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Allergic Proctocolitis Is a Risk Factor for Functional Gastrointestinal Disorders in Children.
Giovanni Di Nardo1, Cesare Cremon2, Simone Frediani3
1Pediatric Gastroenterology Unit, Santobono-Pausilipon Children's Hospital, Naples, Italy; Pediatric Gastroenterology Unit, International Hospital Salvator Mundi, Rome, Italy.
Infants with allergic proctocolitis may develop functional gastrointestinal disorders (FGIDs) later in childhood. This early-life condition is a new risk factor for persistent digestive symptoms in children.
Area of Science:
- Pediatric Gastroenterology
- Allergy and Immunology
- Childhood Health Outcomes
Background:
- Allergic proctocolitis is a condition causing self-limiting rectal bleeding in infants.
- Functional gastrointestinal disorders (FGIDs) are common in childhood and can have long-term impacts.
- The potential link between early-life allergic conditions and later FGIDs is not well-established.
Purpose of the Study:
- To investigate if allergic proctocolitis in infancy predisposes children to developing FGIDs later in childhood.
- To identify risk factors associated with FGIDs in children with a history of allergic proctocolitis.
Main Methods:
- A cohort study involving 80 infants diagnosed with allergic proctocolitis and 80 matched controls.
- Longitudinal follow-up via telephone interviews every 12 months until age 4.
- Assessment of FGIDs using the Questionnaire on Pediatric Gastrointestinal Symptoms, Rome III version.
Main Results:
- 15.0% of children with allergic proctocolitis developed FGIDs, compared to 5.0% of controls (P=0.035).
- Children with allergic proctocolitis had an adjusted odds ratio of 4.39 for developing FGIDs.
- Duration of hematochezia was the only significant independent predictor for FGIDs development (OR, 3.14).
Conclusions:
- Allergic proctocolitis is identified as a novel risk factor for FGIDs in children.
- Early-life allergic inflammation may trigger persistent digestive symptoms, supporting the concept of 'postinflammatory' FGIDs.
- This finding broadens the understanding of FGID etiology beyond infectious triggers.
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