Worldwide, thyroid dysfunction accounts for between 30 and 40% of the total number of patients who go to the endocrinology department. The prevalence of hyperthyroidism in the general population is between 0.2% and 1.3%.
Thyrotoxicosis is more common in women and affects approximately 2% of women and 0.2% of men. Thyrotoxicosis caused by Graves’ disease occurs mainly between 20 and 40 years of age, while the prevalence of autoimmune forms of thyroiditis that generate excessive synthesis of T3, T4 is higher in smokers.
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Thyrotoxicosis causes
The main causes that generate the excessive synthesis of thyroid hormones T3 and T4 responsible for the onset of clinical manifestations specific to thyrotoxicosis are represented by:
- Graves’ disease
- Only toxica multinodulara
- Solitary toxic adenoma
- TSH-secreting pituitary adenoma, pituitary adenoma
- Gestational hyperthyroidism caused by human chorionic gonadotropin HCG produced by the placenta during pregnancy
- Congenital hyperthyroidism, neonatal Graves’ disease
- Metastatic follicular thyroid carcinoma.
Learn more about thyroid goiter and nodular goiter: diagnosis and treatment
Thyrotoxicosis that is not associated with hyperthyroidism can be due to postpartum thyroiditis, subacute forms of thyroiditis and overdose of hormone replacement treatments in people with arrhythmias, hypothyroidism or who have required thyroidectomy. Infarction of a thyroid adenoma, acute thyroiditis of an infectious cause and that induced by exposure to radiation are less frequent causes of thyrotoxicosis that are not associated with hyperthyroidism.
The main risk factors of thyrotoxicosis include:
- Family history of thyroid disease (especially Graves’ disease)
- Belonging to the female sex
- Pregnancy period
- Pre-existing autoimmune conditions such as type I diabetes, pernicious anemia and Addison’s disease.
Thyrotoxicosis symptoms
With the exception of cervical swelling (thyroid goiter), periorbital edema that associates eyelid retraction and ocular asynergism, conjunctival inflammation and ophthalmoplegia specific to Graves’ disease, the clinical manifestations due to the excess of thyroid hormones are varied and can mislead the cliniciandelaying the establishment of a precise diagnosis due to the associated polymorphism.
- Heart rhythm disturbances represented especially by sinus tachycardia, along with the feeling of permanent fatigue, weight loss and constant irritability can be attributed to periods of prolonged physical and mental stress and the burnout frequently encountered in the current social context.
- Intolerance to heat, hypersweating, trembling of the extremities, unjustified anxiety, muscle weakness, hyperreflexia, hair loss, menstrual cycle irregularities (oligomenorrhea), gynecomastia (in men) are other clinical manifestations due to the excess of thyroid hormones that can be associated by people with thyrotoxicosis.
In severe forms of thyrotoxicosisalso known as thyrotoxic crises, the patient may present:
- Sinus tachycardia that can degenerate with the appearance of atrial fibrillation, especially in patients with pre-existing valvular diseases or coronary disease in an advanced stage of evolution
- Febrile syndrome of non-infectious cause
- State of agitation or temporal-spatial confusion
- Digestive disorders: nausea, vomiting or diarrhea that can be mistakenly attributed to a gastrointestinal pathology
- Impairment of liver function
- Loss of consciousness.
Stress and the activity of thyroid hormones
Exposure of the body to physical and/or mental stress generates a series of chemical and hormonal reactions throughout the body which is part of the so-called “fight or flight” mechanism (fight or flight mode).
This adaptive mechanism is effective for short periods of time, but in the long term it favors the appearance of hormonal imbalances manifested by the hyperproduction of cortisol (known as the stress hormone), hypo or hyper thyroid function with a major impact on all organs and systems of the body.
Other factors that influence the activity of thyroid hormones
Hyperthyroidism in pregnancy it can have several causes, the mild forms being associated in the first trimester of pregnancy with the synthesis of beta HCG which causes an increase in fT4 in the presence of a low TSH.
Tireotoxicoza gestationala it remits spontaneously (disappears by itself) in most cases with the progression of pregnancy, towards weeks 14 and 20, and can sometimes be associated with hyperemesis gravidarum. This transient change in thyroid hormones associated with pregnancy does not require specific treatment with synthetic antithyroid drugs and is differentiated from Graves’ disease by the absence of preconceptional symptoms (absence of goiter, exophthalmos) and the paraclinical changes represented by anti-TRab antibodies.
In certain situations, thyrotoxicosis can be induced by an overdose of hormone replacement therapy such as levothyroxine or the administration of certain antiarrhythmic drugs. Amiodarone is a class III antiarrhythmic administered to patients with ventricular and supraventricular arrhythmias that contains 39% iodine that is stored in the adipose tissue, liver, myocardium, lungs and thyroid gland.
Type I amiodarone affects patients associated with a pre-existing thyroid condition such as nodular goiter or subclinical Basedow Graves’ disease, while type II amiodarone generates thyrotoxicosis in people who do not have an underlying thyroid pathology, by accumulating increased amounts of iodine in approximately 30 months after initiation of antiarrhythmic treatment.
When is consultation with an endocrinologist recommended?
The main manifestations frequently attributed to periods of physical and mental overwork but which must be addressed to the endocrinologist to rule out the existence of an evolving thyrotoxicosis are:
- Unintentional weight loss in the context of a normal or increased appetite
- The feeling of permanent fatigue associated with muscle weakness
- Palpitations.
If these manifestations are neglected, thyrotoxicosis can develop with the appearance of severe complications that associate vital risk for the patient due to cardiac and central nervous system manifestations.
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Diagnosis of thyrotoxicosis
From a paraclinical point of view, hyperthyroidism is diagnosed through laboratory investigations to determine the serum concentrations of TSH, fT4, T4 and T3, these laboratory analyzes being performed at the request of the referring physician.
The etiological diagnosis of thyrotoxicosis is made with the help of thyroid scintigraphy that uses technetium 99 to differentiate focal capture with one or more “warm” thyroid nodules specific to Basedow Graves’ disease from thyrotoxicosis induced by iodine, the administration of replacement thyroid hormones or thyroiditis.
Thyrotoxicosis treatment
Symptomatic treatment to reduce the clinical manifestations associated with thyrotoxicosis, it involves the administration of beta blockers and calcium channel blockers that relieve arrhythmias in patients with underlying cardiovascular diseases.
Etiological management of thyrotoxicosis it is carried out with the help of antithyroid medication, radioactive iodine and surgical treatment, the therapeutic plan recommended to the patient being influenced by:
- The severity of the manifestations
- The dimensions of the thyroid gland
- The patient’s desire to get pregnant in the near future
- Associated comorbidities.
Each of the listed treatment options presents risks and benefits that the attending physician discusses in detail with the patient before initiating the therapy.
Agranulocytosis (decrease in the number of leukocytes) and hepatotoxicity with the risk of evolution towards fulminant hepatic necrosis are the main adverse effects of antithyroid therapy. The use of reactive iodine is contraindicated during pregnancy due to the compound’s teratogenic effects.
Surgical treatment recommended for patients with thyrotoxicosis it can cause accidental damage to the recurrent laryngeal nerve, hypoparathyroidism and intraoperative bleeding depending on the experience of the surgeon, the equipment used and the complexity of the case addressed.
Complications of thyrotoxicosis
Manifested severe thyrotoxicosis (thyrotoxic crisis). through tachycardia, altered mental status, liver failure and hyperpyrexia (high fever) is a medical emergency that usually occurs in elderly patients and is associated with a mortality rate between 8 and 25%. This life-threatening complication is treated by administering intravenous fluids, corticosteroids and beta-blockers under the careful monitoring of the patient by specialized medical personnel.
Other complications of thyrotoxicosis include osteoporosis, Graves’ eye disease, atrial fibrillation, congestive heart failure, and stroke.
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2024-03-05 23:12:19
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