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Comparative characteristics of biological activity. All children with salt-wasting 21-hydroxylase deficiency require additional mineralocorticoid preparations. Indications for the appointment of mineralocorticoid therapy are. A high level of renin activity in blood plasma with a normal level of K + and the absence of clinical symptoms of salt loss. The dose of fludroxycortisone (Cortinef) is 0.05-0.3 mg/day. Such therapy makes it possible to compensate for the lack of mineralocorticoids, to achieve more rapid suppression of excess ACTH secretion with the use of lower doses of glucocorticoids.

The need for mineralocorticoids is maximum in children of the first year of life and is 0.1-0.3 mg per day. The daily dose is prescribed in three doses (at 7.00-15.00-23.00). Additionally, an excess amount of table salt is introduced into the diet - up to 2 g per day. In the future, the need to continue therapy with mineralocorticoids is based on indicators of plasma renin activity. In older children, the dose of mineralocorticoids is reduced to 0.05-0.15 mg per day. The daily dose is administered in two doses (at 8.00 and 18.00).

The prognosis for life and intelligence, provided timely and adequate treatment is started, is favorable, for reproduction - relatively favorable severe damage to the liver, nervous system, eyes and other organs. Depending on the type of abnormal enzyme, there are three types of galactosemia. Due to the complete absence of the enzyme galactose-1-phosphate-uridyltransferase (GALT), type I galactosemia or classical galactosemia develops. With a decrease in the activity of the GALT enzyme from 5 to 50%, galactosemia of the Los Angeles or Duarte type develops. With changes in the activity of galactokinase (GALA), type II galactosemia occurs.

The frequency of different types of galactosemia varies from 1.667000 to 1.3800. The average frequency of classical type I galactosemia varies from 1.23500 in Ireland and 1.44000 newborns in the UK to 1.101000 in Sweden and 1.667000 in Japan. Galactosemia of the Duarte type and due to systemic GALE deficiency are more common and occur in a population with an average frequency of 1.10000 newborns (1.9200 in Germany, 1.3800 in Australia, 1.23000 in Japan). The population frequency of GALA deficiency is not entirely clear and is approximately estimated as 1.100000 newborns.

Galactosemia is caused by mutations in the structural genes encoding enzymes of the galactose operon. The gene for the cytosolic GALT enzyme is mapped to 9p13, the gene for the microsomal enzyme GALE is mapped to 1p36-p35, and the GALA gene is mapped to 17q24. At present, the presence of at least 10 mutations in the GALE gene, about 20 in the GALA gene, and about 200 in the GALT gene have been confirmed. Metabolism of galactose is normal. Galactose belongs to carbohydrate compounds, is an important source of energy for the cell and serves as a necessary plastic material in the synthesis of glycoproteins, glycolipids and other complex compounds used by the body to form cell membranes, nerve endings, in the processes of myelination of neurons, etc.

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The main source of dietary or exogenous galactose is dairy products containing lactose (a disaccharide of glucose and galactose), and to a lesser extent - vegetables and fruits. Some amounts of endogenous galactoses are formed during the reactions of intracellular catabolism of glycosaccharides, glycoproteins and glycolipids.
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