Interpretation
The most common carbohydrate malabsorption disorder is lactose intolerance.
All infants have the intestinal enzyme mechanism necessary to break the milk sugar disaccharide lactose into its components, glucose and galactose, thereby allowing absorption to occur.
Congenital lactase deficiency is a rare disorder in which lactase levels in the mucosa are low or absent at birth. Symptoms can occur as soon as milk is taken. Stools have a low pH and contain glucose produced by bacteria action on undigested lactose.
Acquired lactase deficiency is suspected with symptoms of flatulence, abdominal discomfort, bloating, or diarrhoea after the consumption of one or two glasses of milk, especially in ethnic groups with a high prevalence of lactose intolerance.
Absent or low intestinal lactase in the neonate, however, cannot be taken as proof of congenital deficiency because lactase is normally the slowest of the oligo-saccharidases to reach normal peak activities in the newborn gut. A definitive diagnosis must be deferred until after maturation of the lactase synthesis system can be expected to have occurred. In the interim, amelioration is dependent on adjustment of dietary composition guided by symptoms.
Reducing substances may be positive in some metabolic disorders such as galactosaemia and fructosuria.
Testing the pH of the stool is useful when querying disaccharide intolerance as significant amounts of organic acids are produced from the unabsorbed sugars which turns the stool pH more acidic.
Antibiotics can alter the intestinal flora and affect acid production.
False-positive reactions due to drugs (salicylates, penicillin, ascorbic acid, nalidixic acid, cephalosporins, and probenecid) may occur.
Faeces may be contaminated with urine, in which case glycosuria will give false-positive results.
Reference Intervals
pH 5.5 – 7.9
Any sugar indicated as being present is considered abnormal.
Test Method
Clintest for sugar, pH indicator paper.
