Fecal Inflammatory Protein Levels in Children with Autism Spectrum Disorder vs Healthy Siblings
Overview
This study compared fecal α1-antitrypsin, immunoglobulin A, and calprotectin levels in 57 children with ASD and their 57 biological siblings without ASD. No statistically significant differences were found, though exploratory subgroup analyses suggested potential variations related to ASD severity. The findings align with prior meta-analyses showing no consistent evidence of gut inflammation in ASD.
Background
Autism spectrum disorder (ASD) is a neurodevelopmental condition often accompanied by gastrointestinal symptoms. Inflammatory proteins in stool, such as α1-antitrypsin (A1AT), immunoglobulin A (IgA), and calprotectin (Cal), have been proposed as biomarkers to understand gut inflammation in ASD. Prior studies have yielded inconsistent results, and sibling-matched designs help control for shared environmental and genetic factors. Understanding gut immune markers may clarify the role of inflammation in ASD pathogenesis and aid in biomarker development.
Data Highlights
Protein
ASD Group
Sibling Group
Statistical Significance
IgA
Trend toward higher levels
Lower levels
Not significant
Calprotectin
Trend toward higher levels
Lower levels
Not significant
α1-Antitrypsin
Trend toward lower levels
Higher levels
Not significant
Key Findings
No statistically significant differences in fecal α1-antitrypsin, IgA, or calprotectin between children with ASD and their healthy siblings.
Exploratory subgroup analysis indicated higher IgA levels in children with moderate ASD compared to siblings.
Altered S100A8/S100A9 ratio observed in children with severe ASD, suggesting possible immune dysregulation.
Subgroup analyses were underpowered and hypothesis-generating, requiring validation in larger cohorts.
Findings are consistent with meta-analyses reporting no consistent evidence of gut inflammation in ASD.
Clinical Implications
Current evidence does not support routine use of fecal α1-antitrypsin, IgA, or calprotectin as biomarkers for gut inflammation in ASD. Clinicians should interpret fecal inflammatory protein levels cautiously in ASD patients, considering the lack of significant differences compared to siblings. Larger, well-powered studies are needed before these markers can inform diagnosis or management.
Conclusion
This sibling-controlled study found no significant differences in key fecal inflammatory proteins between children with ASD and their healthy siblings, aligning with prior research that questions the role of gut inflammation in ASD. Further research with larger, sex-matched cohorts is necessary to clarify these findings.
