Protective effects of nedocromil sodium on cellular and biohumoral components present in the bronchial alveolar lavage fluid and in peripheral blood in atopic asthmatics.
Nedocromil sodium, a disodium salt of a pyroquinolinedicarboxylic acid, raises the bronchial hyperresponsiveness threshold, because it inhibits the mediators released by the various cells, and reduces the involvement and activation of inflammatory cells. The aim of this study was to evaluate the state of activation of the immunocompetent cells and the main chemical mediators present in the bronchoalveolar lavage (BAL) fluid from 10 atopic asthmatic patients, before and after treatment with nedocromil sodium. The following examinations were performed before treatment and after 120 days of therapy with nedocromil sodium at 16 mg/day (two 2-mg puffs x 4): the level of chemical mediators and the state of activation of immunocompetent cells in BAL fluid; immunological analytes in activation of immunocompetent cells in BAL fluid; immunological analytes in peripheral blood; aspecific bronchial challenge test with ultrasonicated bidistilled H2O fog to evaluate variations in the hyperreactivity threshold; questionnaire to determine any adverse effects of treatment (cough, breathlessness, sleep disorders). Our findings demonstrate that nedocromil sodium prevents the release of chemotactic and inflammatory mediators by the effector cells and thus stabilizes microvascular permeability and epithelial damage, so raising the threshold of response to bronchoconstriction stimuli. Lastly, nedocromil sodium is associated with a better preventive therapeutic efficacy and good tolerance and can therefore be suggested as a valid drug to be used in the long-term treatment of bronchial asthma.
Mazzarella
G
G
Institute of Tuberculosis and Lung Diseases S. Marcatili, 1st Medical and Surgical School, 2nd University of Naples, Italy.
Grella
E
E
Romano
L
L
Perna
A
A
Marzo
C
C
Guarino
C
C
Cammarata
A
A
Bianco
A
A
Liccardo
G
G
D015121:6-Ketoprostaglandin F1 alpha / Q000032:analysis; D000328:Adult; D000418:Albumins / Q000032:analysis; D001249:Asthma / Q000097:blood / Q000188:drug therapy* / Q000276:immunology; D001798:Blood Proteins / Q000032:analysis; D016535:Bronchial Hyperreactivity / Q000188:drug therapy / Q000276:immunology; D001985:Bronchial Provocation Tests; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry* / Q000166:cytology*; D015232:Dinoprostone / Q000032:analysis; D047091:Eosinophil Granule Proteins; D006801:Humans; D006967:Hypersensitivity / Q000276:immunology; D007136:Immunoglobulins / Q000097:blood; D007155:Immunologic Factors / Q000032:analysis* / Q000097:blood; D007962:Leukocytes / Q000187:drug effects*; D007975:Leukotriene B4 / Q000032:analysis; D008214:Lymphocytes / Q000187:drug effects / Q000473:pathology; D008264:Macrophages / Q000187:drug effects*; D008297:Male; D017835:Nedocromil / Q000494:pharmacology / Q000627:therapeutic use*; D010447:Peptide Hydrolases / Q000032:analysis; D012260:Ribonucleases; D013929:Thromboxane B2 / Q000032:analysis
D000418:Albumins; D001798:Blood Proteins; D047091:Eosinophil Granule Proteins; D007136:Immunoglobulins; D007155:Immunologic Factors; D017835:Nedocromil; D007975:Leukotriene B4; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; D012260:Ribonucleases; D010447:Peptide Hydrolases; C023073:tosylarginine methyl ester hydrolase; D015232:Dinoprostone