Serum leptin levels in asthmatic children treated with an inhaled corticosteroid

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dc.contributor.authorGurkan, F
dc.contributor.authorAtamer, Y
dc.contributor.authorEce, A
dc.contributor.authorKocyigit, Y
dc.contributor.authorTuzun, H
dc.contributor.authorMete, N
dc.date.accessioned2024-04-24T16:18:57Z
dc.date.available2024-04-24T16:18:57Z
dc.date.issued2004
dc.departmentDicle Üniversitesien_US
dc.description.abstractBackground: Recent observations suggest the presence of an interaction between leptin and the inflammatory system; however, there is no adequate knowledge about the role of leptin in atopic states such as asthma. Objectives: To evaluate the potential role of leptin in relation to bronchial asthma and inhaled corticosteroid therapy. Methods: Twenty-three children with mild-to-moderate, newly diagnosed asthma enrolled in this 2-period trial. The control group consisted of 20 age- and sex-matched children. Serum leptin levels were measured in patients at initiation and after 4 weeks of budesonide treatment and were compared with control group measurements. Results: Asthmatic children had higher mean +/- SD serum leptin levels at admission (19.3 +/- 5.1 ng/mL) than after budesonide treatment (10.6 +/- 1.6 ng/mL) and vs control group measurements (9.8 +/- 1.6 ng/mL) (P < .001). There was a significant correlation between serum leptin levels before and after budesonide treatment (r = 0.68; P = .007). Mean +/- SD body mass indices in patients and controls were 16.7 +/- 2.1 and 16.9 +/- 2.6 kg/m(2), respectively. Serum leptin levels did not correlate with body mass indices before budesonide treatment in the study group (r = -0.13; P = .65) but correlated well after budesonide treatment (r = 0.58; P = .009) and in the control group (r = 0.65; P = .008). Conclusions: The role of leptin elevation in children with asthma might be a regulatory mechanism rather than being etiologic, but a question may be raised whether it is possible that leptin may contribute to poor patient outcomes. Further research, both basic and clinical, is essential to explain the exact mechanism.en_US
dc.identifier.doi10.1016/S1081-1206(10)61501-3
dc.identifier.endpage280en_US
dc.identifier.issn1081-1206
dc.identifier.issue3en_US
dc.identifier.pmid15478389
dc.identifier.scopus2-s2.0-4644320458
dc.identifier.scopusqualityQ1
dc.identifier.startpage277en_US
dc.identifier.urihttps://doi.org/10.1016/S1081-1206(10)61501-3
dc.identifier.urihttps://hdl.handle.net/11468/16349
dc.identifier.volume93en_US
dc.identifier.wosWOS:000224064800014
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoenen_US
dc.publisherAmer Coll Allergy Asthma Immunologyen_US
dc.relation.ispartofAnnals of Allergy Asthma & Immunology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subject[No Keyword]en_US
dc.titleSerum leptin levels in asthmatic children treated with an inhaled corticosteroiden_US
dc.titleSerum leptin levels in asthmatic children treated with an inhaled corticosteroid
dc.typeArticleen_US

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