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Symptoms and signs of hyperthyroidism

Thyrotoxicosis is a condition in which tissues are exposed to high levels of circulating thyroid hormones. The most common cause of thyrotoxicosis is Hyperthyroidism[1], ie excessive thyroid function. Usually in practice, the two terms are often confused.

Etiopathogenesis[edit | edit source]


  • Graves' disease - the most common cause of hyperthyroidism; antibodies against receptors for TSH (TRAK);[2]
  • 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
  • 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[edit | edit source]

It is caused by a 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[3],
  • 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 symptom: weakened convergence of bulbs.[2]

Diagnostics[edit | edit source]

  • 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.[2]

Diferencial diagnosis[edit | edit source]

Treatment[edit | edit source]

  1. Inicial:
    • thyrostatics (block T3 and T4 synthesis) - thiamazole HVLP (Thyrozole), carbimazole or propylthiouracil
    • beta-blockers (hyperkinetic circulation)
  2. Definitive:
    • long-term treatment with thyrostatics
    • (sub)total thyroidectomy (after repeated relapses after discontinuation of thyrostatics)
    • 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[edit | edit source]

  • 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).[3]

Links[edit | edit source]

Related articles[edit | edit source]

External links[edit | edit source]

Reference[edit | edit source]

  1. HOLUB, V. Tyreotoxikóza. Postgraduální medicína [online]. 2003, roč. -, vol. -, s. -, dostupné také z <>. 
  2. a b c MUNTAU, Ania Carolina. Pediatrie. 4. vydání. Praha : Grada, 2009. s. 77-78. ISBN 978-80-247-2525-3
  3. a b LEBL, J, J JANDA a P POHUNEK, et al. Klinická pediatrie. 1. vydání. Galén, 2012. 698 s. s. 187. ISBN 978-80-7262-772-1.

Used literature[edit | edit source]

  • 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]. <>.