The effect of peripheral blood eosinophilia on inflammatory markers in asthmatic patients with lower respiratory tract infections.

BACKGROUND: To investigate the behaviour of the inflammatory marker neutrophil-to-lymphocyte ratio (NLR) in the presence of peripheral blood eosinophilia (PBE) in paediatric asthma patients with lower respiratory tract (LRT) infections. METHODS: This retrospective study enrolled consecutive patients aged ≥5 years who were diagnosed with asthma and whose haemogram values were available. The patients were further subdivided based on the presence or absence of LRT infections and allergies. NLR and C-reactive protein (CRP) were evaluated in relation to the presence or absence of PBE (≥4% eosinophils). RESULTS: A total of 991 patients were enrolled in the study. Patients with LRT infections had significantly higher leucocyte and neutrophil counts, a greater NLR and a higher level of CRP compared with patients without LRT infections. Overall, patients with PBE had significantly lower NLRs and CRP regardless of the presence or absence of an LRT infection. The PBE percentage showed moderate inverse correlations with NLR ( r = -0.34) and CRP ( r = -0.20). CONCLUSION: The presence of PBE was significantly associated with lower NLR and CRP regardless of the presence or absence of an infectious condition.

The GABAA receptor γ2 subunit (R43Q) mutation in febrile seizures.

BACKGROUND: Febrile seizure is the most common form of childhood seizure. Although its exact cause is unclear, many researchers emphasize the importance of its genetic predisposition. Recent genetic studies revealed the importance of the mutations of the gamma-aminobutyric acid A receptor as the etiology of the febrile seizures. R43Q mutation affecting the γ2-subunit N-terminal domain has been related to childhood absence epilepsy and febrile seizure. METHODS: We investigated R43Q mutations of the GABRG2 gene, located on the long arm of chromosome 5 encoding the γ2-subunit of the gamma-aminobutyric acid A receptor. We studied 44 patients with febrile seizure and 49 children without any febrile seizure who were admitted to our clinic. RESULTS: We found that 36% of our patient group, the children who experienced febrile convulsions, had heterozygous R43Q mutation. Statistical studies revealed that heterozygous R43Q mutation of gamma-aminobutyric acid A receptor γ2 subunit was higher in the study group than in the control group (P < 0.01). CONCLUSIONS: Heterozygous gamma-aminobutyric acid A receptor γ2 subunit (R43Q) mutation may have an effect in the development of febrile seizures.