Disaccharidase deficiency

The selection disaccharidase deficiency as one of the defeat of the small intestine is dictated by the following considerations:
1. The existence of a significant number of patients with clinical symptoms associated with the violation of hydrolysis of disaccharides, and the most frequently milk sugar (lactose fresh milk).
2. The absence of these patients histopathological changes of the mucous membrane of the small intestine according to light microscopy.
3. Marked reduction disaccharidase activity in the determination of one (often lactase) or more enzymes in the homogenate of the mucous membrane of the small intestine and flat blood sugar curve with a load corresponding carbohydrate.
Therefore, under disaccharidase deficiency should understand a number of clinical manifestations associated with the violation of hydrolysis of disaccharides in the absence of histopathological changes in the mucous membrane of the small intestine.
The etiology and pathogenesis. There are congenital and acquired disaccharidase deficiency. The first is related to a congenital defect in the mucous membrane, which violates the synthesis of enzymes. In such cases, the carbohydrate intolerance is manifested in the form of dyspepsia from early childhood. Acquired disaccharidase deficiency occurs as a result of violations complex and still insufficiently studied biochemism in cells associated with the formation of disaccharides. There are indications (Berndt et al., 1969), according to which violation of the hydrolysis of carbohydrates (disaccharides) associated with the disease of microvilli. According to this view disaccharidase deficiency should be considered as pathology wall digestion (A. M. Ugolev, 1967). Along with this Hartman (1968), conducting research in these patients the surface of the mucous membrane of the small intestine with the use of electronic microscope, did not reveal changes of microvilli.
The clinical picture. The diagnosis. Symptoms disaccharidase deficiency is largely dependent on the meals containing the disaccharides (one or more)that are not hydrolyzed in the small intestine, most often it is fresh milk (lactase). Relatively quickly after taking such food (watch!) there is a malaise, feeling of heaviness in the abdomen, bloating it, belching, then attaches diarrhea. The chair is abundant, sour reaction, frothy. Sole and Mokry (1966) described 1235 in cases of intolerance to milk, of which a significant number of patients expected disaccharidase deficiency.
In addition to these clinical, to establish reliable primary disaccharidase deficiency should ensure that no histopathological changes in the small intestine (aspiration biopsy). Confirmation of this disease is the absence or substantial reduction of growth glycemic curve after load the appropriate carbohydrate and reduction in the enzymatic activity of the mucous membrane of the small intestine, obtained by biopsy.
Treatment. The most effective method of treatment disaccharidase deficiency is to exclude from dietary intake of those carbohydrates that there is intolerance. Most often this refers milk sugar (fresh milk). In the literature there are data on the treatment disaccharidase deficiency of plant enzymes (Berndt et al., 1969)splitting carbohydrates (substitution therapy). Some clinical effect in nerezko expressed disaccharidase deficiency have sulfa drugs (sulgin, ftalazol, etazol on 1,0 four times a day) due to the suppression of fermenting bacteria and certain decrease motor activity of the small intestine.