GHT improves IBS-related QOL, is superior to SMT alone, and shows a long-term effect even in refractory IBS.

The pathophysiology of functional dyspepsia is poorly understood, thus diagnostic and therapeutic options for this disease are limited. We assessed the relevance of a simple test for chemical hypersensitivity by applying an oral capsaicin load. After a preliminary dose-finding study, 61 healthy controls and 54 functional dyspepsia patients swallowed a capsule containing 0.75 mg capsaicin. A graded questionnaire evaluated severity of symptoms before and after capsule ingestion; an aggregate symptom score was calculated by adding all symptom scores. Controls developed moderate symptoms (symptom score: 6.0+/-4.1; median: 5.0). The 75% quartile (9.0) was considered the upper limit of normal. Functional dyspepsia patients had significantly higher symptom scores (10.0+/-6.5) than controls. About 54% of functional dyspepsia patients tested positive; clinically this group was not different from the group testing negative besides being on average younger and suffering more from bloating. In additional 13 patients with functional dyspepsia who tested positive (symptom score: 15.8+/-0.9), symptom response to placebo capsules (1.9+/-0.6) was similar to controls. In reliability testing, the Cronbach alpha-value of the capsaicin test was 0.86. The capsaicin test is a simple and non-invasive method to detect a subgroup of functional dyspepsia with chemical hypersensitivity.

Half of functional dyspepsia patients had chemical hypersensitivity, determined with an oral capsaicin load. Placebo response was negligible. The results of the capsaicin test were not associated with specific dyspepsia symptoms or Rome subgroups.

Repeated ingestion of capsaicin over a prolonged period reduces symptoms in functional dyspepsia, but initially induces upper abdominal symptoms. Sensitizing chemonociception might be the cause for this initial effect of capsaicin. The aim was to evaluate the effect of prolonged capsaicin ingestion on duodenal chemo- and mechanonociception. Healthy subjects ingested capsules containing either 0.25 mg capsaicin tid (n = 8) or placebo (n = 8) for 28 days. Before (day 0) and after (day 29) capsule ingestion the duodenum was distended with a balloon and perfused with a capsaicin solution. Mechanically and chemically induced sensation was evaluated by a graded questionnaire. Aggregate perception scores were calculated. Perception scores during balloon distensions with 12 and 18 mmHg were significantly lower after 4 weeks capsaicin when compared to baseline (P < 0.05). Balloon volumes to induce first sensation (63 +/- 14 mL (day 0) vs 92 +/- 22 mL (day 29); P < 0.05) and discomfort (101 +/- 12 mL vs 137 +/- 22 mL; P = 0.05) where significantly higher after 4 weeks capsaicin application; balloon pressures to induce sensations were not significantly different. Intraluminal capsaicin application induced first sensation after 3.4 +/- 1.5 min (day 0) and 7.5 +/- 4.6 min (day 29) (P < 0.05) and discomfort after 15.9 +/- 9.8 min and 22.4 +/- 7.3 min (P < 0.05). The quality of perception was not altered by repeated capsaicin ingestion. In the placebo group, mechano- and chemonociception remained unaltered at day 29. Four weeks ingestion of capsaicin desensitized both chemonociceptive and mechanonociceptive pathways in healthy volunteers. Symptom reduction after prolonged treatment with capsaicin in dyspeptic patients might be attributed to a dual desensitizing effect of capsaicin on chemonociceptors and mechanonociceptors.

SUMMARY BackgroundIntestinal chemo-nociception is a recently described mechanism of perception of intraluminal stimuli that might involve pathways independent from mechano-nociception.

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Differences in upper GI symptoms distinguished capsaicin positive and negative patients. Symptom improvement after long-term capsaicin ingestion was indirect proportional to the capsaicin test result.

Duodenal acid activated mechanisms that lead to a decreased sensitivity for intraluminal capsaicin; these mechanisms might protect duodenal chemonociceptors from being sensitized by acid. Whether this mechanism is impaired in patients with upper gastrointestinal functional disease remains to be determined.