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Paresthesias

♦ Lack of brush-border disaccharidase causes malabsorption of the corresponding disaccharide. A lack of lactase, which splits lactose into glucose and galactose, is common. Lactase deficiency, which goes hand in hand with intolerance to milk and lactose-containing foods, is rarely congenital, but often develops after weaning. There are marked ethnic differences.

♦ Defects of specific mucosal carriers cause specific malabsorption. In Hartnup disease, for example, there is a specific carrier defect ve for certain neutral amino acids; in cystinuria L, for cationic (basic) amino acids and cystine. <D (The uptake of the affected amino acids as di-tin peptides is undisturbed, because the mucosa tes has its own carrier for dipeptides). = ♦ Global defects of mucosal digestion and h, absorption occur in diffuse mucosal diseases, ra such as celiac disease, tropical sprue, Crohn's ^ disease, Whipple's disease, AIDS, infections St (e.g., with Salmonella), radiation enteritis, id and after resection of large portions of the small intestine.

♦ In addition to alcohol (pancreatic insufficiency, chronic liver disease), a number of drugs cause malabsorption: colchicine (inhibits division of crypt cells and disacchari-dases), neomycin and similar antibiotics (inhibit division of crypt cells and disacchari-dases; precipitate bile salts and micellar fatty acids), methotrexate (inhibits folate absorption), cholestyramine (binds bile salts), certain laxatives, biguanides, etc.

♦ Especially in fat absorption, processing within the mucosal cells (formation of chylo-microns) is an important partial step whose disturbance in abetalipoproteinemia (^ p. 247) results in fat malabsorption (^ D). Another cause is lymphatic blockage (lymph-angiectasia, lymphoma, etc.).

♦ Finally, malabsorption naturally occurs if blood flow through the intestine is disturbed (ischemia, e.g., in vasculitis).

The consequences of malabsorption are dependent on the kind of malabsorbed substance:

♦ Malabsorption of proteins (^C) can lead to muscular atrophy and weight loss, while any resulting hypoproteinemia will result in

♦ Malabsorption of carbohydrates in the small intestine (^C) means that some of them are metabolized to short-chain fatty acids and to gases (CO2, H2) resulting in distension and flatulence. If more than 80g/d of carbohydrates fail to be absorbed, osmosis-induced watery diarrhea occurs (^ p. 150).

♦ Malabsorption of fats (^ D) is characterized by fatty stools (steotorrhea) and leads to weight loss from a lack of these high-calorie components of food. Malabsorption of the fat-soluble vitamins A, D, E, and K occurs especially if fat malabsorption is caused by a lack of bile salts or by other reasons of abnormal formation of micelles (^ D). This is because these vitamins can only reach the absorbing mucosa in an uninterrupted lipo-philic milieu for which micelles are essential. If vitamin K deficiency occurs, the glutamyl residues of prothrombin and other blood clotting factors cannot be y-carboxylated in the liver, and thus bleeding may occur. Vitamin D deficiency causes rickets in children and osteomalacia in adults. In vitamin A deficiency hyperkeratosis and night blindness develops.

♦ Malabsorption of the water-soluble vitamin cobalamine (B12) (for causes, see above) and folate (e.g., in global malabsorption or methotrexate administration) leads to macrocytic anemia (^ p. 34), termed pernicious anemia if there is a cobalamine deficiency, to glossitis and aphthous ulcers as well as neurological defects (nerve degeneration) if there is a cobalamine deficiency.

♦ Iron malabsorption (see also p. 38) leads to hypochromic anemia.

of small intestine

Desynchronization of chyme emptying and bile pankreatic secretion secretion

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