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In the future, the need to order clindamycin gel 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).

Plasma levels of deoxycorticosterone, deoxycortisol, cortisol and aldosterone are low or absent.

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 clindac online 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.

Symptoms and signs of 21-hydroxylase deficiency in children.

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. There are currently no reliable data on the prevalence of galactosemia in USA populations, and according to generalized literature data, its frequency is approximately 1.16242. The estimated population frequency of heterozygous carriage is 1.300.

Treatment is with glucocorticoids, in combination with mineralocorticoids if necessary, and, for some gender-ambiguous newborn girls, with surgical reconstruction.

Etiology. 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 buy clindac gel. 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.

The salt-losing form causes hyponatremia (sometimes severe), hyperkalemia and hypotension, and virilization.

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. 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 clindamycin galactose are formed during the reactions of intracellular catabolism of glycosaccharides, glycoproteins and glycolipids.

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In healthy people, galactose, under the action of clindamycin gel, is phosphorylated into galactose-1-phosphate, from which, together with UDP-glucose, under the action of the bifunctional enzyme GALT, glucose-1-phosphate and UDP-galactose are formed, which, with the participation of the GALE enzyme, is reversibly reduced to UDP-glucose. and further to glucose-1-phosphate. A part of glucose-1-phosphate under the action of phosphoglucomutase is converted into glucose-6-phosphate, which is actively used in the processes of intracellular metabolism or accumulates in the form of glycogen (Fig. 4)./span>