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Abstract:
Decreased alpha-1-antitrypsin (alpha 1AT) levels have been observed in children affected by bronchiolitis; however, variant alleles Pi (S, Z) which are usually associated with reduction of the inhibitor do not show a higher incidence in children affected by this disease. Subtypes M2 and M3 of alpha 1AT have recently been considered to play a role in the development of allergic states in children as well as in chronic obstructive lung disease in adults. In the present study we have investigated the incidence of PiM subtypes in 98 children affected by bronchiolitis. No greater incidence of subtypes M2 and M3 was observed in these children than in controls. These results rule out the hypothesis of a pathogenetic role of M subtypes in the development of bronchiolitis in children.
Insights
This study found no link between alpha-1-antitrypsin (alpha 1AT) M subtypes and bronchiolitis in children. The M2 and M3 variants do not appear to cause this common childhood respiratory illness.
Area of Science:
- Pediatrics
- Pulmonology
- Genetics
Background:
- Decreased alpha-1-antitrypsin (alpha 1AT) levels are noted in pediatric bronchiolitis.
- Known alpha 1AT deficiency alleles (Pi S, Z) are not more common in affected children.
- Alpha 1AT M subtypes (M2, M3) are hypothesized to contribute to pediatric allergic conditions and adult COPD.
Purpose of the Study:
- To investigate the incidence of alpha-1-antitrypsin (alpha 1AT) PiM subtypes in children with bronchiolitis.
- To determine if M2 and M3 subtypes are associated with the development of bronchiolitis in pediatric patients.
Main Methods:
- Study included 98 children diagnosed with bronchiolitis.
- Genotyping was performed to identify the presence of alpha-1-antitrypsin (alpha 1AT) PiM subtypes (M2, M3).
- Incidence of M2 and M3 subtypes in bronchiolitis patients was compared to control groups.
Main Results:
- No increased incidence of alpha-1-antitrypsin (alpha 1AT) M2 or M3 subtypes was found in children with bronchiolitis compared to controls.
- The study did not observe a higher prevalence of these specific alpha 1AT variants in the patient cohort.
Conclusions:
- The findings do not support a pathogenetic role for alpha-1-antitrypsin (alpha 1AT) M subtypes (M2, M3) in the development of bronchiolitis in children.
- This research rules out the hypothesis linking specific alpha 1AT M subtypes to childhood bronchiolitis etiology.