Comparison of venous and capillary blood samples in lactose tolerance testing.
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About 70% of the world's adult population is unable to digest lactose, the sugar found naturally only in milk. This disability leads to gastrointestinal symptoms called lactose intolerance. In Finland, many patients visit health care centres because they are suffering from gastrointestinal symptoms. A few of them are diagnosed as being lactose intolerant. However, a far larger number diagnose themselves as suffering from lactose intolerance. Therefore the diagnostic tests used should be carefully validated and standardized in clinical laboratories throughout the country. The aim of this questionnaire study was to clarify the situation centres with adult patients in Finnish health care and to try to standardize procedures for administering lactose tolerance tests.
The standard lactose tolerance test involves measuring a patient's blood glucose after the ingestion of lactose. If the patient has lactase deficiency and is unable to hydrolyze lactose and absorb its monosaccharides, glucose and galactose, the blood glucose does not usually increase greater than 20 mg/100 ml. Since factors other than the absorption of glucose can cause an increase in the blood glucose of greater than 20 mg/100 ml in a diabetic, this test could be unreliable when it is performed on a diabetic. The present study was performed to determine whether the lactose-ethanol tolerance test could be used to diagnose lactoase deficiency in diabetics. This test involves measuring the blood galactase level, instead of the blood glucose, and the administration of ethyl alcohol to a subject prior to the test to delay the clearance of galactose from the circulation. The results indicate that the standard lactose tolerance test in which the blood glucose is measured is unreliable when performed on insulin-dependent diabetics, but that it can be reliable when performed on non-insulin-dependent diabetics. The lactose-ethanol tolerance test gave results in each type of diabetic which were qualitatively similar to those of nondiabetics. It was concluded that the latter test is a useful screening test for lactase deficiency in diabetics.
Because of the traditional "nonmilking" attitude in Vietnam, a high incidence of lactose malabsorption would be expected in Vietnamese. However, confirming data are not available, and for this reason 31 adult Vietnamese were studied by obtaining diet histories and performing oral lactose tolerance tests. Twenty-three had drunk from one glass of milk a month to three glasses a day as adutls in Vietnam, and eight had noted milk-related symptoms. Since arrival in the United States, 30 had drunk milk and six had experienced symptoms. All 31 adult Vietnamese tested had flat lactose tolerance tests, signifying lactose malabsorption, with 20 subjects having symptoms during or after the tests.
Inability to hydrolyze lactose does not always cause symptoms. The lactose tolerance test commonly used in diagnosis pinpoints the biochemical anomaly but does not establish whether it causes a functional disability. I therefore compared a milk tolerance test (500 ml milk) with the standard lactose tolerance test in 40 healthy adult volunteers for rise in blood sugar. A maximum glucose rise of 9 mg/100 ml or less indicated lactose malabsorption. Only one subject was misclassified by the milk tolerance test when compared with the lactose tolerance test (specificity 91.7%; sensitivity 100%). The test not only reproduces the worst symptoms that the subject is likely to suffer due to usual milk intake, but also accurately identifies the lactose malabsorber, thus yielding more information than the standard lactose tolerance test.
Some formulas designed for premature infants contain glucose polymer (GP) as part of their carbohydrate content. GP tolerance tests and lactose tolerance tests were performed on 11 healthy premature infants at 2 to 3 weeks of age to compare their ability to digest and absorb GP and lactose. Total plasma reducing substances (TPRS), plasma insulin (PI), and plasma glucose were measured 10 minutes before and 30, 60, and 120 minutes after the oral carbohydrate test meal. Lactose and GP stimulated a significant increase in TPRS at 30 and 60 minutes and produced similar glycemic responses. However, GP stimulated PI response whether measured as the area under the PI response curve or as the PI/TPRS ratio. It was concluded that although GP and lactose evoke similar glycemic responses, they differ in their abilities to stimulate insulin secretion. The mechanism controlling this differential insulin response is unknown.
The aim of this study was to continue our previously published work and to compare the different indirect diagnostic methods for hypolactasia with the lactase to sucrase ratio obtained by jejunal biopsy. The following tests were performed in 63 adult patients: the breath hydrogen test, the lactose tolerance test with ethanol (serum galactose measurement after oral lactose load with ethanol), the urinary lactose tolerance test (urinary galactose measurement after oral lactose load with ethanol), and the strip test (like the former but using a special test strip for urinary galactose). Specificities of all these tests were good (96-98%). The 3-h breath hydrogen test was less sensitive (69%) than the other methods (81-94%). The strip test is recommended for the general practitioner for the diagnosis of this common cause of abdominal complaints.
A method has been devised for the analysis of tolerance curves, and tested on data collected for the diagnosis of lactose malabsorption with lactose tolerance tests. Two different models were fitted to over 100 experimental curves; the need to allow small changes over time in the glucose baseline level became evident, indicating that a model allowing a time trend is preferable. The results are briefly discussed and the biological significance of the quantities estimated by the method is discussed.
In order to collect data on (1) the prevalence of lactose malabsorption and (2) the value of indirect diagnostic methods for hypolactasia in diabetics, we compared lactose tolerance tests using serum glucose, serum galactose (after oral ethanol intake) and breath hydrogen excretion as diagnostic cutoff in 144 nondiabetic and 46 diabetic subjects. A good rate of concordance was found for the hydrogen breath test and galactose-dependent lactose tolerance test. The glucose-dependent lactose tolerance test was found to be of satisfactory diagnostic value in nondiabetic subjects and was useless for diagnostic purposes in diabetics. Lactose malabsorption was no more frequent in diabetics than in controls and lactose intolerance was found to be less frequent in the diabetic group. A distinction between hypolactasia and other gastrointestinal disorders in diabetics is possible by ambulatory indirect tests.
BACKGROUND: Non-absorbable carbohydrates are widely used in the therapy of hepatic encephalopathy. It has been argued that their effects depend on intestinal fermentation. In some geographic areas other than Chile up to 27% of healthy inhabitants are not able to increase breath hydrogen after a lactulose load, a parameter of intestinal fermentation of carbohydrate. Lactose has been proposed as an alternative to non-absorbable disaccharides in patients with lactase deficiency. AIM: To investigate intestinal fermentation of lactulose and lactose malabsorption in Chilean patients with liver cirrhosis. PATIENTS AND METHODS: 22 healthy controls and 52 patients with liver cirrhosis (16 with hepatic encephalopathy) were prospectively studied by means of lactulose or lactose hydrogen breath tests and lactose tolerance test. MAIN RESULTS: In the control group, 19% were non-hydrogen excretors after lactulose, meanwhile a significant rise in breath hydrogen concentration was observed in all cirrhotic patients (p < 0.01). Lactose tolerance test was indicative of lactase persistance in 37% of cirrhotics and in 43% of controls (NS). Finally, 41% of cirrhotics and 50% of controls had a normal lactose hydrogen breath test (NS). These results were not significantly modified by the presence of hepatic encephalopathy. CONCLUSION: Our data suggest that a lack in bacterial fermentation is not a cause of lactulose therapy failure in Chilean patients with hepatic encephalopathy. Lactose might be an inappropriate substitute to lactulose treating a significant proportion of patients with this condition in our country.