Impact of bile acid malabsorption on steatorrhoea and symptoms in patients with chronic diarrhoea.

OBJECTIVE: Bile acids are important for fat absorption. The relationship between bile acid malabsorption and steatorrhoea and gastrointestinal symptoms in patients with chronic diarrhoea has only been studied on a limited scale. DESIGN: Ninety-four patients referred for chronic diarrhoea were prospectively investigated with the 75SeHCAT test, a faecal fat excretion test and registration of symptoms in addition to the standard clinical work-up. METHODS: The correlation between the 75SeHCAT value and the faecal fat excretion was calculated for different groups of patients. Symptoms were registered in a questionnaire over a period of seven consecutive days. RESULTS: Forty-two patients had a 75SeHCAT value < 10%. Mild steatorrhoea was common in patients with non-organic bile acid malabsorption (50%) and in patients with functional diarrhoea (38%). There was no correlation between low 75SeHCAT values and steatorrhoea, although some patients with severe organic disease had a concomitant malabsorption of fat and of bile acids. In coeliac disease, severe steatorrhoea was common even in patients with high 75SeHCAT values. Patients with bile acid malabsorption had more frequent (P < 0.008) and looser (P= 0.0021) stools compared with patients with functional diarrhoea. There was no difference in abdominal pain, distension or flatulence. CONCLUSION: Mild steatorrhoea is common in both non-organic bile acid malabsorption and functional diarrhoea. The 75SeHCAT value cannot predict the risk of steatorrhoea. The high prevalence of bile acid malabsorption in patients with chronic diarrhoea and the absence of specific symptoms, except frequent and more liquid stools, indicates that the 75SeHCAT test should be performed early in the investigation of these patients.

Comparison of the 1-gram (14)C-D-xylose breath test and the 50-gram hydrogen glucose breath test for diagnosis of small intestinal bacterial overgrowth.

BACKGROUND/AIMS: Culture of small bowel aspirate is the most direct method and the gold standard for diagnosing small intestinal bacterial overgrowth. However, cultures are cumbersome and fluoroscopy is required for obtaining aspirate. Therefore, different breath tests such as the xylose breath test and the hydrogen breath test have been developed. There is no general agreement as to which test is to be preferred. In the only previous direct comparison between these two tests an advantage for the 1-gram-(14)C-D-xylose breath test was found. The aim of the study was to compare the 50-gram glucose hydrogen breath test and the 1-gram (14)C-D-xylose breath test in relation to results of cultures of small bowel aspirate. METHODS: Forty-six consecutive patients, mean age 57 (range 27-87) years, 12 men and 34 women, were included because of suspicion of small intestinal bacterial overgrowth. After small bowel aspiration, all patients received a solution of 1 g xylose, labelled with 50 microg (14)C-D-xylose, and 50 g glucose dissolved in 250 ml water. The concentration of breath hydrogen was analyzed every 15 min for 2 h and (14)CO(2) was analyzed every 30 min for 4 h. A positive hydrogen breath test was defined as a rise in hydrogen concentration of 15 ppm. A positive xylose test was defined as an accumulated dose 4.5% after 4 h. Two definitions for a positive culture were used, either growth of 10(5 )colonic-type bacteria/ml or growth of 10(5) bacteria/ml of any type. RESULTS: Twenty-four patients had growth of 10(5) bacteria, of whom 10 had growth of 10(5) colonic-type bacteria in small bowel aspirate. Twenty-two patients had no significant growth. The hydrogen breath test and the xylose breath test had a sensitivity for growth of 10(5) bacteria of 58 and 42%, respectively. For growth of 10(5 )colonic-type bacteria the sensitivity was 90% for the hydrogen breath test and 70% for the xylose breath test. The specificity was similar for the two tests. CONCLUSION: Although no significant difference between the two tests was found, there was a tendency in favor of the 50-gram glucose hydrogen breath test. The simplicity in combination with high sensitivity makes the hydrogen breath test suitable as a screening method to select patients for further investigation.

Bile duct bacterial isolates in primary sclerosing cholangitis and certain other forms of cholestasis--a study of bile cultures from ERCP.

BACKGROUND/AIMS: The pathogenesis of the inflammatory lesion in primary sclerosing cholangitis is unknown. We have recently demonstrated a high positivity rate of bacterial cultures in bile and bile ducts of explanted livers from primary sclerosing cholangitis patients compared with patients with primary biliary cirrhosis. In particular, alpha-hemolytic Streptococci was a frequent finding, suggesting an etiopathogenic role of that particular bacteria in primary sclerosing cholangitis. We therefore wanted to study naive primary sclerosing cholangitis patients and compare them with primary sclerosing cholangitis patients that have previously undergone endoscopic retrograde cholangiopancreatography, in order to evaluate the potential role of these bacteria in the etiopathogenesis in primary sclerosing cholangitis. METHODOLOGY: Samples for bacterial cultures were obtained during a diagnostic endoscopic retrograde cholangiopancreatography. PARTICIPANTS: 12 naive primary sclerosing cholangitis patients, 10 patients with primary sclerosing cholangitis, previously investigated using endoscopic retrograde cholangiopancreatography, 47 patients with choledocholithiasis, 19 patients with cancer obstructing the common bile duct, and 29 patients with other forms of biliary disorders. RESULTS: Positive cultures were obtained from 3 of the naive primary sclerosing cholangitis patients and from 6 of the primary sclerosing cholangitis patients with previous endoscopic retrograde cholangiopancreatography (NS). The most frequent finding in all the primary sclerosing cholangitis patients was alpha-hemolytic Streptococci. Bacteria were cultured from the bile in 64% of the patients with choledocholithiasis, higher than the 25% in the naive primary sclerosing cholangitis patients (P < 0.03), and in 56% of patients with obstructing cancer (NS) but in only 24% of patients with other forms of biliary disorders, all of whom, except 4, had normal cholangiograms. In the 22 patients with primary sclerosing cholangitis, 75% of the positive bacterial cultures consisted of Gram-positive isolates and 25% were enteric bacteria, which differed statistically from the 74% enteric bacteria and 26% Gram-positive bacteria in the patients with common duct stone (P < 0.01). CONCLUSIONS: Alpha-hemolytic Streptococci do not seem to play a primary role in the etiopathogenesis of primary sclerosing cholangitis since most naive primary sclerosing cholangitis patients were found to have negative bacterial cultures. This does not exclude the possibility that they play a role in the progression of primary sclerosing cholangitis following infection in conjunction with the first endoscopic retrograde cholangiopancreatography.

Serum antibodies to H+,K+-ATPase, serum pepsinogen A and Helicobacter pylori in relation to gastric mucosa morphology in patients with low or low-normal concentrations of serum cobalamins.

OBJECTIVES: To compare the diagnostic performance of serum antibodies to H+,K+-ATPase (EC 3.6.1.36), serum pepsinogen A (EC 3.4.23.1) and the Schilling test in diagnosing chronic atrophic body gastritis; to study the interrelationships between H+,K+-ATPase antibodies, serology for Helicobacter pylori, and gastric morphology. DESIGN: Patients with suspected cobalamin deficiency and serum cobalamin < 200 micromol/l were investigated using upper gastrointestinal endoscopy, the Schilling test and serum tests for H+,K+-ATPase antibodies, pepsinogen A, and H. pylori. SETTING: The Department of Internal Medicine, Sahlgrenska University Hospital, Göteborg, Sweden. PATIENTS: Ninety seven consecutively referred patients. MAIN OUTCOME MEASURES: Sensitivity and specificity of assays for serum H+,K+-ATPase antibodies, serum pepsinogen A, and the Schilling test. RESULTS: Assays of serum antibodies to H+,K+-ATPase and of serum pepsinogen A displayed equal diagnostic sensitivity for atrophic gastritis (around 0.90 for the severe forms) and higher than that for the Schilling test (0.65). The diagnostic specificity for pepsinogen A (1.0) was higher than for H+,K+-ATPase antibodies (about 0.80). The prevalence of antral gastritis and positivity for H. pylori antibodies declined with the transition of body gastritis into severe atrophy, while the prevalence of H+,K+-ATPase antibodies increased. CONCLUSION: Pepsinogen A is preferable to serum H+,K+-ATPase antibodies in the diagnosis of gastric body mucosal atrophy. The formation of H+,K+-ATPase antibodies does not seem to be a primary event in the development of gastric body muscosal atrophy.

Advantages of serum pepsinogen A combined with gastrin or pepsinogen C as first-line analytes in the evaluation of suspected cobalamin deficiency: a study in patients previously not subjected to gastrointestinal surgery.

OBJECTIVES: Since there is a significant overlap in serum cobalamin concentrations between healthy and cobalamin-deficient individuals, we wanted to compare two different principles for use as supplementary tests to serum cobalamin concentration in patients with suspected cobalamin malabsorption and deficiency. DESIGN: Clinical study of consecutive patients. SETTING: The catchment area of Sahlgrenska University Hospital, Göteborg. SUBJECTS: A total of 112 patients with suspected cobalamin deficiency who had not previously undergone gastrointestinal surgery. INTERVENTIONS: Gastroduodenoscopy with biopsies taken from the gastric body and the duodenum, Schilling test, and measurement of serum methylmalonic acid (MMA), total homocysteine (Hcy), pepsinogens A and C, and gastrin. MAIN OUTCOME MEASURES: Number of patients with gastric body atrophy identified with the combination of MMA and Hcy, and pepsinogen A combined with pepsinogen C or gastrin. RESULTS: About 95% of the patients with severe gastric body atrophy had abnormal concentrations of serum pepsinogen A and/or gastrin or pepsinogen A/C ratio, whereas 65% had abnormal metabolite concentrations. Serum pepsinogen A combined with pepsinogen C identified 100%, and combined with gastrin 88%, of the patients with gastric body atrophy and elevated metabolite tests, and 67 and 75%, respectively, of those who had not yet developed elevated metabolite tests. CONCLUSIONS: Pepsinogen A, combined with pepsinogen C or gastrin, should be the first option in evaluating patients with suspected cobalamin deficiency who have not previously undergone gastrointestinal surgery.

Early predictors of glucocorticosteroid treatment failure in severe and moderately severe attacks of ulcerative colitis.

OBJECTIVE: To analyse the ability of simple clinical and biochemical parameters to predict glucocorticosteroid (GCS) treatment failure in patients with acute attacks of ulcerative colitis. DESIGN/METHODS: Retrospective analysis of clinical and biochemical data. SETTING: Four Swedish university hospitals. PATIENTS: Ninety seven patients with acute attacks of ulcerative colitis severe enough to warrant treatment with intravenous GCS, hospitalized during the years 1988-93. MAIN OUTCOME MEASURE: Colectomy within the first 30 days after hospitalization, defined as 'clinical steroid resistance'. RESULTS: Thirty days after admission, 39 patients (40%) were in complete clinical and endoscopic remission while 33 (34%) had undergone colectomy. During follow-up for 24 months, four patients among the 39 initially in remission underwent colectomy. Among the 25 patients (26%) not attaining remission after 30 days, an additional nine patients subsequently required colectomy. Steroid resistance was associated with duration of disease (2.7 vs 8.1 years, P=0.0037) and steroid treatment before hospitalization (70 vs 42%, P=0.010). In particular, elevation of body temperature (37.4 vs 36.9 degrees C, P=0.012), persistence of diarrhoea (6.8 vs 3.6 bowel movements/day, P<0.0001) and passage of blood (83 vs 42%, P=0.0003) as well as CRP elevation (36.3 vs 18.0 mg/l, P=0.007) on day 3 after treatment initiation were identified as predictors of a poor response. CRP > or = 25 mg/l and > 4 bowel movements/day on day 3 of hospitalization independently predicted a high risk for colectomy within 30 days. CONCLUSIONS: Sustained elevation of body temperature, persistent bloody diarrhoea and continued CRP elevation on day 3 of intravenous GCS treatment strongly predict clinical steroid resistance in acute attacks of ulcerative colitis. In the group of poor or non-responders, colectomy or more aggressive medical treatment should be considered at an early stage.

Diagnosis of small intestinal bacterial overgrowth in clinical praxis: a comparison of the culture of small bowel aspirate, duodenal biopsies and gastric aspirate.

BACKGROUND/AIMS: This study was undertaken to validate the usefulness of the culture of duodenal biopsy specimens and gastric aspirate compared to the culture of small bowel aspirate for diagnosing small intestinal bacterial overgrowth. We also investigated the occurrence of predisposing conditions in these patients. METHODOLOGY: Seventy five consecutive patients, admitted because of symptoms which caused us to suspect small intestinal bacterial overgrowth, were studied. For all patients, specimens for the culture of small bowel aspirate, duodenal biopsies and gastric aspirate were obtained during upper endoscopy. RESULTS: Eighteen patients showed growth of gram negative bacteria, 22 growth of gram positive bacteria and 35 showed no significant growth in cultures of small bowel aspirate. Cultures of duodenal biopsies revealed gram negative bacteria in 11 patients, gram positive bacteria in 9 and no growth in 55. Cultures of gastric aspirate revealed gram negative bacteria in 7 patients, gram positive bacteria in 12 and no growth in 51. Ten of the 18 patients with gram negative overgrowth and 13 of the 22 patients with gram positive overgrowth had a predisposing condition. In contrast, only 4 of the 35 without overgrowth had a predisposing condition. CONCLUSIONS: The culture of duodenal biopsy specimens or gastric aspirate is a less sensitive method than the culture of small bowel aspirate. Most patients with culture-proven small intestinal bacterial overgrowth had at least one predisposing condition.

Serum methylmalonic acid and total homocysteine in patients with suspected cobalamin deficiency: a clinical study based on gastrointestinal histopathological findings.

We compared the sensitivity and specificity of the two metabolite tests, methylmalonic acid (MMA) and total homocysteine (Hcy) in serum, and serum cobalamin (Cbl) in patients referred to our hospital because of suspected cobalamin deficiency and a serum cobalamin value at the referring unit <200 pmol/L. All 111 patients included were investigated using upper gastrointestinal endoscopy with biopsy specimens taken from the gastric and duodenal mucosa to find a morphological basis for cobalamin malabsorption as well as the Schilling test for the validation of the serum tests. All patients were treated with cobalamin and new blood samples were taken after 4 weeks. We found no difference in sensitivity and specificity between serum MMA, Hcy, and Cbl in identifying patients with and without conditions compatible with cobalamin malabsorption. Elevated serum MMA and Hcy were also found in about 15% of the group of patients with normal Schilling tests and without a morphological basis for cobalamin malabsorption. Moreover, most patients in this group responded with decreased values of the metabolite tests following cobalamin treatment, suggesting that neither elevated metabolites nor a decrease in these values following cobalamin treatment are specific for cobalamin deficiency.

Schilling and protein-bound cobalamin absorption tests are poor instruments for diagnosing cobalamin malabsorption.

OBJECTIVES: To assess the advantage of a protein-bound cobalamin absorption test (PBAT) over the Schilling test in patients with suspected cobalamin (vitamin B12) malabsorption. DESIGN: Clinical study of consecutive patients referred from primary care units, medical and neurological clinics. SETTING: The catchment area of Sahlgrenska University Hospital, Göteborg. SUBJECTS: Referred patients (n = 155) with suspected cobalamin deficiency and at least one serum cobalamin value < 200 pmol L-1. INTERVENTIONS: All patients were investigated with upper gastrointestinal endoscopy with biopsies taken from the gastric body and duodenal mucosa. Serum methylmalonic acid (MMA) and homocysteine (Hcy) were determined in all 109 patients not on cobalamin substitution. A dual isotope cobalamin absorption test was then performed with the concomitant administration of crystalline (Schilling) and protein-bound cobalamin (PBAT). MAIN OUTCOME MEASURES: Number of patients with gastric body atrophy diagnosed with each absorption test and the relation between these results and functional cobalamin deficiency defined as elevated MMA and Hcy, that normalized after cobalamin substitution treatment. RESULTS: The majority of patients with abnormal absorption tests had already developed elevated MMA and/or Hcy. PBAT was more sensitive than the Schilling test in identifying patients with gastric body atrophy but the sensitivity was too low for clinical use. About 1/3 of the patients with gastric body atrophy and normal absorption tests had elevated MMA and/or Hcy, indicating cobalamin deficiency. CONCLUSION: PBAT may be somewhat more sensitive than the Schilling test but neither test is sensitive enough for diagnosing cobalamin malabsorption at an early stage.

Value of serologic markers for clinical diagnosis and population studies of coeliac disease.

BACKGROUND: There is a need for serologic markers in selecting patients with symptoms compatible with coeliac disease for intestinal biopsy and for population screening. Few comparative studies have been done. METHODS: Sera from 55 patients with coeliac disease and 65 referents, aged between 8 months and 79 years, were investigated. Anti-gliadin, anti-reticulin, anti-endomysium, and anti-jejunal antibodies were measured. The sensitivities, specificities, and positive predictive values for different disease prevalence levels were calculated. Confidence intervals, rarely used in this type of study, were calculated. RESULTS AND CONCLUSIONS: In most tests the antibody levels were age-correlated. The highest sensitivities in combination with high specificities were found for IgA anti-gliadin antibodies in children less than 5 years of age and IgA anti-endomysium antibodies in older children and adults. These tests were most useful for testing a population with a high disease prevalence, such as patients with gastrointestinal symptoms, although the results for many tests had overlapping confidence intervals. For screening unselected populations with a low disease prevalence, in which a test with maximum specificity is desired, only anti-endomysium antibodies had sufficiently high predictive value to be of practical use.

Serum levels of the carcinoma-associated antigen CA 50 in ulcerative colitis.

The aim was to study the serum level of the carcinoma-associated antigen CA 50 as a marker of dysplasia in ulcerative colitis. Seventy-four patients with a mean history of ulcerative colitis of 16 years (SD, 9 years) underwent colonoscopic examination of the entire colon. Dysplasia was diagnosed by light microscopy of multiple biopsy specimens obtained during colonoscopy. Increased serum levels of the antigen CA 50 were found in four patients, of whom two had no signs of dysplasia. Six out of eight patients with moderate dysplasia had serum levels of CA 50 not exceeding a reference level determined as the mean + 2 SD of the results in sera of 500 blood donors. Of 5 patients with ulcerative colitis for more than 30 years, 2 had increased levels of CA 50, whereas only 2 out of 69 with shorter disease duration did (p less than 0.02). Longitudinal studies are required to determine whether measurement of carcinoma-associated antigens will provide clinical information for the treatment of patients with ulcerative colitis.

Serum antibodies to gliadin in coeliac disease after gluten withdrawal.

Serum gliadin antibodies of the IgA and IgG classes were determined by the diffusion-in-gel enzyme-linked immunosorbent assay (DIG-ELISA) in 10 adult patients with villous atrophy of the small-intestinal mucosa. After introduction of a gluten-free diet a gradual decrease in serum gliadin antibody levels occurred, reaching statistical significance at 3 months of treatment for the IgA class (p less than 0.01) and at 6 months for the IgG class (p less than 0.05). A decrease of serum gliadin antibody levels after gluten withdrawal was related to an improvement of the intestinal mucosa and should thus be indicative of whether the patient is following the dietary recommendations. However, determination of gliadin antibody levels cannot replace small-intestinal biopsy, as there are a few patients in whom the antibody levels are not related to the morphology of the gut mucosa.

Serum antibodies to gliadin and small-intestinal morphology in dermatitis herpetiformis. A controlled clinical study of the effect of treatment with a gluten-free diet.

Serum gliadin antibodies of the IgA and IgG classes were determined by the diffusion-in-gel enzyme-linked immunosorbent assay in 41 patients with dermatitis herpetiformis before treatment with a gluten-free diet. Increased gliadin antibody levels were found more frequently in patients with subtotal villous atrophy (9 out of 17 patients, or 53%; p less than 0.05) than in patients with partial villous atrophy (2 out of 13 patients, or 15%) or normal villous appearance (2 out of 10 patients, or 20%). The gliadin antibody levels were negatively correlated with the urinary xylose excretion (r = -0.40, p less than 0.02 for the IgA class and r = -0.64, p less than 0.001 for the IgG class). Intestinal morphology improved and mean gliadin antibody levels of the IgA and IgG classes decreased during treatment with a gluten-free diet for 16-36 months (mean, 20 months) (p less than 0.005, n = 26), whereas no significant changes of the gliadin antibody levels or the small-intestinal morphology were observed in the other 15 patients, who continued on a non-restricted diet for 17-35 months (mean, 20 months). Thus, gliadin antibody levels in sera from patients with dermatitis herpetiformis seem to be correlated with the severity of the intestinal disease. However, all patients with villous atrophy are not detected by determination of serum gliadin antibodies.

On the natural history of hypergastrinemia.

We determined total gastrin and pepsinogen I in frozen serum samples from 175 overnight-fasted women 54 years old, and from 81 overnight-fasted women 60 years old, who took part in a population study in 1968-69. We also assayed samples from some of these women, who participated in clinical follow-up studies in 1974-75 and 1980-81: all of the women in the initial group whose serum gastrin concentration exceeded the 85th centile value and, as a reference group, a randomized subsample of women whose initial serum gastrin concentration was less than the 80th centile. Samples with total gastrin concentration greater than 400 ng/L were also assayed for gastrin-17 and gastrin-34. We found that: a pronounced increase of serum gastrin persisted throughout the study period for most of these postmenopausal women, indicating that conversion of type A gastritis (antrum-sparing) to pan-gastritis is uncommon; unexplained high concentrations of pepsinogen I in relation to the reference interval for young and middle-aged adults, as well as in relation to serum gastrin, were common; and the gastrin-17/gastrin-34 ratio is not correlated with the outcome of pronounced hypergastrinemia.

Plasma enteroglucagon in the control of childhood celiac disease.

To study whether or not plasma enteroglucagon reflects changes of the small intestinal mucosa during different phases of celiac disease, we studied fasting and postprandial concentrations of plasma enteroglucagon, as well as small intestinal mucosa morphology, in children with celiac disease and in a reference group of children without gastrointestinal disorders. The children with celiac disease were studied before dietary treatment, during gluten-free diet, and during gluten challenge. In untreated celiac children we found high mean basal and postprandial plasma enteroglucagon concentrations compared with the reference group (p less than 0.001). After a gluten-free diet period of 0.2-4.5 years (mean, 1.0 year), when the small intestinal histology was normal or only mildly abnormal, there was a decrease of both mean basal plasma enteroglucagon concentration (from 81 to 17 pmol/L; p less than 0.001) and mean postprandial plasma enteroglucagon concentration (from 129 to 39 pmol/L; p less than 0.001). During a subsequent gluten challenge, which resulted in a mucosal relapse, there was a rise in mean postprandial plasma enteroglucagon concentration (from 39 to 74 pmol/L; p less than 0.005), although there was a substantial overlap in values from treated and challenged patients. These findings suggest that plasma enteroglucagon levels, particularly after a mixed meal, are correlated with the small intestinal mucosal morphology in childhood celiac disease. Determination of plasma enteroglucagon may facilitate the control of the dietary adherence during gluten-free diet and may in some children indicate mucosal relapse during gluten challenge. Thus, the number of control biopsies may be reduced.

Analytical and clinical evaluation of a radioimmunoassay for gastrin.

Prior to a study of the pathophysiological significance of chronic atrophic gastritis and hypergastrinemia, we evaluated a new radioimmunoassay kit for serum total gastrin (Diagnostic Products Corp.). The mean intra-assay CV ranged from 2 to 5% (2386 patients' samples in 47 assay runs done during four months). Total CVs for two controls ranged from 4 to 10%. Within-assay bias was 5%. Oleate decreased the values, indicating that intravenous heparin, which releases endothelial lipase, causing in vitro lipolysis, should be avoided if indwelling catheters are used for sampling, e.g., during provocation tests for gastrin release. Of three other commercial kits examined, two were affected by oleate. Other anions such as heparin and EDTA also affected the assay. Values for gastrin in heparinized plasma from surgical patients representing a variety of disorders agreed well with results obtained by a reference laboratory. We confirm the usefulness of this assay for discriminating clinical situations and conclude that ligand assays, besides those for thyroid assessment, should be assessed for interference from nonesterified fatty acids. Preliminary data also suggest a marked age dependence of serum gastrin concentration.

Serum gliadin antibodies for detection and control of childhood coeliac disease.

Serum gliadin antibodies of the IgA and IgG isotypes were determined by means of the diffusion-in-gel enzyme-linked immunosorbent assay (DIG-ELISA) in children during different phases of coeliac disease. Fourteen children were studied before onset of dietary treatment, 16 during a period of gluten-free diet and 16 during gluten challenge. The control groups consisted of 44 children with other gastrointestinal diseases and 14 children without gastrointestinal disorders. All of the children studied had been subjected to small-intestinal biopsy. On the basis of the results obtained in this study the diagnostic sensitivity with regard to untreated coeliac disease was found to be 100% and the diagnostic specificity 97%. In 10 coeliac children followed during the phases of diagnostic evaluation antibody levels decreased in all during dietary treatment and increased in 8 during a subsequent gluten challenge. It is suggested that determination of IgA and IgG gliadin antibodies by means of DIG-ELISA may be used as a diagnostic test for coeliac disease in children and that this test may be useful in monitoring the dietary treatment in children with known coeliac disease. Moreover, the DIG-ELISA is an inexpensive and technically simple method.

Plasma enteroglucagon related to malabsorption in coeliac disease.

Plasma enteroglucagon was measured before and during three hours after a standard meal in 21 untreated adult patients with suspected coeliac disease who all had villous atrophy of the small intestinal mucosa and malabsorption, and in nine control subjects. In 11 of these patients the diagnosis of coeliac disease was confirmed and 10 were again investigated on a gluten free diet. The coeliac patients had higher basal (37 +/- 9 pmol/l, mean +/- SE, p less than 0.05) and postprandial (70 +/- 9 pmol/l, p less than 0.005) mean plasma enteroglucagon concentrations than the control subjects (basal 14 +/- 4 pmol/l, postprandial 25 +/- 5 pmol/l). The 10 coeliac patients on gluten free diet for five to 20 months had a basal mean plasma enteroglucagon concentration not significantly lower than before treatment (25 +/- 5 pmol/l) but significantly lower postprandial enteroglucagon concentrations than before treatment (40 +/- 7 pmol/l, p less than 0.025). Postprandial plasma enteroglucagon concentration after 90 minutes in untreated patients correlated positively to the faecal fat excretion (r = 0.58, p less than 0.02). It correlated negatively to the urinary five hour D-xylose excretion after an oral load of 165 mmol D-xylose (r = -0.71, p less than 0.01). Thus, the postprandial plasma enteroglucagon concentrations in untreated coeliac disease were related to the degree of malabsorption and they normalised during treatment with a gluten free diet.

Determination of enteroglucagon in plasma for detection of celiac disease in children.

To evaluate the plasma enteroglucagon assay as a test for the detection of celiac disease, we have determined basal and postprandial concentrations of enteroglucagon in plasma of children who underwent small-intestinal biopsy because of suspected celiac disease. In the 14 children with untreated celiac disease both basal [81 (SD 33) pmol/L] and postprandial [129 (SD 26) pmol/L] concentrations of enteroglucagon were significantly higher (p less than 0.001) than in the 45 children with other gastrointestinal disorders [24 (SD 9) pmol/L, and 50 (SD 22) pmol/L, respectively] and in the 15 children without gastrointestinal disorders [14 (SD 10) pmol/L, and 35 (SD 8) pmol/L, respectively]. All children with celiac disease had either basal or postprandial plasma enteroglucagon concentrations exceeding the mean + 2 SD of the results for the children with other gastrointestinal disorders. Eight of 10 children with celiac disease in whom both concentrations were measured had increased values for both. In our study the sensitivity for detection of celiac disease was 100% and the specificity 97%. Evidently determination of plasma enteroglucagon concentration is effective in diagnosing celiac disease, thereby improving the selection of patients for small-intestinal biopsy.