Sugar malabsorption in functional bowel disease: clinical implications.

Fernández-Bañares, F; Esteve-Pardo, M; de Leon, R; Humbert, P; Cabré, E; Llovet, J M; Gassull, M A · Am J Gastroenterol · 1993

case_control · Level III

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Abstract

To investigate the relationship of sugar malabsorption to the development of clinical symptoms in functional bowel disease. Twenty-five consecutive outpatients [five men, 20 women; mean age 38.7 +/- 2.6 (SEM) yr] with functional bowel disease and symptoms suggestive of carbohydrate malabsorption were studied. Twelve healthy subjects [six men, six women; mean age 35.7 +/- 3.7 (SEM) yr] acted as the control group. Sugar malabsorption was assessed by breath-hydrogen test after an oral load of various solutions containing lactose (50 g), fructose (25 g), sorbitol (5 g), fructose plus sorbitol (25 + 5 g), and sucrose (50 g). The severity of symptoms developing after sugar challenge was studied. In addition, the effect on clinical symptoms of a diet free of the offending sugars, compared to a low-fat diet, was assessed. Frequency of sugar malabsorption was high in both patients and controls, with malabsorption of at least one sugar in more than 90% of the subjects. Median symptom scores after both lactose [median 6; interquartile (IQ) range 3-7] and fructose plus sorbitol (median 2; IQ range 0-4) malabsorption were significantly higher than after sucrose load (median 1; IQ range 0-1.5) in functional bowel disease patients (p = 0.001 and p = 0.007, respectively). However, there were no differences in healthy controls. In addition, symptoms score after both lactose and fructose plus sorbitol malabsorption was significantly higher in patients than in control subjects (p = 0.02 and p = 0.008, respectively). On the other hand, H2 production capacity, as measured following lactulose load, was significantly higher in patients than in controls. The clinical symptoms improved in 40% of the evaluated patients after restriction of the offending sugars. These results suggest that sugar malabsorption may be implicated in the development of abdominal distress in at least a subset of patients with functional bowel disease.

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