1155
BREATH HYDROGEN AS A DIAGNOSTIC
We have tested a simple method for the collection of exhaled H2 in the clinical situation.9 After an oral lactose load we compared the rise in breath H2 concentration with symptoms, maximum rise in bloodglucose, and, in patients requiring jejunal biopsy, with mucosal lactase activity.
METHOD FOR HYPOLACTASIA DAVID J. A. JENKINS ALVIN NEWMAN * LAURENCE M. BLENDIS
GEOFFREY METZ TIMOTHY J. PETERS
Department of Gastroenterology and Medical Research Council Gastroenterology Unit, Central Middlesex
Hospital,
and
Royal Postgraduate
Medical
Patients and Methods
School,
Twenty-five consecutive patients investigated in the
London
unit either for diarrhoea or abdominal symptoms of unknown cause were given 50 g. of lactose in 200 ml. of water by mouth. Any gastrointestinal symptoms such as borborygmi, excessive flatus, pain, discomfort, or diarrhoea were recorded. Samples of endexpiratory alveolar air from a single breath using a modified Haldane-Priestley tubewere collected every 30 minutes, and the H2 concentration was measured by gas chromatography. The results, expressed as change in H2 concentration at 120 minutes compared with fasting level, were compared with the maximum rise in bloodglucose during that period. Jejunal biopsy was done in patients with specific indications, part of the tissue being used for routine histology and part for assay of lactase activity. Disaccharidase activities were assayed independently by a modification 11 of the technique of Dahlqvist.12 Results were expressed as nmoles substrate hydrolysed per minute per mg. protein.13 In these cases the mucosal lactase activity was compared with the other variables being studied. The criterion for hypolactasia used in the study was a mucosal lactase activity of less than 100 milliunits per mg. protein. In the patients who did not have a biopsy, a maximum rise in blood-glucose of 20 mg. per 100 ml. or more was considered normal.
gastroenterology
(H2), collected by endexpiratory sampling, was measured in twenty-five patients with abdominal symptoms or diarrhœa after ingesting 50 g. of lactose. This was compared with established tests of hypolactasia. Fifteen patients with a blood-glucose rise of more Sum ary
Breath hydrogen
than 20 mg. per 100 ml. had less than 4 parts per million (p.p.m.) rise in breath H2 at 2 hours. In contrast, ten patients with blood-glucose rises of less than 20 mg. per 100 ml. had more than a 20 p.p.m. H2 rise (mean 85·8 p.p.m.±S.D. 44·3) at 2 hours. Similarly, two patients with normal jejunal lactase activity had no significant H2 production, whereas six patients with hypolactasia had more than a 20 p.p.m. rise in H2. Symptoms related to milk or lactose ingestion were found to be unreliable. End-expiratory sampling of breath H2 would seem to be a simple, non-invasive, and accurate method of diagnosing hypolactasia, which is also very acceptable to patients. This should make it a valuable tool both in diagnostic gastroenterology and in epidemiological surveys.
Results
Introduction SINCE lactose malabsorption is common in adultsi a rapid and simple method for its detection would be of great potential use in the investigation of patients with unexplained abdominal complaints such as diarrhoea, flatulence, or pain, and also more generally in studies of the incidence of lactose intolerance in different ethnic groups. At present the diagnosis depends on recording gastrointestinal symptoms and measuring the blood-glucose rise during a lactosetolerance test (L.T.T./.2 However, the mucosal lactase activity of jejunal-biopsy specimens remains the ultimate criterion. This must be so since symptoms after lactose ingestion can often be misleading and the changes in glucose levels in peripheral blood are influenced by other factors apart from the absorption
’I I
I II
B
I
Six patients, on direct questioning before the test, had the impression that milk was a cause or exacerbating feature of their symptoms. Four were shown to be intolerant to the lactose load, but two had completely normal results on testing (table i). During the L.T.T. fifteen of the twenty-five patients had a maximum blood-glucose rise of greater than 20 mg. per 100 ml., and they all had a 2-hour H2 rise of less than 4 parts per million (p.p.m.) (figure). They were also symptom-free, except one young woman being investigated for chronic flatulence who com-
BREATH HYDROGEN AS A DIAGNOSTIC
We have tested a simple method for the collection of exhaled H2 in the clinical situation.9 After an oral lactose load we compared the rise in breath H2 concentration with symptoms, maximum rise in bloodglucose, and, in patients requiring jejunal biopsy, with mucosal lactase activity.
METHOD FOR HYPOLACTASIA DAVID J. A. JENKINS ALVIN NEWMAN * LAURENCE M. BLENDIS
GEOFFREY METZ TIMOTHY J. PETERS
Department of Gastroenterology and Medical Research Council Gastroenterology Unit, Central Middlesex
Hospital,
and
Royal Postgraduate
Medical
Patients and Methods
School,
Twenty-five consecutive patients investigated in the
London
unit either for diarrhoea or abdominal symptoms of unknown cause were given 50 g. of lactose in 200 ml. of water by mouth. Any gastrointestinal symptoms such as borborygmi, excessive flatus, pain, discomfort, or diarrhoea were recorded. Samples of endexpiratory alveolar air from a single breath using a modified Haldane-Priestley tubewere collected every 30 minutes, and the H2 concentration was measured by gas chromatography. The results, expressed as change in H2 concentration at 120 minutes compared with fasting level, were compared with the maximum rise in bloodglucose during that period. Jejunal biopsy was done in patients with specific indications, part of the tissue being used for routine histology and part for assay of lactase activity. Disaccharidase activities were assayed independently by a modification 11 of the technique of Dahlqvist.12 Results were expressed as nmoles substrate hydrolysed per minute per mg. protein.13 In these cases the mucosal lactase activity was compared with the other variables being studied. The criterion for hypolactasia used in the study was a mucosal lactase activity of less than 100 milliunits per mg. protein. In the patients who did not have a biopsy, a maximum rise in blood-glucose of 20 mg. per 100 ml. or more was considered normal.
gastroenterology
(H2), collected by endexpiratory sampling, was measured in twenty-five patients with abdominal symptoms or diarrhœa after ingesting 50 g. of lactose. This was compared with established tests of hypolactasia. Fifteen patients with a blood-glucose rise of more Sum ary
Breath hydrogen
than 20 mg. per 100 ml. had less than 4 parts per million (p.p.m.) rise in breath H2 at 2 hours. In contrast, ten patients with blood-glucose rises of less than 20 mg. per 100 ml. had more than a 20 p.p.m. H2 rise (mean 85·8 p.p.m.±S.D. 44·3) at 2 hours. Similarly, two patients with normal jejunal lactase activity had no significant H2 production, whereas six patients with hypolactasia had more than a 20 p.p.m. rise in H2. Symptoms related to milk or lactose ingestion were found to be unreliable. End-expiratory sampling of breath H2 would seem to be a simple, non-invasive, and accurate method of diagnosing hypolactasia, which is also very acceptable to patients. This should make it a valuable tool both in diagnostic gastroenterology and in epidemiological surveys.
Results
Introduction SINCE lactose malabsorption is common in adultsi a rapid and simple method for its detection would be of great potential use in the investigation of patients with unexplained abdominal complaints such as diarrhoea, flatulence, or pain, and also more generally in studies of the incidence of lactose intolerance in different ethnic groups. At present the diagnosis depends on recording gastrointestinal symptoms and measuring the blood-glucose rise during a lactosetolerance test (L.T.T./.2 However, the mucosal lactase activity of jejunal-biopsy specimens remains the ultimate criterion. This must be so since symptoms after lactose ingestion can often be misleading and the changes in glucose levels in peripheral blood are influenced by other factors apart from the absorption
’I I
I II
B
I
Six patients, on direct questioning before the test, had the impression that milk was a cause or exacerbating feature of their symptoms. Four were shown to be intolerant to the lactose load, but two had completely normal results on testing (table i). During the L.T.T. fifteen of the twenty-five patients had a maximum blood-glucose rise of greater than 20 mg. per 100 ml., and they all had a 2-hour H2 rise of less than 4 parts per million (p.p.m.) (figure). They were also symptom-free, except one young woman being investigated for chronic flatulence who com-
