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Subclinical intestinal inflammation in siblings of children with Crohn's disease
Mimi Pham1, Steven T Leach, Daniel A Lemberg
1Department of Gastroenterology, Sydney Children's Hospital, Randwick, Sydney, Australia.
Insights
Subclinical intestinal inflammation was detected in siblings of pediatric Crohn's disease patients using fecal S100A12. This gut inflammation may indicate a risk factor for developing Crohn's disease later in life.
Area of Science:
- Gastroenterology
- Immunology
- Genetics
Background:
- Crohn's disease pathogenesis involves intestinal permeability, inflammation, and genetic/environmental factors.
- Identifying early indicators of disease risk is crucial for Crohn's disease management.
Purpose of the Study:
- To evaluate subclinical intestinal inflammation in healthy first-degree relatives of pediatric Crohn's disease patients.
- To utilize non-invasive fecal markers for assessing gut inflammation prevalence.
Main Methods:
- Collected stool samples from Crohn's disease patients, their siblings, and parents.
- Measured fecal S100A12 and calprotectin levels using ELISA and PhiCal assays.
- Compared marker levels against healthy pediatric and adult controls.
Main Results:
- Fecal S100A12 levels were significantly elevated in siblings and patients compared to controls (p < 0.001).
- Fecal calprotectin levels were lower in siblings than pediatric controls (p = 0.03).
- No elevated fecal markers were observed in parents compared to adult controls.
Conclusions:
- Subclinical gut inflammation is present in first-degree relatives of Crohn's disease patients.
- Elevated fecal S100A12 in siblings suggests a potential risk marker for Crohn's disease.
- Further research is warranted to understand the implications of subclinical inflammation in disease development.
Background:
Intestinal permeability and altered inflammatory responses, along with genetic and environmental factors, likely contribute to the pathogenesis of Crohn's disease.
Aims:
This study aimed to assess the presence and prevalence of subclinical intestinal inflammation among apparently healthy, first-degree relatives of pediatric patients with Crohn's disease, using non-invasive fecal markers.
Methods:
Stool samples were collected from 13 patients with Crohn's disease, 36 siblings and 41 parents. S100A12 levels were measured using an in-house ELISA assay and calprotectin levels were determined using the PhiCal test, with levels compared to normal healthy population controls.
Results:
Fecal S100A12 levels in siblings (median, 14 mg/kg; 95% confidence interval [CI], 9-32 mg/kg) and patients (71 mg/kg; CI 4-286 mg/kg) differed significantly from pediatric controls (1 mg/kg; CI 1-5 mg/kg; p < 0.001). In contrast, fecal calprotectin levels in siblings (22 mg/kg; CI 15-31 mg/kg) were lower than that of pediatric controls (31 mg/kg; CI 19-52 mg/kg; p = 0.03). Fecal markers were not elevated in parents compared to adult controls.
Conclusions:
This study provides further evidence of subclinical intestinal inflammation amongst first-degree relatives of patients with Crohn's disease. The presence of sub-clinical gut inflammation may be a risk factor for the subsequent development of Crohn's disease.
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