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Hyperthyroidism - a clinical syndrome caused by persistent excess of thyroid hormones in the body. There are three pathogenic variant of this syndrome:

1. Hyperproduction of thyroid hormone (hyperthyroidism) thyroid gland produces excess thyroid hormones. This is the most frequent and has the most male masturbation - research scientists important clinical variant of thyrotoxicosis, it is developing with Graves' disease (diffuse toxic goiter), multinodular toxic goiter and some other diseases.

2. Destructive (tireolitichesky) hyperthyroidism develops as a result of the destruction of thyroid follicles and getting into the bloodstream of excess thyroid hormones contained in the colloid and thyrocytes. Such pathogenic variant of thyrotoxicosis develops in the subacute (DeKervena thyroiditis), postpartum, painless (silent) and tsitokinindutsirovannom thyroiditis.

3. Medical thyrotoxicosis develops with an overdose of drugs of thyroid hormones.

In this article I would like to dwell on the diagnosis and treatment of two diseases that occur with the syndrome of persistent thyrotoxicosis and dominant in its etiological structure: in Graves' disease (diffuse toxic goiter) and multinodular toxic goiter.

Graves' disease is an organ-specific autoimmune disease characterized by persistent pathological increase production of thyroid alcohol and potency are not compatible hormones, usually diffusely enlarged thyroid gland, which in 5075% of cases combined with endocrine ophthalmopathy. The pathogenesis of Graves' disease is to develop catalytic antibodies to the receptor-stimulating hormone (TSH), which are responsible for enduring hyperstimulation thyrocytes. Graves' disease is one of the most common autoimmune diseases, the prevalence reaches 0.1% of the population. Sick of predominantly young women, the peak incidence occurs between ages 25 and 40 years. In regions with adequate iodine (for example, in the U.S., UK, Canada, Scandinavian countries), Graves' disease is the most common cause of hyperthyroidism (incidence multinodular toxic goiter is relatively low).

And multi-nodular toxic goiter in most cases of iodine deficiency disease in which persistent abnormal hyperproduction due to the formation of thyroid hormones in thyroid autonomous viagra functioning thyrocytes. If the normal iodine is a disease is quite rare, in regions of iodine deficiency, which include the entire territory of the Russian Federation, as well as much of continental Europe, multinodular toxic goiter competes with Graves' disease in the first place in the etiological structure of the syndrome of hyperthyroidism. It is interesting to note that if the leadership in endocrinology, released in the U.S. and Britain, are beginning to discuss the problem of hyperthyroidism with Graves' disease, and only at the end of this section, we briefly mention a multinodular toxic goiter, the guidelines issued by, for example, Germany starting the chapter on thyrotoxicosis exclusively discuss the functional autonomy of the thyroid gland, the most frequent clinical variant of which is multinodular toxic goiter.

Let us dwell in somewhat more detail on the pathogenesis of functional autonomy of the thyroid gland. As already mentioned, it is iodine deficiency disorders and in fact the outcome of a long, lasting many decades, and morphogenesis of iodine deficiency goiter (Fig. 1). In conditions of iodine deficiency thyroid gland is exposed to the complex incentives that ensure adequate production of thyroid brand viagra hormones in conditions of scarcity main substrate for their synthesis. As a result, the most susceptible individuals is an increase in thyroid gland is formed diffuse euthyroid goiter (stage I). Depending on the severity of iodine deficiency, it can be formed in 1080% of the total population. Individual thyroid cells are more sensitive to these incentive effects, so get preferential growth. Since forming nodular and multinodular euthyroid goiter (stage II). At the next, III stage described compensatory processes begin to acquire pathological significance. In some actively dividing thyrocytes start delayed reparative processes, and therefore the accumulated mutations, among which the most important purchase so-called activators, resulting in daughter cells acquire the ability to autonomously, that is, outside the regulatory effects of thyroid stimulating hormone (TSH), to produce thyroid hormones. The final stage of morphogenesis of the natural iodine deficiency goiter is nodular and multinodular toxic goiter (stage IV). This process takes many decades, and as a consequence of nodular and multinodular toxic goiter is most common in the elderly. According to most experts, one of the most serious light and moderate iodine deficiency is the high incidence of multinodular toxic goiter and nodular in the older age group. According to several population-based studies, the incidence of thyrotoxicosis in a population living in conditions of iodine deficiency in general more, and it is linked with high incidence of multinodular toxic goiter. In addition, as shown in table 1, against the backdrop of the introduction of mass iodine prophylaxis the incidence of thyrotoxicosis in a population is gradually decreasing.