Although the NAEP guidelines were published 7 years ago, compliance with the guidelines was low. It was especially poor for use of preventive medication and routine peak-flow measurement. Furthermore, the results showed that asthma specialists provided more thorough care than did primary care physicians in treating patients with asthma. Combining the results of the regression analyses revealed that some of the variation in rates of emergency department visits and hospitalizations among some subpopulations can be explained by the underuse of preventive medication. This study serves the goal of documenting the quality of care and services currently provided to patients with asthma through a large health maintenance organization and provides baseline information that can be used to design and assess effective population-based asthma disease management intervention programs.
Tumour necrosis factor (TNF) alpha affects immune response and airway inflammation, which are characteristics of asthma. Genetic factors may impact TNFa levels, and several polymorphisms in the TNF gene cluster on chromosome 6p21 have been associated with TNFa production and potential increased risk of asthma. The present paper evaluates the relation between two single nucleotide polymorphisms (SNPs) in the TNF gene cluster and asthma risk. The SNPs investigated here are guanine (G) to adenosine (A) substitutions in the TNFa and lymphotoxin alpha (LTa) genes. The TNFa SNP is at position -308 in the promoter region (TNFa-308), while the LTa SNP is in the first intron NcoI recognition sequence (LTa-NcoI). (For both SNPs the G allele is denoted as 1, and the A allele 2.) We determined TNFa-308 and LTa-NcoI genotypes in 511 individuals: 236 asthma cases and 275 non-asthmatic controls. Data were analysed by logistic regression of asthma status on the genotypes and potential confounders. TNFa-308*2 was positively associated with asthma, and this relation was strengthened when restricting cases to individuals reporting acute asthma: the adjusted odds ratio (OR) comparing carriers of one or two TNFa-308*2 alleles versus none was 1.86 (95% confidence interval (CI)=1.03 ± 3.34, P=0.04). Further restricting the subjects to those with a family history of asthma, and those of European-American ancestry strengthened the association even more: adjusted OR=3.16 (95% CI=1.04 ± 9.66; P=0.04). LTa-NcoI*1 was weakly associated with asthma, and analysis of both genes suggests that only the TNFa-308*2 allele increases risk of asthma.
Results from this observational study reinforce the positive impact that anticoagulation services have on anticoagulation therapy outcomes, emphasizing the importance of providing such services for patients undergoing treatment with warfarin.
A B S T R A C T Lymphocytes from normial noinallergic donors and patients with atopic disorders were analyzed for subpopulations bearing Fc receptors for immtnunoglobulin (Ig)E (Fce) and IgG (Fcy), surface IgM (sIgM) and IgD
6 patients suffering from severe atopic dermatitis with high serum IgE were investigated. 3 of the patients had elevated plasma histamine levels (1.5–2.0 ng/ml). Compared to 9 nonatopic normal volunteers, the patient showed increased in vitro histamine release from peripheral leukocytes after stimulation with iothalamate and methacholine: while there was no significant histamine release at a methacholine concentration of 10––4M in normals, 4 of the patients with atopic dermatitis showed measurable histamine release under these conditions in vitro. The uptake of radiolabeled serotonin by platelets in vitro was decreased in 2 of the patients. There was no significant difference in serotonin release induced in vitro by different concentrations of thrombin, epinephrine and methacholine; 2 patients showed an increased platelet release reaction after iodipamide stimulation. It is concluded that a general tendency to release vasoactive mediators, even after ‘nonimmunologic’ stimulation, might play a role in the pathogenesis of atopic dermatitis.
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