D-Xylose Test in Enteric Fever, Cirrhosis, and Malabsorptive States
Authors: M. H. Shamma'a, S. A. S. Ghazanfar
Journal: BMJ (1960)

Interest in the physiology of intestinal absorption has increased considerably during the last decade. This has been prompted by the availability of improved tech niques of investigation of the function of the small intestine. It has become possible to demonstrate, categorize, and study the type and extent of deficient absorption in many clinical states. The available evidence emphasizes the multiplicity of factors capable of altering the physiology of the small intestine. These include metabolic disturbances in sprue, alterations in ground substance as seen in Whipple's disease (Puite and Tesluk, 1955), massive resection of the small intestine (Jackson and Linder, 1951), intestinal diverticulosis and fistulae (Baddenoch et al, 1955), neoplastic involvement of the small intestine (Sleisenger et al, 1953), ulcerogenic tumours of the pancreas (Maynard and Point, 1958), and ischaemia of the small-intestine tract (Joske et al., 1958). The present study deals with the state and mechanism of intestinal absorption of carbohydrates in two unre lated conditions?enteric fever and cirrhosis of the liver ?utilizing the D-xylose excretion test. D-Xylose is among the naturally occurring pentoses, chiefly found in plant products. It has a molecular weight of 150. Its structural formula is: CHO-HCOH-HOCH-HCOH-CH2OH It is not normally found in human blood. Like most sugars it is predominantly absorbed from the small intestine, more in the proximal than in the distal part. The transport of sugars across the intestinal mucosa involves more than diffusion. Despite the lower molecular weight of pentoses, which enhances diffusion, they have been shown to be absorbed more slowly than hexoses. Thus, Cori (1925) and McCance and Madders (1930) found the various absorption rates of sugars to be the following: galactose 110, glucose 100, fructose 43, mannose 19, xylose 15, arabinose 9. They also found that above a concentration range of 10-13% the rate of absorption is independent of concentration. It has always been thought that active absorption involves phosphorylation of sugars. This hypothesis has been generally accepted, though direct evidence for it has been lacking. The phosphorylation of D-xylose is still debatable. Sols (1956) maintains that it is not phosphorylated in vitro. His quantitative data indicate that the normal role of mucosal hexokinase is to initiate glycolysis for the tissues' own needs and not for active absorption. The data of Hele (1953) prove the contrary, and Turner (1950) even suggested the probability of a xylokinase in the mucosa of the small intestine. In normal individuals 65% of the xylose is absorbed (Christiansen et al, 1959). It is unaltered by the liver (Fishberg and Friedfeld, 1932). Of the oral dose of 25 g., about 6 g. is excreted in the urine within the first five hours. Benson et al (1957), studying two well nourished subjects with ileostomies, found that no xylose was detected in the ileostomy discharge after the fifth hour and that 10% of the oral dose was excreted in the urine during the next 19 hours. About 50% of the dose appeared to be destroyed by the body. Dom?nguez and Pomerene (1934) employed D-xylose as a renal-function test. Helmer and Fouts (1937) first reported on its use in intestinal absorption. They found no consistent abnormality in absorption of xylose in pernicious anaemia but noted defective absorption in three cases of non-tropical sprue. Fourman (1948) found decreased absorption of D-xylose in three patients with tropical sprue, in two with steatorrhoea, and in two with steatorrhoea due to healed tuberculous mesenteric adenitis. Since then many publications on the subject have appeared (Brien et al, 1952 ; Gardner, 1956 ; Finlay and Wightman, 1958).