Original article
Fermentation of endogenous substrates is responsible for increased fasting breath hydrogen levels in celiac disease

https://doi.org/10.1016/j.lab.2003.11.006Get rights and content

Abstract

Fasting breath hydrogen (FBH) levels are frequently increased in celiac disease (CD). In this study we sought to determine whether the unknown source of the fermented substrates is endogenous glycoproteins shed or exuded through the damaged mucosa. To test the role of nonabsorbable exogenous substrates, we subjected 39 untreated and 23 treated CD patients and 37 healthy volunteers to the H2 breath test after administration of lactulose after both an unrestricted and a restricted pretest meal. To test the relevance of endogenous substrates, we measured breath H2 excretion during a 9-hour fast and after the administration of lactulose solution. To determine whether the luminal content of CD patients contains an increased amount of fermentable substrates, we incubated samples of jejunal juice from 7 untreated CD patients, 6 healthy volunteers, and 6 dyspeptic patients in vitro with a fecal homogenate obtained from a healthy H2-producer volunteer and measured the cumulative H2 production. Untreated CD patients showed higher FBH levels than did treated patients and healthy volunteers. Only in untreated CD did FBH levels show no difference if a restricted or an unrestricted dinner was eaten the evening before the test. Nine-hour FBH levels were significantly higher in untreated CD than in healthy volunteers, whereas no difference was found after administration of lactulose. In vitro H2 production was significantly higher in untreated CD patients than in controls. Increased FBH levels in CD do not depend on fermentation of malabsorbed exogenous substrates; endogenous substrates are increased in the lumens of CD patients and may be responsible for increased FBH levels.

Section snippets

Patients

Thirty-nine untreated CD patients (20 of them women; mean age 33 ± 5 years, range 22-45) and 23 treated ones (12 women; mean age 35 ± 5 years, range 23 - 47) took part in the study. In 25 untreated patients CD was suspected on the basis of the presence of the classical symptoms of malabsorption (diarrhea, steatorrhea, weight loss); in the remaining 14, CD was diagnosed on the basis of the following conditions: iron-deficiency anemia (n = 7), first-degree kinship with a CD patient (n = 3),

Results

Table I confirms that FBH levels are significantly higher in patients with untreated CD than in patients with treated disease or in healthy volunteers. We noted no difference between the last 2 groups. Dividing the group of patients with untreated CD on the basis of the pattern of clinical presentation, we saw that patients with overt malabsorption at the time of diagnosis had FBH levels significantly higher than those in patients with minor symptoms (Fig 1).

With regard to mouth-to-cecum

Discussion

Increased FBH excretion is a common feature in patients with untreated CD,10, 12 but until now, the pathophysiological mechanism responsible for this finding was unknown. The prevalence of increased FBH levels was higher in patients with malabsorption symptoms (diarrhea, steatorrhea, weight loss) than in patients without overt malabsorption (iron-deficiency anemia, first-degree kinship with a CD patient, dermatitis herpetiformis, alopecia areata, recurrent aphthous stomatitis). This finding

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