title: Serum-soluble TRAIL levels in patients with severe persistent allergic asthma: its relation to omalizumab treatment.
abstract: BACKGROUND
  In this study we compare the Omalizumab treatment modality in the dynamics of cell apoptosis regulating molecules in both severe persistent asthma patients who had no other any allergic disease, newly diagnosed patients with allergic asthma, and healthy volunteers.
  
  
  METHODS
  Severe persistent allergic asthma patients were subjected to measurement of serum soluble TRAIL (TNF-related apoptosis-inducing ligand) levels during the active disease phase and the stable phase which occurred 4 months after Omalizumab treatment. Serum sTRAIL concentrations were measured by a solid phase sandwich enzyme-linked immunosorbent assay. Concentration levels were compared with those of age- and sex-matched newly diagnosed patients with allergic asthma, and healthy controls. All assays were carried out in duplicate. Total serum IgE levels, antinuclear antibody (ANA), rheumatoid factor (RF), hepatitis markers, C3, C4 and eosinophil levels were evaluated in all patients.
  
  
  RESULTS
  ANA, RF, hepatitis markers were negative in all patients. Complement 3 and 4 levels were normal in all patients. Prick tests in all patients were detected in mite and grass allergy. These results correlated with specific IgE. There were no differences between the healthy controls, newly diagnosed allergic asthma patients, and non-treated severe persistent allergic asthma patients during the active phase. Interestingly, the levels in variances of the patients who had the effective omalizumab treatment were significantly lower than the healthy controls, while the mean values were not statistically significant.
  
  
  CONCLUSIONS
  Our study gives a different perspective on severe persistent allergic asthma and omalizumab treatment efficacy at the cell apoptosis-linked step by the serum sTRAIL levels.
authors.affiliation: Allergy and Clinical Immunology Unit, Antalya Education and Training Hospital, Antalya, Turkey. adidyal@yahoo.com
authors.forename: Arzu Didem
authors.initials: AD
authors.lastname: Yalcin
authors.forename: Atil
authors.initials: A
authors.lastname: Bisgin
authors.forename: Aysegul
authors.initials: A
authors.lastname: Kargi
authors.forename: Reginald M
authors.initials: RM
authors.lastname: Gorczynski
mesh_terms: D000293:Adolescent; D000328:Adult; D018927:Anti-Asthmatic Agents / Q000627:therapeutic use*; D000888:Antibodies, Anti-Idiotypic / Q000627:therapeutic use*; D000974:Antibodies, Antinuclear / Q000097:blood; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use*; D001249:Asthma / Q000097:blood* / Q000188:drug therapy / Q000209:etiology; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D006967:Hypersensitivity / Q000097:blood* / Q000150:complications / Q000188:drug therapy; D007073:Immunoglobulin E / Q000097:blood; D008297:Male; D008875:Middle Aged; D000069444:Omalizumab; D012217:Rheumatoid Factor / Q000097:blood; D053221:TNF-Related Apoptosis-Inducing Ligand / Q000097:blood*; D055815:Young Adult
chemical_list: D018927:Anti-Asthmatic Agents; D000888:Antibodies, Anti-Idiotypic; D000974:Antibodies, Antinuclear; D061067:Antibodies, Monoclonal, Humanized; D053221:TNF-Related Apoptosis-Inducing Ligand; C505653:TNFSF10 protein, human; D000069444:Omalizumab; D007073:Immunoglobulin E; D012217:Rheumatoid Factor