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Triiodothyronine T3 and thyroxine T4 inhibit the secretion of thyrotropin TSH both hipervuncion and indirectly, by inhibiting the secretion of thyrotropin-releasing hormone TRH.
TSH stimulates the synthesis and secretion of T4 and T3 by the thyroid gland.
T4 is converted to T3 in the liver and many other tissues by the action of T4 monodeiodinases. Some of the T4 and T3 is conjugated with glucuronide and sulfate in the liver, excreted in the bile, and partially hydrolyzed in the intestine; the Hiperfuncikn and T3 formed there may be reabsorbed. Drug interactions can occur at any of these sites. However, screening for hypothyroidism in hospital patients is not effective.
The best current recommendation is to maintain a low threshold for suspecting hypothyroidism, particularly in its more obscure presentations, and to reserve testing for these patients. However, a cost utility analysis using a computer decision model to assess the consequences and costs of thyroid stimulating hormone screening recently came to the conclusion that testing 35 year old hipeffuncion and women, with repeat estimates every five years for 50 years, would be beneficial.
This last estimate may be too high as the 20 year Whickham survey found no evidence of increased mortality or ischaemic heart disease in women with thyroid antibodies or raised thyroid stimulating hormone concentrations. Since raised thyroid stimulating hormone alone is a predictor of overt hypothyroidism, more cases at risk will be ascertained which in turn will alter costs.
Nevertheless, the final conclusion was that screening for hypothyroidism is as favourable as screening for hypertension in the same age group, providing a similar increase in quality adjusted days. It is also important to note that screening based on thyroid stimulating hormone concentrations will of course also turn up subclinical and overt thyrotoxicosis,8 and arguably this is even more important to recognise and treat.
Further hiperuncion based on existing local screening schemes are therefore needed to determine the true place of thyroid stimulating hormone testing for the general population.
At present the benefits remain debatable. One reasonable alternative is the case finding approach, focusing testing on patients visiting their doctors for an unrelated reason; this is particularly effective in women over 40 with non-specific symptoms.
Also, any woman who develops postpartum thyroiditis should be offered annual follow up, as about a quarter of these women will develop overt hypothyroidism within the next five years. Delaying testing until the third week after admission avoids the transient disturbances due to the effects of acute psychiatric illness. Once helper T cells are activated, they induce B cells to secrete thyroid antibodies. Increased serum concentrations of thyroid antibodies are present in up to 10 percent of the general population in the United States5 and in approximately 25 percent of U.
In the third U. National Health and Nutrition Examination Survey of persons 12 years of age or older, high serum concentrations of thyroid antibodies were present in In studies in England, 10 percent of postmenopausal women with high serum thyroid antibody concentrations had subclinical hypothyroidism and 0.
The former are closely associated with overt thyroid dysfunction, and their presence tends to correlate with thyroidal damage and lymphocytic inflammation. Thyroid peroxidase antibodies are complement-fixing and thus directly cytotoxic to thyrocytes,10 but there is limited evidence that this toxic effect is a primary destructive mechanism in autoimmune thyroiditis. Antibodies that block thyrotropin receptors have been reported in up to 10 percent of patients with Hashimoto’s thyroiditis.
Thyroglobulin antibodies are present less frequently, and their role is unclear. Antibodies to colloid antigen, thyroid hormones, and the sodium iodide symporter have also been detected in patients with autoimmune thyroiditis.
N Engl J Med ; The most common cause is chronic autoimmune thyroiditis, which occurs in 3 percent of adults and 10 percent of postmenopausal women It is also common after treatment of hyperthyroidism by surgery or iodine and may result from the use of drugs such as lithium carbonate.
Subclinical hypothyroidism is usually detected during follow-up of patients with a history of thyroid disease or as a result of biochemical screening for nonspecific symptoms, such as tiredness or weight gain.
Whether patients with subclinical hypothyroidism benefit from thyroxine replacement is uncertain. There is some evidence that subclinical hypothyroidism is accompanied by reversible changes in the function of target organs, which are similar to but less marked than those that occur in overt hypothyroidism.
These changes include impaired left ventricular function,26 reduced hearing,27 and increased capillary permeability to protein Clinicians favoring therapy for patients with subclinical hypothyroidism will be most influenced by the knowledge that between 25 and 50 percent of such patients feel better while taking thyroxine39,40 and by the fact that the annual rate of evolution from subclinical to overt hypothyroidism is approximately 5 percent among patients with hyperthyroidism treated with iodine or surgery41,42 and among those with chronic autoimmune thyroiditis In patients over 65 years of age, the latter disorder is associated with a higher risk of overt hypothyroidism 20 percent per year In patients with confirmed subclinical hypothyroidism, it makes sense to prevent the progression to overt hypothyroidism by prescribing thyroxine.
As in patients with overt hypothyroidism, the goal of treatment with thyroxine in patients with subclinical hypothyroidism is to restore the serum thyrotropin concentration to a normal level. If, however, the serum thyrotropin concentration is only slightly elevated e.
Patients with preexisting thyroid autoimmunity are at increased risk for the development of hypothyroidism while receiving amiodarone. Treatment with levothyroxine sodium is indicated in hypothyroid patients, and amiodarone may be continued. The dose of levothyroxine sodium needed to normalize the serum concentration of thyrotropin is often higher than the usual dose, because amiodarone decreases 5′-deiodinase activity in peripheral tissues, thus also decreasing production of T3.
Amiodarone-induced thyrotoxicosis occurs in up to 23 percent of patients receiving amiodarone and is far more prevalent in iodine-deficient regions. Type II amiodarone-induced thyrotoxicosis is a destructive thyroiditis that causes the release of preformed thyroid hormone from the damaged thyroid gland.
Distinguishing between the two forms of amiodarone-induced thyrotoxicosis is difficult, especially since some patients have both types. In patients in the United States, I uptake values are typically low in type I and type II amiodarone-induced thyrotoxicosis. Color-flow Doppler ultrasonography may show hypervascularity in type I disease but reduced blood flow in type II.
Type I amiodarone-induced thyrotoxicosis is best treated with high doses of antithyroid drugs methimazole or propylthiouracilsometimes with the addition of potassium perchlorate to prevent further uptake of iodine by the thyroid. Lithium has also been suggested as therapy for type I disease. Iopanoic acid has recently been reported to be effective in patients with type II amiodarone-induced thyrotoxicosis,62 although less so than corticosteroids,63 and in those with type I disease who require thyroidectomy.
It has a strong affinity for intralysosomal phospholipids, inhibiting their degradation by phospholipases and leading to phospholipidosis and disturbances of lysosomal function.
These inclusion bodies have been found in the lungs, liver, heart, skin, corneal epithelium, and peripheral nerves, which explains the toxic effects in many organs and the proportional relation between toxicity and duration of use and cumulative dosage. These changes do not require further management apart from monitoring with thyroid function tests.
Box 4 gives a brief review of thyroid dysfunction caused by amiodarone, with emphasis on the practical aspects and recent concepts. Tratamiento Continuar amiodarona pero agregar L-tiroxina. There are, however, well-recognized situations in which hypothyroidism is transient.
For example, during the recovery phase of subacute or painless thyroiditis including postpartum thyroiditis ,51 patients may have asymptomatic or mild hypothyroidism for a few weeks. Hypothyroidism caused by chronic autoimmune thyroiditis may remit spontaneously,52 particularly if excessive iodine intake has been implicated The use of iodine-containing antiseptics applied vaginally during labor54 or topically to the skin of newborn infants55 may result in transient hypothyroidism, and the condition may also occur in infants born to mothers with chronic autoimmune thyroiditis because of the transplacental passage of thyrotropin-receptor-blocking antibodies Patients with untreated or inadequately treated Addison’s disease may have somewhat elevated serum thyrotropin concentrations that usually decline to the normal range during glucocorticoid-replacement therapy Hypothyroidism may also be transient after a subtotal thyroidectomy; the common failure to appreciate this possibility has led to unnecessary treatment and a falsely high estimate of the frequency of postoperative thyroid failure.
A low serum thyroxine concentration and a high serum thyrotropin concentration, with or without associated features of mild hypothyroidism, occur in about 30 percent of patients three months after surgery, but by the sixth month the serum thyroxine concentration and usually the serum thyrotropin concentration have returned to normal levels in the majority of such patients A similar pattern of thyroid function may occur after treatment of hyperthyroidism with iodine Permanent hypothyroidism should therefore not be diagnosed before six months have elapsed since surgery or iodine treatment of hyperthyroidism.
Measurement of the serum thyroxine and thyrotropin concentrations at six months will indicate whether continued treatment with a higher dose is necessary in the case of a raised serum thyrotropin concentration or whether the thyroxine should be discontinued in the case of a normal or low thyrotropin concentration ; the patient should be reevaluated in four to six weeks.
El aparato cardiovascular El aparato digestivo El sistema nervioso. Preferiblemente el paciente debe recibir las misma marca durante todo su tratamiento. No usar Hormona tiroidea disecada Combinaciones de hormonas tiroideas Triyodotironina Endocr Pract ;8: It is perhaps surprising that any problems are perceived, other than compliance, with a treatment that has been available in one form or another for over a century. However, the availability of increasingly sensitive assays for thyrotropin1 has led to controversy about the dose of thyroxine needed for replacement therapy and about the safety of long-term suppressive treatment.
Other issues include whether patients with subclinical hypothyroidism defined as an elevated serum thyrotropin concentration but a normal serum thyroxine concentration in an asymptomatic patient should be treated or simply followed, the need for variations in the dose of thyroxine in patients with hypothyroidism, and the recognition of transient thyroid failure N Engl J Med ; Combinations of thyroxine and triiodothyronine are available as either synthetic preparations, such as liotrix, or preparations derived from animal thyroid glands, such as thyroid extract or thyroglobulin.
Patients receiving combination therapy have a supraphysiologic rise in the serum triiodothyronine concentration several hours after taking the combined drugs, which may be associated with troublesome palpitations, and it is not sufficiently recognized that the serum thyroxine concentration should be in the lower part of the normal range, often leading to an inappropriate increase in dose.
For these reasons, combination therapy cannot be recommended. The main advantage of treatment with thyroxine is that the serum concentration of triiodothyronine — formed in extrathyroidal tissue from the ingested thyroxine — is controlled physiologically, which may be of benefit during illness or fasting, when extrathyroidal production of triiodothyronine is usually decreased and the serum concentration is low N Engl J Med ; Before assays for thyrotropin were available, the recommended daily dose of thyroxine for patients with primary hypothyroidism was to microg.
The appropriate dose for an individual patient was largely a matter of clinical judgment, although it was customary to maintain the serum total thyroxine concentration above the normal range as a compensation for the lack of triiodothyronine secretion by the thyroid.
The recommended dose was reduced when serum thyrotropin assays became available and when it was realized that most triiodothyronine is produced by extrathyroidal deiodination of thyroxine. The total daily secretion of thyroxine is related to body mass, but it is not customary to prescribe thyroxine in microgs per kilogram of body weight. In patients under 30 to 40 years of age and in those in whom hypothyroidism has developed rapidly and was detected early e.
Three to four months after the start of treatment, measurement of the serum concentrations of free or total thyroxine and thyrotropin will dictate any need for a minor adjustment in the dose. Patients with hypothyroidism of long duration notice an improvement in well-being two to three weeks after starting treatment.
Reductions in weight and puffiness and increases in the pulse rate and pulse pressure occur early in the treatment, but hoarseness, anemia, and changes in skin and hair may take many months to resolve.
Does it matter whether the serum thyrotropin concentration is suppressed to a level of 0. The secretion of thyrotropin is sensitive to very small changes in serum thyroxine and triiodothyronine concentrations, even within their respective normal ranges,5 but is the pituitary unique in this respect among target organs?
In rats 50 percent of the triiodothyronine occupying nuclear receptors in the anterior pituitary is derived from intrapituitary monodeiodination of thyroxine, whereas in other organs, such as the liver and kidneys, only 20 percent of nuclear triiodothyronine is derived from intracellular thyroxine, with most coming from thyroxine in the circulation6.
If these findings applied to humans, suppression of thyrotropin secretion would not necessarily be accompanied by changes indicative of excessive thyroxine and triiodothyronine in other target organs. As a result of treatment with thyroxine, the combination of a low serum thyrotropin concentration, a normal or raised thyroxine concentration, and a normal triiodothyronine concentration, known as subclinical hyperthyroidism, would therefore be of no clinical importance.
Doses of thyroxine that suppress thyrotropin secretion, however, have more widespread effects, such as increasing the nocturnal heart rate, shortening the systolic time interval, increasing urinary sodium excretion and serum enzyme activities in the liver and muscles, and decreasing the serum cholesterol concentration7,8.
These effects are similar to, but less marked than, those in overt hyperthyroidism. Serum osteocalcin, a marker of bone formation, is increased in patients receiving suppressive doses of thyroxine, presumably as a result of the increase in bone resorption Therefore, a primary concern about overreplacement with thyroxine is its possibly deleterious effect on bone.
Significant decreases in bone mineral density at various sites have been found in some but by no means all studies of pre- and postmenopausal women receiving long-term thyroxine therapy in doses sufficient to lower thyrotropin secretion to a level below the normal range,12,13,14,15,16,17,18,19,20,21,22 but there is no evidence of an increased rate of fracture4, Hence adequate compliance is needed to achieve and maintain euthyroidism.
The sensitive assay for thyroid stimulating hormone has advantages over assays for thyroxine, triiodothyronine, and free thyroxine, and both the free thyroxine index and older versions of the thyroid stimulating hormone radioimmunoassay. The sensitive assay helps to differentiate normal concentrations of thyroid stimulating hormone in euthyroid subjects from low concentrations for example, hypothyroidism secondary to pituitary insufficiency, subclinical hyperthyroidism.
The assay is also independent of changes in concentrations of thyroxine binding globulin, which occur, for example, during pregnancy and hormone replacement therapy.
In the absence of clear evidence of malabsorption for example, with bowel bypass surgery or sprue there is no evidence that malabsorption of thyroxine exists as an isolated entity.
This results in increased free thryoxine concentrations and an increased free thryoxine index but an inappropriately raised thyroid stimulating hormone concentration.