Our library of drug research abstracts drawn from the medical literature is updated on a regular schedule, and you can be assured that new flonase research articles will be listed here shortly after becoming available to us.
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Medical research on flonase
J Mol Med. 2008 Jul 4;
Mortaz E, Rad MV, Johnson M, Raats D, Nijkamp FP, Folkerts G
The combination of inhaled corticosteroids and long-acting beta(2)-adrenoceptor agonists is increasingly used in chronic obstructive pulmonary disease (COPD). Recently, we have demonstrated that combination of salmeterol and fluticasone propionate (FP) additionally suppress the production of IL-8 by human monocyte. In this study, the molecular mechanism behind the effectiveness of this combination therapy is investigated in human neutrophils. Human neutrophils were preincubated with salmeterol or FP or the combination. The amount of interleukin-8 (IL-8), elastase and matrix metalloproteinases (MMP)-2 and -9 releases, and reactive oxygen species (ROS) generation and expression of MAP kinase phosphatase (MKP-1) and glucocorticoid receptor (GR) were determined. Cigarette smoke medium (CSM) induces an increased expression of CXC receptors and the production of ROS that may explain the strong production of IL-8 by neutrophils. The expression of CXC receptors, the production of ROS, and the release of elastase and MMP-2 and -9 were not influenced by salmeterol, FP, or the combination. Interestingly, the combination therapy had an additive suppressive effect on the CSM-induced production of IL-8. The latter could be explained by an increased mRNA expression of MKP-1, the GR and an increased translocation of the GR to the nucleus. This leads eventually to suppression of both the NF-kappaB and MAPK pathways and, hence, to less IL-8 production by the neutrophil. These data are in support for the use of a combination therapy in COPD patients.
Ann Allergy Asthma Immunol. 2008 Jun; 100(6): 601-7
Robroeks CM, van de Kant KD, van Vliet D, Kester AD, Hendriks HJ, Damoiseaux JG, Wodzig WK, Rijkers GT, Dompeling E, Jöbsis Q
BACKGROUND: Extra-fine hydrofluoroalkane-beclomethasone differs from other inhaled corticosteroids by its fine aerosol characteristics. Therefore, extra-fine hydrofluoroalkane-beclomethasone may be particularly useful for treating peripheral airway inflammation in asthma. OBJECTIVE: To analyze the anti-inflammatory effects of extra-fine hydrofluoroalkane-beclomethasone vs fluticasone dry powder inhaler (DPI) in asthmatic children by measuring bronchial and alveolar nitric oxide (NO) and inflammatory markers in exhaled breath condensate (EBC). METHODS: In a 6-month crossover study, 33 children aged 6 to 12 years with moderate persistent asthma were randomly treated with extra-fine hydrofluoroalkane-beclomethasone (200 microg daily via an Autohaler) and fluticasone DPI (200 microg daily via a Diskus). The primary outcome variables were alveolar NO concentration and bronchial NO flux. The secondary outcome variables were levels of inflammatory markers in EBC, lung function indices, symptoms, exacerbations, and adverse effects. All the variables were recorded at baseline and after each treatment period. RESULTS: Mean +/- SE alveolar NO concentration and bronchial NO flux were comparable after treatment with hydrofluoroalkane-beclomethasone vs fluticasone DPI (4.7 +/- 0.5 vs 4.3 +/- 0.5 ppb, P = .55, and 1,124.3 +/- 253.6 vs 1,029.1 +/- 195.5 pL/s, P = .70, respectively). In addition, levels of inflammatory markers in EBC, lung function indices, and symptoms did not differ between treatments. Patients used fewer beta2-agonists during the last 2 weeks of hydrofluoroalkane-beclomethasone treatment. CONCLUSION: The anti-inflammatory effects of hydrofluoroalkane-beclomethasone are similar to those of fluticasone DPI in children with moderate persistent asthma.
Allergy. 2008 Jul; 63(7): 932-8
Bateman ED, Bousquet J, Busse WW, Clark TJ, Gul N, Gibbs M, Pedersen S,
BACKGROUND: Uncontrolled asthma is characterized by variability. Current asthma guidelines recommend focussing on the achievement and maintenance of control but few studies have examined in detail, using composite measures of control, the stability and potential duration of control once achieved. In this post-hoc analysis of the results of the Gaining Optimal Asthma controL (GOAL) study, we examine the association between the level of asthma control achieved during the step-up phase of the study and the stability of control experienced during the maintenance phase. METHODS: GOAL was a 1-year, randomized, stratified, double-blind study of 3421 patients with uncontrolled asthma, which compared salmeterol/fluticasone propionate combination with fluticasone propionate in achieving two composite, guideline-based measures of control: totally controlled and well-controlled asthma. We analysed the proportion and duration of time spent in control, the effect of treatment on asthma stability, and the impact of asthma control stability on unscheduled use of healthcare resources. RESULTS: In patients achieving well-controlled or totally controlled asthma, at least well-controlled asthma was maintained for a median of almost 3 and 6 months, and for more than 85% and 95% of weeks of follow-up, respectively. A high level of stability was confirmed in a Markov analysis investigating transitional probability of change in control status. Variability in control was associated with increased probability of an unscheduled healthcare resource use (odds ratio: 1.06, P < 0.001). CONCLUSIONS: Most patients achieving guideline-defined control can maintain at least a similar level of control with regular, stable dosing, with little likelihood of losing control.
South Med J. 2008 Jun 14;
Nepal M, Padma H
Allergic granulomatous vasculitis, or Churg-Strauss syndrome, is a small vessel, multisystem vasculitis that can affect multiple organs. It is usually idiopathic, but recent case reports have implicated leukotriene receptor antagonists (LTRA) and inhaled corticosteroids in the development of this rare syndrome. We report a case that acutely developed skin-limited Churg Strauss-like cutaneous allergic granulomatous vasculitis after initiating therapy with inhaled fluticasone and salmeterol for poorly controlled asthma symptoms. Our result thus highlights the importance of keeping the differential diagnosis of drug-induced Churg-Strauss syndrome in patients who have recently been prescribed inhaled steroids like fluticasone when they present with rashes of varying severity.
Mortality in COPD: inevitable or preventable? Insights from the cardiovascular arena.
COPD. 2008 Jun; 5(3): 187-200
Halpin D
Mortality due to chronic obstructive pulmonary disease continues to rise, whereas mortality rates related to cardiovascular disease appear to be slowing, or even declining. This is due at least in part to more widespread use of preventative therapies that have been shown to reduce cardiovascular mortality, raising the question of whether appropriate use of therapies for chronic obstructive pulmonary disease which potentially reduce mortality could have a similar impact. This article discusses approaches used successfully in managing heart disease and considers whether these can be applied to chronic obstructive pulmonary disease and whether a better understanding of the strongest predictors of mortality in chronic obstructive pulmonary disease is needed. It reviews the role of inhaled corticosteroids, both alone and in combination with long-acting beta(2)-agonists, in individuals with chronic obstructive pulmonary disease, including the role of combination therapy with inhaled corticosteroids/long-acting beta(2)-agonists (budesonide/formoterol or salmeterol/fluticasone propionate) in decreasing exacerbations and improving health status, potentially providing survival benefits in chronic obstructive pulmonary disease. This review also discusses the potential impact of treatments indicated for cardiovascular disease on chronic obstructive pulmonary disease and possible links between the two diseases.
Beta2-agonists potentiate corticosteroid-induced neutrophil survival.
COPD. 2008 Jun; 5(3): 163-9
Perttunen H, Moilanen E, Zhang X, Barnes PJ, Kankaanranta H
Neutrophils are considered to play a role in the pathogenesis of chronic obstructive pulmonary disease (COPD) and severe asthma. Recent guidelines recommend the use of a combination of inhaled corticosteroids (ICS) and long-acting beta2-agonists (LABA) in the treatment of COPD with exacerbations and asthma not adequately controlled by ICS alone. LABA have been proposed to have a synergistic effect with corticosteroids by activating glucocorticoid receptors. The aim of this study was to investigate the effect of beta2-agonists on the inhibitory effects of corticosteroids on human neutrophil apoptosis. In addition, the effects of beta2-agonists on spontaneous neutrophil apoptosis and on GM-CSF- and LTB4-afforded survival were also evaluated. Neutrophils were isolated from human blood under sterile conditions and cultured for 16 hours. Apoptosis was assessed by relative DNA fragmentation assay. Morphological analysis was used as a control method to confirm the occurrence of apoptosis. Salbutamol, formoterol and salmeterol prolonged the lifespan of budesonide- and fluticasone propionate-treated neutrophils by inhibiting apoptosis. Formoterol and salbutamol partly reversed the inhibitory effect of GM-CSF on neutrophil apoptosis. In contrast, the effects of beta(2)-agonists on spontaneous neutrophil apoptosis and on LTB(4)-afforded survival were negligible. beta2-agonists potentiate corticosteroid-induced neutrophil survival at clinically relevant drug concentrations. Whether these effects translate into clinically relevant changes in lung neutrophil numbers remains to be demonstrated.
Is salmeterol/fluticasone propionate equivalent to tiotropium bromide in the treatment of COPD?
Am J Respir Crit Care Med. 2008 Jul 1; 178(1): 105; author reply 106-7
Gillissen A
[Adrenal insufficiency during inhaled corticosteroid treatment in a child with asthma]
Ugeskr Laeger. 2008 Jun 9; 170(24): 2161
Bjerre JV, Bender L, Naeraa RW, Rix M
We report a 12 year-old asthmatic girl with adrenal insufficiency during inhaled corticosteroid treatment. Symptoms, investigations and treatment are discussed.
Methods Find Exp Clin Pharmacol. 2008 Mar; 30(2): 149-71
Moral MA, Tomillero A
Gateways to Clinical Trials are a guide to the most recent clinical trials in current literature and congresses. The data in the following tables has been retrieved from the Clinical Trials Knowledge Area of Prous Science Integrity, the drug discovery and development portal, http://integrity.prous.com.This issue focuses on the following selection of drugs: 131-I-Chlorotoxin, 423557; Abatacept, Ad.Egr.TNF.11D, Adalimumab, AE-941, Ambrisentan, AMR-001, Anacetrapib, Anakinra, Aripiprazole, Atazanavir sulfate; BAY-639044, Bazedoxifene acetate, Belimumab, Bevacizumab, Bortezomib, Botulinum toxin type B, Brivaracetam, Bucindolol hydrochloride; Carfilzomib, Carisbamate, CCX-282, CD20Bi, Ceftobiprole, Certolizumab pegol, CF-101, Cinacalcet hydrochloride, Cypher; Darifenacin hydrobromide, Degarelix acetate, Denosumab, Desvenlafaxine succinate, Dexlansoprazole, Dexverapamil, Drotrecogin alfa (activated), Duloxetine hydrochloride, Dutasteride; Efalizumab, EPs-7630, Escitalopram oxalate, Etoricoxib; Fluticasone furoate, Fondaparinux sodium, Fospropofol disodium; Hexadecyloxypropyl-cidofovir, HIV gp120/NefTat/AS02A, HPV-6/11/16/18; INCB-18424, Incyclinide, Inhalable human insulin, Insulin detemir; KNS-760704, KW-0761; Lacosamide, Lenalidomide, Levetiracetam, Licofelone, Lidocaine/prilocaine; mAb 216, MEDI-528, Men ACWY, Meningococcal C-CRM197 vaccine, Methylnaltrexone bromide; Nemifitide ditriflutate, Nicotine conjugate vaccine, Nilotinib hydrochloride monohydrate; Octaparin; Parathyroid hormone (human recombinant), Pegaptanib octasodium, Pitrakinra, Prasterone, Pregabalin; Ranelic acid distrontium salt, Rasagiline mesilate, Retigabine, Rimonabant, RTS,S/AS02D; Sarcosine, Sitaxentan sodium, Solifenacin succinate, Sunitinib malate; Taranabant, Taxus, Teduglutide, Teriparatide, Ticagrelor, Travoprost, TRU-015; USlipristal acetate, Urocortin 2; Vardenafil hydrochloride hydrate; YM-155, Yttrium 90 (90Y) ibritumomab tiuxetan; Zanolimumab, Zoledronic acid monohydrate, Zotarolimus, Zotarolimus-eluting stent.
Environ Health Perspect. 2008 Jun; 116(6): 799-805
Alexis NE, Lay JC, Haczku A, Gong H, Linn W, Hazucha MJ, Harris B, Tal-Singer R, Peden DB
BACKGROUND: Ozone exposure induces airway neutrophilia and modifies innate immune monocytic cell-surface phenotypes in healthy individuals. High-dose inhaled corticosteroids can reduce O(3)-induced airway inflammation, but their effect on innate immune activation is unknown. OBJECTIVES: We used a human O(3) inhalation challenge model to examine the effectiveness of clinically relevant doses of inhaled corticosteroids on airway inflammation and markers of innate immune activation in healthy volunteers. METHODS: Seventeen O(3)-responsive subjects [> 10% increase in the percentage of polymorphonuclear leukocytes (PMNs) in sputum, PMNs per milligram vs. baseline sputum] received placebo, or either a single therapeutic dose (0.5 mg) or a high dose (2 mg) of inhaled fluticasone proprionate (FP) 1 hr before a 3-hr O(3) challenge (0.25 ppm) on three separate occasions at least 2 weeks apart. Lung function, exhaled nitric oxide, sputum, and systemic biomarkers were assessed 1-5 hr after the O(3) challenge. To determine the effect of FP on cellular function, we assessed sputum cells from seven subjects by flow cytometry for cell-surface marker activation. RESULTS: FP had no effect on O(3)-induced lung function decline. Compared with placebo, 0.5 mg and 2 mg FP reduced O(3)-induced sputum neutrophilia by 18% and 35%, respectively. A similar effect was observed on the airway-specific serum biomarker Clara cell protein 16 (CCP16). Furthermore, FP pretreatment significantly reduced O(3)-induced modification of CD11b, mCD14, CD64, CD16, HLA-DR, and CD86 on sputum monocytes in a dose-dependent manner. CONCLUSIONS: This study confirmed and extended data demonstrating the protective effect of FP against O(3)-induced airway inflammation and immune cell activation.