Incidence and clinical significance of lactose malabsorption in ulcerative colitis and Crohn's disease

The incidence of lactose malabsorption was investigated in 85 patients with ulcerative colitis and 71 patients with Crohn's disease by means of lactose tolerance tests and disaccharidase determinations in small intestinal mucosa. Eight patients with ulcerative colitis (9%) and four with Crohn's disease (6%) had lactose malabsorption. A control group displayed a similar incidence. It is concluded that lactose malabsorption is not particularly common in ulcerative colitis and Crohn's disease. If it is present, its aetiology seems to be unrelated to the intestinal disease.Transitional lactose malabsorption was detected in two cases during a relapse of ulcerative colitis.Institution of a lactose-free (or lactose-poor) diet was an important supporting measure in seven patients who were unaware of their milk intolerance, in particular in two with ileostomy. Therefore, it is recommended that a lactose tolerance test should always be performed in patients with ulcerative colitis or Crohn's disease.Twenty-one patients with ulcerative colitis and nine with Crohn's disease, none of whom had lactose malabsorption, were placed on milk-free diets. A beneficial effect was noticed in five of the patients with ulcerative colitis, and in three of those with Crohn's disease. The mechanism is unknown.Evidence is presented that milk allergy is not responsible for the beneficial effect of a lactosefree diet in patients with associated lactose malabsorption.     

Incidence and clinical significance of protein-bound vitamin B12 malabsorption

Patient records from January 1975 to December 1984 were analysed to assess the possible incidence of protein-bound vitamin B12 malabsorption. This condition is characterised by a low serum vitamin B12 level and a normal Schilling test but impaired absorption of vitamin B12 bound to protein. We found that 48 (25%) patients with a low serum cobalamin level unexplained by other causes had a normal Schilling test. Megaloblastic haemopoiesis was found in 25 of these. From this group, all 10 patients who had a test of protein-bound vitamin B12 absorption showed impaired absorption. Protein-bound vitamin B12 malabsorption may represent an early phase of pernicious anaemia when hypochlorhydria precedes intrinsic factor deficiency and should be tested for when the serum vitamin B12 level is decreased and the Schilling test is normal.     

Regression of lactose malabsorption in coeliac patients after receiving a gluten-free diet

OBJECTIVE: In a recent study by our group, it was shown that a large proportion of patients with lactose malabsorption and with no bacterial overgrowth are affected by silent coeliac disease (CD). Our aim was to evaluate the effect of a gluten-free diet on lactose malabsorption assessed using the hydrogen lactose breath test (LBT) and also the relationship with normalization of duodenal biopsies in coeliac patients. MATERIAL AND METHODS: Fifteen patients (11 F, 4 M; mean age 35.8+/-6) affected by CD with a positive LBT and negative glucose breath test were enrolled. All were started on a gluten-free diet and were re-evaluated after 6 months by LBT and after 12 months by both LBT and upper gastrointestinal endoscopy with biopsies. RESULTS: LBT normalization was observed in 1 out of 15 patients (6.7%) after 6 months and in 9 of the remaining 14 (64.2%) after 12 months. Duodenal biopsies showed normal villi in 8 patients, partial villous atrophy in 5 and total atrophy in 2. CONCLUSIONS: The present study shows that a large proportion of CD patients experience a regression of lactose malabsorption after receiving a gluten-free diet. This may be related to normalization of the brush border with an improvement of lactase enzyme activity. LBT should be performed after 12 months in CD patients on a gluten-free diet in order to assess the persistence/disappearance of lactose malabsorption, thus avoiding an unnecessary lactose-free diet.     

Adult coeliac disease: prevalence and clinical significance

BACKGROUND AND AIMS: Although coeliac disease is a common condition, the role of population screening is not clear. The aim of this study was to determine the prevalence and clinical significance of coeliac disease in the adult population of Christchurch, New Zealand. METHODS: A total of 1064 adults randomly selected from the 1996 Christchurch electoral rolls were enlisted. The subjects were screened for coeliac disease using the anti-endomysial antibody test (EMA), and all those with positive tests were reviewed and underwent a small bowel biopsy. RESULTS: Twelve of the 1064 persons tested (1.1%) were EMA positive and all had small bowel biopsy histology consistent with coeliac disease. Two of the 12 subjects were previously known to be EMA positive although neither had a small bowel biopsy. One additional subject with known and treated coeliac disease was also enrolled but was EMA negative. Thus, the overall prevalence of coeliac disease was 13 of 1064 subjects (1.2%, or 1:82), 10 of whom were newly diagnosed (0.9%, or 1:106) and three were previously known or suspected to have coeliac disease (0.3%, or 1:355). The prevalence in both sexes was similar. Nine of the 12 EMA-positive coeliac disease subjects identified by the use of screening reported symptoms, of which tiredness and lethargy were the most common. The subjects were of normal stature, although females tended to be lean. None of the subjects were anaemic, but four were iron deficient and four folate deficient. Five of the 12 had sustained bone fractures. Bone mineral density was reduced in males but not in females. CONCLUSIONS: The prevalence of coeliac disease in the adult population of Christchurch, New Zealand, is 1.2%. Unrecognized coeliac disease which was detected by population screening was three-fold more common than proven or suspected coeliac disease. Population screening may identify subjects who could benefit from treatment.     

Incidence of small-intestinal mucosal abnormalities and of clinical coeliac disease in the relatives of children with coeliac disease

Evidence is presented of a higher than normal incidence both of clinical coeliac disease and of small-intestinal mucosal abnormalities in relatives of children with coeliac disease. In such relatives the incidence of mucosal abnormality may differ from the incidence of clinical coeliac disease. The data show an absence of any simple Mendelian pattern of inheritance: in place of the hypothesis that inheritance is through a dominant gene of reduced penetrance, it is argued that the pathogenesis of coeliac disease is multifactorial, the genetic basis of susceptibility being polygenic and interacting with environmental factors. On this hypothesis the relative contributions of inheritance and environment to liability to the clinical condition are estimated, the genetic component being 45% +/- 9. Environmental factors appear more important in the development of mucosal abnormality.     

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.     

Individual sensitivity to lactose in lactose malabsorption

The clinical significance of lactose malabsorption and the individual sensitivity to lactose were investigated in 20 patients with verified lactose malabsorption. Thirteen patients were relieved of all symptoms while seven improved only on a lactose-free diet. The healthy patients did not experience any symptoms following provocation with lactose-free milk but following provocation with increasing amounts of lactose, the tendency to diarrhea and abdominal discomfort increased considerably. Three patients experienced discomfort after provocation with only 5 g lactose. On provocation with increasing amounts of lactose the seven patients who had not recovered also developed increased abdominal discomfort but none of them developed increased tendency to diarrhea. It is concluded that, in addition to lactose malabsorption, these patients must suffer from irritable colon with tendency to constipation.This investigation was supported by The Danish Medical Research Council and The Danish Hospital Foundation for Medical Research, Region of Copenhagen, Faroe Islands and Greenland.     

Hydrogen breath test quantification and clinical correlation of lactose malabsorption in adult irritable bowel syndrome and ulcerative colitis

Lactose malabsorption was studied, by hydrogen breath test, in 72 adults suffering from irritable bowel syndrome, in 20 ulcerative colitis patients, and in 69 healthy subjects. The minimum dose of lactose required to cause a positive breath test was determined, and the symptoms caused and the resulting hydrogen eliminated quantified. A high incidence of lactose malabsorption was shown at standard doses (up to 50 g) in both the healthy subjects (70%) and the patients (86% and 85%, respectively). In the irritable bowel syndrome and the ulcerative colitis groups, symptoms occurred with a smaller quantity of breath hydrogen, presumably in association with a greater individual sensitivity of the colon to distension. The threshold lactose dose was notably lower in the diseased subjects who registered as evidence a prevalence of malabsorption at a 20-g lactose load. The pathogenetic role of lactose malabsorption in the irritable bowel syndrome is emphasized, as is the importance of the personal lactose tolerance.     

Phytochemical malabsorption:clinical significance

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Sorbitol malabsorption in normal volunteers and in patients with coeliac disease.

Sorbitol is a hexahydroxy alcohol used as a sugar substitute in many dietetic foods and as a drug vehicle. Previous studies have suggested that sorbitol ingestion may be an additional cause of non-specific gastrointestinal distress. We evaluated sorbitol malabsorption in 30 healthy volunteers, seven patients with untreated coeliac disease and nine patients with coeliac disease on a gluten free diet, using a four hour H2 breath test. After ingestion of test solutions containing sorbitol 10 and 20 g and of four sweets (6.8 g sorbitol), 90%, 100%, and 62% of healthy volunteers, respectively had significantly raised H2 excretion, indicating malabsorption of sorbitol. Of all healthy subjects tested, 45% after 10 g, 100% after 20 g, and 50% after four sweets complained of symptoms of carbohydrate intolerance during the eight hours after sorbitol. After a 5 g dose given at concentrations of 2%, 4%, 8%, 16%, malabsorption was shown in 10%, 12%, 22%, and 43% of the healthy volunteers. Symptoms of intolerance at 5 g were experienced only at concentrations of 8% and 16%. Unlike healthy volunteers and coeliac patients on a gluten free diet, 100% of untreated coeliacs malabsorbed a 2% solution of 5 g sorbitol. These results show that malabsorption and intolerance of sorbitol may result from ingestion of doses and/or concentrations usually found in many foods and drugs; they underline the need to consider this as a possible and hitherto underestimated cause of gastrointestinal symptoms.     

Sideroblastic anaemia in adult coeliac disease

Anaemia due to pyridoxine deficiency has not previously been described in adult coeliac disease. The patient described here had a sideroblastic bone marrow showing the characteristic perinuclear rings of iron-containing granules and biochemical evidence of pyridoxine deficiency. These changes disappeared completely when the patient was put on a gluten-free diet.