Background: Several environmental factors trigger attacks of asthma by immunological and non-immunological mechanisms. Among these factors are cited the passive or second hand smoking (SHS) which has a deleterious effect on the prognosis of childhood asthma and induces a resistance to treatment by corticosteroids. The aim of the present study was to identify parents of children with asthma who are smokers and to explore the possible negative impact of SHS exposure on the disease of asthmatic children. Materials and Methods:A cross sectional study was conducted from February 2012 to February 2013.The study population consisted of children with asthma. The information concerning the patients was collected from their medical records filled out by the physician in a clinical setting in direct communication with the patients, or their parents when it is a little child. A group of 100 children age between 2 and 15 years, with asthma were recruited for the study. The study children were divided into two groups: cases with 28 children from smoking families, and controls with 73 children from non-smoking families. Analysis of the number of respiratory infections, asthma exacerbations per year, and the average number of hospitalization was done in both groups.Results: Pearson chi2 test was adopted. We showed that smoking among the father was positively correlated with a higher number of hospitalizations for asthma, higher incidence of lower respiratory tract infections and asthma exacerbations. Similarly, the maternal smoking was positively correlated with a higher number of hospitalizations for asthma, lower respiratory tract infections and asthma exacerbations. Conclusion:Passive smoking causes respiratory illness, asthma, poor growth, neurological disorders in children. To avoid the risk of respiratory and allergic diseases by environmental tobacco smoke, absolute smoking cessation by parents is strongly recommended.

Henoch-Schönlein purpura (HSP) is a small-vessel vasculitis with cutaneous, articular, gastrointestinal, and renal manifestations. Leukocytoclastic vasculitis and IgA deposits are classically found when involved skin and kidneys are biopsied. The disease's etiology remains unknown, although many bacterial and viral infections have been described as triggering factors. A 53-year-old woman presented with fever, arthralgia, and non-thrombocytopenic purpura. She also had a segmental pulmonary collection with peripheral alveolar consolidation. Staphylococcus aureus and mycobacteria growth was found on sputum cultures. In addition to intravenous antibiotics and anti-mycotic drugs, high-dose corticosteroids were urgently administered due to the development of severe intestinal symptoms. A cutaneous biopsy later confirmed HSP. Microbial identification yielded Mycobacterium xenopi . In the review of the literature, we only found 12 cases of Mycobacterium tuberculosis and one case of Mycobacterium avium-intracellulare complex that were associated with HSP. Nearly, half of the cases responded to anti-mycotic treatment alone. The rest required immunosuppressants. We report the first case of M. xenopi pulmonary infection in HSP. This disease process can have a severe course, which requires rapid recognition and treatment.

RATIONALE: Systemic Seminal Plasma Hypersensitivity (SPH) is caused by specific IgE to human prostate specific antigen (hPSA). Presensitization to dog PSA (Can f 5) was reported to be associated with SPH in women sensitized to dog due to cross-reactivity. Conformational epitope mapping of hPSA is required to elucidate this cross-reactivity and to design hypoallergenic derivatives for desensitization. METHODS: Sequence-and structure-based bioinformatic analyses were performed to identify potential hPSA epitope(s). Sequences of hPSA and other known serine protease allergens were retrieved from the uniprot database. The hPSA structure was obtained from its monoclonal antibodybound form (2ZCH.pdb) to study its antigenic surface and to model the Can f 5 structure. Site-directed mutagenesis of top solvent-exposed residues was performed to assess their role in IgE binding. RESULTS: About 45% (5054.97 A 2) of hPSA surface is polar. Four areas, including a region Arg85-Ser99 (containing the mAb binding site) have been identified as potential epitopes. A close evolutionary relationship between hPSA and Can f 5 (57% sequence identity; 89% sequence similarity) was noted. The alpha-C backbone superimposition (global RMSD51.1 A) indicated an overall structural similarity, while conserved surfaceexposed patches indicated possible cross-reactivity between hPSA and Can f 5. Preliminary results of site-directed mutagenesis indicated the importance of specific surface exposed residues (e.g. R85) in IgE binding. CONCLUSIONS: Epitope residues are dispersed on hPSA surface. Conserved patches might be responsible for cross-reactivity between hPSA and Can f 5 in some patients. Peptide microarray-based epitope mapping and detailed characterization of mutant hPSA proteins are ongoing to confirm these findings.