Visceral hypersensitivity and intolerance symptoms in lactose malabsorption

Abstract

Lactose malabsorption is not always associated with intolerance symptoms. The factors responsible for symptom onset are not yet completely known. As differences in visceral sensitivity may play a role in the pathogenesis of functional symptoms, we evaluated whether an alteration of visceral sensitivity is present in subjects with lactose intolerance. Thirty subjects, recruited regardless of whether they were aware of their capacity to absorb lactose, underwent an evaluation of intestinal hydrogen production capacity by lactulose breath test, followed by an evaluation of lactose absorption by hydrogen breath test after lactose administration and subsequently an evaluation of recto-sigmoid sensitivity threshold during fasting and after lactulose administration, to ascertain whether fermentation modifies intestinal sensitivity. The role of differences in gastrointestinal transit was excluded by gastric emptying and mouth-to-caecum transit time by (13)C-octanoic and lactulose breath tests. Lactulose administration induced a significant reduction of discomfort threshold in subjects with lactose intolerance but not in malabsorbers without intolerance symptoms or in subjects with normal lactose absorption. Perception threshold showed no changes after lactulose administration. Severity of symptoms in intolerant subjects was significantly correlated with the reduction of discomfort thresholds. Visceral hypersensitivity should be considered in the induction of intolerance symptoms in subjects with lactose malabsorption.

A comparison of diagnostic tests for lactose malabsorption - which one is the best?

“…But even ELL-symptoms showed unacceptable diagnostic properties and poor agreement with any of the other test (table 4 and 5). This fits with the clinical observation that the prevalence of perceived lactose intolerance, which is also related to visceral hypersensitivity, is significantly higher than that of LM, and that subjects with LM can consume a variable but limited amount of lactose without developing symptoms [9,11,20]. …”

The effect of gluten on intestinal fermentation, gastric and gallbladder emptying in healthy volunteers

“…Accordingly, our data could be consistent with previous results showing both an improvement of symptoms after gluten withdrawal in non-coeliac patients claiming a close link with consumption of cereals [41] and the worsening of symptoms in patients suffering from conditions characterised by alterations of visceral sensitivity [27]. It is, in fact, likely that the actual presence of alterations of visceral sensitivity may represent an important cofactor in the pathophysiology of symptoms, as described in IBS [14], but also in patients with lactose intolerance [36]: in this condition, in fact, in malabsorber patients, only the subgroup with visceral hypersensitivity shows an intolerance syndrome. Our hypothesis, in fact, is that in a patient suffering from alterations of visceral sensitivity, the ingestion of gluten, a chemically and physically complex compound [2], might enhance abdominal symptom severity, highlighting the relationship between gluten ingestion and symptom onset.…”

“…All these alterations are known to be responsible for symptoms [36][37][38][39]. However, it is not possible to exclude the role for FODMAPs in our results.…”

Polymorphism in the oxytocin promoter region in patients with lactase non-persistence is not related to symptoms

“…In the present study, we chose only homozygote patients to obtain well-defined groups concerning lactase persistence, as individual variations in the lactose absorption, particularly among heterozygotes have been reported [2,4]. Factors causing this variation of symptoms in response to the same volume of milk intake, or according to different milk products, may include the amount of lactose not absorbed in the gut, differences in the bacterial flora and their metabolism of lactose in colon [22], and the rate of gastric emptying and individual perception of symptoms [5,6]. In the present study, the A/A genotype of rs6133010 in the promoter region of the OXT gene was more frequent in asymptomatic controls and in lactase persistent subjects than in lactase non-persistent, although statistically significant only in persistent subjects.…”

“…Frequently indistinguishable symptoms are seen in the subgroup of patients with lactase non-persistence, which is also common in the adult population [2,3], and reported complaints in this group are surprisingly less correlated to the volume of milk intake, than previously assumed [4]. Differences in gastric emptying and individual perception of symptoms have been discussed [5,6]. Many neuropeptides, e.g.…”