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Hypothyroidism is a state of hypothyroidism may be due to various causes and final state produced as an insufficient synthesis of thyroid hormones.
Its prevalence is 2% in adult females and 0.1-0.2% in adult men. Congenital hypothyroidism affects 1 in 4000 newborns (NB) may occur by an alteration to any level of the hypothalamic-pituitary-thyroid. Can be classified into:
- Hypothyroidism: It is the most common cause of hypothyroidism. Affects 1-3% of the general population. Represents 95% of all cases of hypothyroidism. It is due to primary involvement of the thyroid gland.
- secondary and tertiary hypothyroidism, represent the remaining 5% of cases. Is due to a pituitary disorder (secondary) or hypothalamic (tertiary). We can refer to it collectively as Central Hypothyroidism.
| What causes primary hypothyroidism occur? |
- chronic autoimmune Hashimoto's thyroiditis, is the most common cause of hypothyroidism in areas without iodine deficiency. It is the most common cause of hypothyroidism in children. It is more common in middle-aged women (40-60 years). 80% have positive antibodies to thyroglobulin and peroxidase. It is associated with autoimmune diseases.
occurs destruction of the gland cells and antibody-mediated. May occur with or without goiter being the latter case the terminal stage of disease that occurs in glandular atrophy.
- iatrogenic hypothyroidism:
- H. Post-thyroidectomy: appears 2-4 weeks after total thyroidectomy and a variable time after subtotal thyroidectomy, appearing mostly in the first year after surgery. Among those who are euthyroid in the first year, approximately 0.5-1% each year becomes hypothyroid.
- H. after treatment with iodine 131 (I-131), most also become hypothyroid in the first year. Among euthyroid annual incidence of hypothyroidism is 0.5-2%.
- H. neck after external radiation: the effect is dose dependent and the phasing.
All these cases present clinically without goiter. Hypothyroidism
- yodoinducido: Both the default as the excess of iodine can cause hypothyroidism:
- The defect of iodine is the most common cause of hypothyroidism and goiter worldwide, affecting about 200 million people.
- Excess iodine can also cause hypothyroidism by inhibiting the organification and synthesis of T3 and T4 (Wolff Chaikoff effect). This is more important in patients with previous thyroid disease: euthyroid Graves Disease, neonatal, autoimmune thyroiditis, treatment with I-131, etc.
- Drugs: Many drugs can interfere with the production of thyroid hormones can act at any level of synthesis (methimazole or methimazole , propylthiouracil, amiodarone , Lithium .) Interfere with its absorption (cholestyramine, iron salts ) or increase your metabolism ( Carbamazepine, Rifampicin, phenobarbital ). All can cause hypothyroidism and goiter.
- Hereditary defects of thyroid hormone synthesis: present with goiter and almost always manifest at birth.
- thyroid agenesis or dysgenesis: is the most common cause of congenital hypothyroidism. No association with goiter.
- Infiltrative Diseases: Hemochromatosis, sarcoidosis, leukemia.
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| What causes produce secondary and tertiary hypothyroidism? |
Secondary hypothyroidism is due to a deficit of TSH their most important causes are: pituitary adenoma (the most common), postpartum pituitary necrosis (Sheehan syndrome), trauma and hypophysitis. The TSH deficiency may be isolated but usually associated with other deficits pituitary.
tertiary hypothyroidism due to a shortfall in production of TRH. You can be the result of hypothalamic dysfunction or adjacent structures or to an alteration in the hypothalamic-pituitary portal system.
| Presentation Forms |
The clinical presentation is variable, depending mainly on age, duration and severity of hormone deficiency.
- Neonatal Hypothyroidism: manifested by persistent physiological jaundice, hoarse cry, constipation, drowsiness, feeding problems. In more severe cases are treated not the entity called Cretinism: short stature, coarse features, prominent tongue, flat nose, lack of hair, dry skin, umbilical hernia, impaired mental development. Hypothyroidism
- Children: linear growth retardation (short stature) and delayed sexual maturation with delayed puberty. Hypothyroidism
- Adult: initially nonspecific symptoms: lethargy, constipation, cold intolerance, stiffness and muscle spasm, menorrhagia ... As it progresses the clinical deficit progresses, impaired intellectual and motor activity, decreased appetite, weight gain, dry skin, hoarse voice ... may end up in the final stage in the clinical flowery Myxedema: Amimi, coarse features, lack of hair, periorbital edema, macroglossia, pallor and coldness of skin.
| How is it diagnosed? |
determination alone most useful is the serum TSH, which is invariably high in all forms of primary hypothyroidism and may be normal or decreased in the pituitary and hypothalamic hypothyroidism.
Falling in total and free T4 is common in all causes of hypothyroidism. The concentration of serum T3 T4 less specific than to confirm the diagnosis since it is affected in cases of systemic diseases in euthyroid patients.
Other biochemical hypothyroidism include hypercholesterolemia, increased LDH, CPK, AST and CEA. They are also frequent findings: abnormal ECG, pernicious anemia and achlorhydria. In central hypothyroidism associated with other hormone deficiencies: Adrenal, FSH, LH and GH. In short:
- primary hypothyroidism: elevated TSH, low free T4.
- Central Hypothyroidism: low free T4, TSH normal or low. Sometimes it can be slightly high due to biologically inactive TSH. Associated with other hormone deficiencies.
To distinguish secondary hypothyroidism tertiary are most useful imaging techniques: MRI brain.
| How is it treated? |
In most patients, the hypothyroidism is permanent and requires lifelong treatment. The goal of treatment is to restore the euthyroid state. If left untreated, is associated with high mortality and morbidity.
treatment of choice is levothyroxine (Dexnon, eutirox, Levothroid) . It is administered orally, is absorbed by 80% and its plasma half-life is 6-7 days. With the administration of one dose per day was obtained constant blood levels of T4 and T3.
The dose should be the one that keeps the TSH within normal limits trying to avoid overdosing and the suppression of TSH may have consequences in some organs such as bone and heart. The initially recommended are:
- In congenital hypothyroidism: 10-15 microg / kg / day.
- :2-4 in children? G / kg / day.
- in adults: 1.6 microg / kg / day.
Patients elders with cardiovascular disease or long-standing hypothyroidism should begin treatment with lower doses (12.5 to 25 microg / day) and gradually increase every 4-6 weeks until adequate. This is due to the risk of these patients to develop arrhythmias or ischemic heart disease. If you suspect the existence of central hypothyroidism, it is first necessary to supplement adrenal axis, because if you start thyroid treatment can trigger acute adrenal insufficiency.
The effectiveness of treatment in primary hypothyroidism by measuring TSH is controlled and maintained within normal ranges. In the secondary and tertiary levels of TSH are not useful for control and then use the free T4 levels should be maintained between the middle and the upper limit of normal.
are needed about 6 weeks for a given dose reaches its full effect so this is the time that must pass to reassess after treatment initiation and dose change is necessary. Once the appropriate dose is reached, control can be spaced by measuring the TSH annually. There are some situations where it is necessary to amend a previously established dose:
- during pregnancy: the need to increase the dose of hormone from the first quarter.
- drugs that interact with the absorption (cholestyramine, ferrous sulfate, sucralfate , aluminum hydroxide) or metabolism. (Anticonvulsants, rifampicin ). Pass is recommended to allow 4-5 hours between administration of the hormone and the drug of first case. Situations that alter
- elimination: renal failure.
- In patients receiving androgen therapy requires fewer doses of hormone.
| Special Considerations |
1. Secondary and tertiary hypothyroidism: Before starting treatment with LT4, if suspected hypothyroidism central, it is first necessary to supplement adrenal axis, because if you start thyroid treatment can trigger acute adrenal insufficiency.
2. Subclinical hypothyroidism, subclinical hypothyroidism is a condition, usually asymptomatic, where we have a serum free T4 within normal limits, with a slightly elevated TSH. It is more common in women with a prevalence in these 7.5-8% according to various studies, while in men the prevalence is 2.8-4.4%. It is more prevalent in patients with Down syndrome, type 1 diabetes mellitus and other autoimmune diseases.
causes that can produce are the same as those produce overt hypothyroidism although most patients have chronic autoimmune thyroiditis. Before the diagnosis is necessary to repeat the determination to confirm the alteration of TSH and in many cases are transient elevations that do not indicate an underactive thyroid.
There is much controversy on the indication of treatment in these patients. Although most are asymptomatic, a proportion of them may have nonspecific symptoms that improve after replacement therapy, on the other hand, treatment would also be indicated to prevent progression to overt hypothyroidism.
As a general rule, most studies treatment recommended in the following cases:
- TSH levels greater than 10-20MU / L.
- peroxidase antibody positive.
- presence of goiter.
- nonspecific symptoms: depression, constipation, fatigue, ...
The treatment is done with Levothyroxine administered in a single daily oral dose, typical doses required are similar for overt hypothyroidism. The aim is to maintain TSH levels within normal limits.
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