Effects of chili on postprandial gastrointestinal symptoms in diarrhoea predominant irritable bowel syndrome: evidence for capsaicin-sensitive visceral nociception hypersensitivity.

Irritable bowel syndrome (IBS) patients often complain of gastrointestinal symptoms after eating chili. However, the effect of chili ingestion on gastrointestinal symptoms in IBS patients has not been characterized. To study the effect of chili-containing foods on postprandial gastrointestinal symptoms in diarrhoea-predominant IBS (IBS-D), 20 IBS-D patients underwent gastrointestinal symptoms and postprandial colonic transit evaluations after ingesting three different meals: (i) a standard meal, (ii) a spicy meal (a standard meal mixed with 2 g chili), and (iii) a standard meal with 2 g chili in capsules, in a randomized crossover fashion. Postprandial gastrointestinal symptoms were scored every 15 min for 2 h using visual analogue scales. Thirty-eight healthy volunteers were used as controls. In healthy volunteers, the spicy meals and meals with chili capsules induced only mild abdominal burning relative to the standard meals (P < 0.05), whereas it induced significant levels of abdominal pain and burning in IBS-D patients (P < 0.05). Other gastrointestinal symptoms and postprandial colonic transit after spicy meals and meals with chili capsules did not differ from standard meals in IBS-D and controls (P > 0.05). Diarrhoea-predominant IBS patients and controls reported similar oral burning symptoms when eating spicy meals (P > 0.05). Both the spicy meal and the standard meal with chili capsules led to similar severity of gastrointestinal symptoms (P > 0.05). Diarrhoea-predominant IBS patients exhibit gut hypersensitivity to chili. Chili ingestion produced more abdominal pain and burning in IBS-D patients than in healthy volunteers, but was associated with similar oral burning symptoms.

Expanding the phenotypic spectrum of Caffey disease.

Infantile cortical hyperostosis (ICH) is an inherited disorder characterized by hyperirritability, acute inflammation of soft tissues, and massive subperiosteal new bone formation. It typically appears in early infancy and is considered a benign self-limiting disease. We report a three-generation Thai family with ICH, the oldest being a 75-year-old man. A heterozygous mutation for a 3040C-->T in exon 41 of COL1A1 was found in affected individuals, further confirming the autosomal dominance of Caffey disease that is caused by this particular mutation. The novel findings in our studies include short stature and persistent bony deformities in the elderly. The height mean Z-score of the five affected individuals was -1.75, compared to 0.53 of the other seven unaffected individuals giving a p-value of 0.008. Short stature may be partly due to progressive height loss from scoliosis, compression fractures of the spine and genu varus. These features, which have not previously been described, expand the phenotypic spectrum of the Caffey disease.