 * PASTOR, Jan. Langenbeck's medical web page [online]. [cit. 2010-05-19]. < https://langenbeck.webs.com/ >.