American journal of respiratory medicine: drugs, devices, and other interventions (Am J Respir Med )

Description

The American Journal of Respiratory Medicine is a peer reviewed journal providing comprehensive coverage of the therapy and management of a wide range of respiratory disorders. The journal publishes up to date, critical reviews and high quality original clinical research relating to the use of drugs, devices, diagnostics and other interventions for the treatment of patients with respiratory disorders. The American Journal of Respiratory Medicine publishes a regular program of independent review articles covering all aspects of the management of respiratory disorders, particularly the place in therapy of newer and established drugs and devices, with the aim of promoting rational therapy and effective patient management within the discipline of respiratory medicine.

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  • Website
    American Journal of Respiratory Medicine website
  • Other titles
    American journal of respiratory medicine (Online)
  • ISSN
    1175-6365
  • OCLC
    49728650
  • Material type
    Document, Periodical, Internet resource
  • Document type
    Internet Resource, Computer File, Journal / Magazine / Newspaper

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Lung cancer is the second most common cancer and the leading cause of cancer-related deaths in the US. It as been shown that when treated in its early stages, survival rates improve. Despite this, controversy remains regarding screening for the early detection of lung cancer, primarily because mortality reductions were not observed in the trials that studied chest x-ray and sputum cytology. Nevertheless, renewed interest in screening, due in part to better screening options, has prompted further research exploring the potential cost-effectiveness of implementing lung cancer screening programs. This article provides a critical review of the literature of economic evaluations of lung cancer screening programs. The focus of this review is the methodology implemented in these studies. Based on an electronic search of the literature (Pubmed, Medline and CancerLit) from Sep 1988–Sep 2001, seven articles that quantified the cost-effectiveness of lung cancer screening programs were identified. For most of the studies, the cost-effectiveness aspect was a minor component with little or no description of the methods. Although some studies focused more on estimating the economic efficiency of screening, their methodology was weak and still not well documented. Only two studies implemented fully a cost-effectiveness analysis and provided the necessary level of detail. If consensus can be reached regarding the clinical benefit of lung cancer screening, future studies related to cost-effectiveness would have to be implemented on much sounder methodology. The publications reviewed do provide preliminary support for the economic efficiency of screening for lung cancer.
    American journal of respiratory medicine: drugs, devices, and other interventions 12/2012; 1(6).
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    ABSTRACT: β2-adrenoceptor agonists (β2-agonists) such as albuterol (salbutamol) and terbutaline and their long-acting analogs salmeterol and formoterol are widely used as bronchodilators in the treatment of asthma. They are chiral drugs historically marketed as racemic mixtures of an active (eutomer) and essentially inactive (distomer) stereoisomer. Despite their obvious therapeutic value and widespread use, β2-agonists have been implicated, somewhat controversially, in causing an increase in asthma mortality and a deterioration of asthma control by a mechanism that remains elusive. Inherent toxicity of the distomers has been widely touted as an explanation and has given rise to pressure for the replacement of the racemates with pure eutomer formulations (the so-called chiral or racemic switch). This has culminated in the recent introduction into clinical practice of the single active stereoisomer of albuterol (levalbuterol) and the promise of other pure β2-agonist eutomer formulations to follow. This article examines the evidence on which these chiral switches are based. Clinical studies designed to reveal negative effects of β2-agonists have searched for reductions in lung function, increases in airway responsiveness to bronchoconstrictor mediators and worsening of asthma control. Crossover studies administering the pure stereoisomers and racemate of albuterol have not shown a clear superiority of the pure eutomer formulation over the racemate in terms of either bronchial hyperresponsiveness, tachyphylaxis to bronchoprotective effects or improvements in lung function. Clinical toxicity of β2-agonist distomers on any aspect of asthmatic lung function has also not been demonstrated in the relatively short-term inhalational studies (single dose or repeated dose studies <1 week) that have been carried out. In animal studies, the administration of β2-agonist racemates and distomers has been shown to enhance bronchial hyperresponsiveness but only in ovalbumin-sensitized animals where the relevance to humans is questionable. The pharmacokinetics and metabolism of β2-agonist stereoisomers appear to be essentially similar whether administered as single stereoisomers or as racemates. Levalbuterol may be slightly more potent than an equivalent dose given as racemate, but there is some evidence that it forms a small amount of the distomer in vivo which detracts somewhat from its purported benefits over use of the racemate. Whilst there remains a clear need for studies of longer duration with sensitive clinical endpoints to evaluate the benefits of β2-agonist eutomers and to investigate distomer toxicity, the chiral switch for β2-agonists in general, and for albuterol in particular, does not appear to be justified on the basis of the evidence available to date.
    American journal of respiratory medicine: drugs, devices, and other interventions 10/2012; 1(5).
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    ABSTRACT: Evidence suggests that allergy is a significant triggering factor in asthma in children and adults alike. In immunoglobulin (Ig) E-mediated allergic reactions, sensitization occurs when allergen-specific B cells are stimulated and switched to IgE antibody production by interleukin (IL)-4 and IL-13 provided by helper T cells type 2 (Th2). The IgE antibodies act by arming cells bearing either the high-affinity (FcεRI) or low-affinity (FcεRII or CD23) receptor. The subsequent interaction of allergen with IgE-FcεRI complexes on mast cells and basophils causes cross-linking of receptors that triggers the release of a variety of inflammatory mediators, cytokines and chemokines. Therefore, the ability to lower circulating free IgE levels is desirable because most individuals are exposed to multiple allergens to which they are sensitive at any given time. Omalizumab (formerly known as rhuMAb-E25) is a recently developed humanized monoclonal anti-IgE antibody directed at the FcεRI binding domain of human IgE. It inhibits binding of IgE to mast cells without provoking mast cell activation. Preliminary clinical data from randomized controlled trials have shown that the addition of omalizumab to standard asthma therapy reduces asthma exacerbations and decreases inhaled corticosteroid and rescue medication use. The compound is also well tolerated. Omalizumab represents a novel therapeutic approach in the management of asthma.
    American journal of respiratory medicine: drugs, devices, and other interventions 10/2012; 1(5).
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    ABSTRACT: Fungal pathogens are increasingly important causes of respiratory disease, yet the number of antifungal agents available for clinical use is limited. Use of amphotericin B deoxycholate is hampered by severe toxicity. Triazole agents currently available have significant drug interactions; fluconazole has a limited spectrum of activity and itraconazole was, until recently, available only in oral formulations with limited bioavailability. The development of resistance to all three agents is increasingly being recognized and some filamentous fungi are resistant to the action of all of these agents. In the past few years, new antifungal agents and new formulations of existing agents have become available. The use of liposomal amphotericin B preparations is associated with reduced, but still substantial, rates of nephrotoxicity and infusion-related reactions. An intravenous formulation of itraconazole has been introduced, and several new triazole agents have been developed, with the view of identifying agents that have enhanced potency, broader spectra of action and improved pharmacodynamic properties. One of these, voriconazole, has completed large-scale clinical trials. In addition, caspofungin, the first of a new class of agents, the echinocandins, which inhibit cell wall glucan synthesis, was approved for use in the US in 2001 as salvage therapy for invasive aspergillosis. It is hoped that the availability of these agents will have a significant impact on the morbidity and mortality of fungal respiratory infections. However, at the present time, our ability to assess their impact is limited by the problematic nature of conducting trials for antifungal therapy.
    American journal of respiratory medicine: drugs, devices, and other interventions 10/2012; 2(5).
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    ABSTRACT: Non-small cell lung cancer (NSCLC) is cured with surgery in a minority of affected persons. Chemotherapy and radiation can palliate and extend survival of patients with disease not amenable to surgery. Consequently, new treatment options are urgently needed. In the era of molecularly targeted therapeutics, the recent direction in cancer research has been to identify and modulate specific events in tumorigenesis. Angiogenesis, or new vessel formation, is one such event elucidated to be fundamental to the development, growth, and metastasis of cancers and is one of the characteristics that differentiates tumor from host. Thus, targeting of tumor neovasculature continues to generate tremendous enthusiasm and effort in drug development. Extensive research into the role of angiogenesis in NSCLC has produced a host of novel targets; their potential inhibitors, now numbering over 40, are in various phases of clinical testing around the world. The current lead compounds include inhibitors of matrix metalloproteinases, angiogenic growth factors and their receptor tyrosine kinases. Despite their impressive activity in animal models, definitive evidence of their antitumor activity in humans is yet to be established. We face several challenges as we look to advance the field of antiangiogenesis for the treatment of cancer, namely, the need for a better understanding of the optimal timing and dosing of antiangiogenic agents, the validation of imaging and quantification methods of tumor angiogenesis, and a new clinical trials design for a more expedient evaluation of novel cytostatic target modulators.
    American journal of respiratory medicine: drugs, devices, and other interventions 10/2012; 1(5).
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    ABSTRACT: Patients with community-acquired pneumonia (CAP) are treated in hospital or in the ambulatory care setting depending on the severity of illness. Despite numerous guidelines proposed, there is no agreement on specific criteria for hospitalization other than the clinicians’ experience. The purpose of this review is to discuss the importance of the appropriate choice and timely administration of antibacterial agents, either in the hospital or in the outpatient setting. Since a high proportion of CAP patients will not have an etiologic agent identified at the time of initiation of treatment, the choice of antibacterial therapy is usually empiric. Antibacterial agents with activity against pneumococci and atypical pathogens causing pneumonia are the preferred choices. Macrolides, doxycycline, or respiratory fluoroquinolones have been recommended by various guidelines committees in North America for the treatment of pneumonia in patients with or without underlying comorbidities. Because of the increasing resistance to β-lactams as well other antibacterial agents such as macrolides, doxycycline, and sulfamethoxazole/trimethoprim (cotrimoxazole), it is important that clinicians are aware of local statistics on resistance to Streptococcus pneumoniae, as infection with this bacterium is associated with high rates of morbidity and mortality. More recently, fluoroquinolone resistance has been reported, but the percentage of pneumococcal strains resistant to this agent is relatively low compared with the other antibacterial agents. Switch (intravenous to oral) therapy is recommended for hospitalized patients with CAP to facilitate early discharge, which has been shown to improve patient satisfaction and reduce hospital costs. Early conversion to oral therapy has not been shown to be associated with increased complications or higher mortality. Following prompt intravenous therapy and stabilization, patients with CAP should be treated with oral therapy in the ambulatory setting.
    American journal of respiratory medicine: drugs, devices, and other interventions 10/2012; 2(5).
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    ABSTRACT: Background: A number of different inhaler devices are available to deliver β2-adrenoceptor agonist (β2-agonist) bronchodilators in asthma. These include hydrofluoroalkane or chlorofluorocarbon (CFC)-free propelled pressurized metered-dose inhalers (pMDIs), many dry powder inhalers and breath-actuated inhalers. Objective: To determine the clinical efficacy of all available hand-held inhaler devices compared with the standard CFC-containing pMDI for the delivery of short-acting β2-agonist bronchodilators in nonacute asthma in both children and adults. Methodology: A systematic review and meta-analysis was carried out of all available randomized, controlled trials (RCTs) using the standard pMDI compared with any other hand-held inhaler device, delivering short-acting β2-agonist bronchodilators in patients with stable asthma. Results: One hundred and eighteen RCTs were included in this review. No clinical differences were found between the standard CFC-containing pMDI and 12 other hand-held inhaler devices for most outcome measures. We found no evidence of clinical differences between studies using either a 1 : 1 (pMDI: another inhaler) or a 2 : 1 dosing ratio. Conclusions: In patients with stable asthma, short-acting β2-agonist bronchodilators in standard CFC-pMDIs are as effective as any other hand-held inhaler device; therefore the cheapest available device that the patient is able to use should always be considered. Pharmaceutical companies should in future submit to regulatory authorities clinical outcome data (as opposed to in vitro data) in support of any dosing schedules greater than 1 : 1 when compared with the standard pMDI. Clinical effectiveness studies that use an intention-to-treat analysis and report more patient-centered outcomes are required.
    American journal of respiratory medicine: drugs, devices, and other interventions 08/2012; 2(4).
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    ABSTRACT: Inhaled β2-adrenoceptor agonists (β2-agonists) are the most commonly used asthma medications in many Western countries. Minor adverse effects such as palpitations, tremor, headache and metabolic effects are predictable and dose related. Time series studies suggested an association between the relatively nonselective β-agonist fenoterol and asthma deaths. Three case-control studies confirmed that among patients prescribed fenoterol, the risk of death was significantly elevated even after controlling for the severity of asthma. The Saskatchewan study not only found an increased risk of death among patients dispensed fenoterol, but also suggested this might be a class effect of β2-agonists. However, in subsequent studies, the long-acting β2-agonist salmeterol was not associated with increased asthma mortality. In a case-control study blood albuterol (salbutamol) concentrations were found to be 2.5 times higher among patients who died of asthma compared with controls. It is speculated that such toxic concentrations could cause tachyarrhythmias under conditions of hypoxia and hypokalemia. The risk of asthma exacerbations and near-fatal attacks may also be increased among patients dispensed fenoterol, but this association may be largely due to confounding by severity. Although salmeterol does not appear to increase the risk of near-fatal attacks, there is a consistent association with the use of nebulized β2-agonists. Nebulized and oral β2-agonists are also associated with an increased risk of cardiovascular death, ischemic heart disease and cardiac failure. Caution should be exercised when first prescribing a β-agonist for patients with cardiovascular disease. A potential mechanism for adverse effects with regular use of β2-agonists is tachyphylaxis. Tachyphylaxis to the bronchodilator effects of long-acting β2-agonists can occur, but has been consistently demonstrated only for formoterol (eformoterol) a full agonist, rather than salmeterol, a partial agonist. Tachyphylaxis to protection against induced bronchospasm occurs with both full and partial β2-agonists, and probably within a matter of days at most. Underlying airway responsiveness to directly acting bronchoconstricting agents is not increased when the bronchodilator effect of the regular β2-agonist has been allowed to wear off, although there may be an increase in responsiveness to indirectly acting agents. While there has been speculation that underlying airway inflammation in asthma may be made worse by regular use of short-acting β2-agonists, in contradistinction, a number of studies have shown that long-acting β2-agonists have positive anti-inflammatory effects. An Australian Cochrane Airways Group systematic review of the randomized, controlled trials of short-acting β-agonists found only minimal and clinically unimportant differences between regular use and use as needed. Regular short-acting treatment was better than placebo. However, a subsequent systematic review has found that regular use of long-acting β-agonists had significant advantages over regular use of short-acting β-agonists. More studies and data are needed on the regular use of β2-agonists in patients not taking inhaled corticosteroids, and in potentially vulnerable groups, such as the elderly and those with particular genotypes for the β-receptor, who might be more prone to adverse effects.
    American journal of respiratory medicine: drugs, devices, and other interventions 08/2012; 2(4).
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    ABSTRACT: Patients with allergic rhinitis frequently present with symptoms of nasal congestion, runny nose, sneezing, daytime somnolence and fatigue associated with decreased cognitive performance and impaired quality of life. Recent research has suggested that daytime somnolence in allergic rhinitis can be attributed to chronic inflammation of the nasal mucosa leading to nasal congestion and obstructed nasal passageways resulting in disturbed sleep. Treating daytime somnolence due to allergic rhinitis requires a reduction in obstruction caused by nasal congestion. Currently available therapy for allergic rhinitis includes topical corticosteroids, sedating and non-sedating antihistamines, topical cromolyn sodium (sodium cromoglycate), decongestants, immunotherapy and topical ipratropium bromide. The effectiveness of antihistamines in patients with allergic rhinitis has long been established. However, results of placebo-controlled trials investigating the effects of azelastine on sleep and daytime somnolence have produced conflicting results. Sleep improved with azelastine therapy, but there was a lack of evidence that azelastine significantly affected daytime sleepiness, sleep severity and nasal congestion. Sedating antihistamines exacerbate daytime somnolence and should be avoided in patients with allergic rhinitis. In a separate study, desloratadine failed to benefit sleep, but did not worsen daytime somnolence. Topical nasal cromolyn sodium is inconvenient to use and is unlikely to have a major effect on nasal congestion. Decongestants do decrease nasal congestion but the effect this has on sleep has not been adequately studied. Recent research has shown that topical corticosteroids are an effective treatment for alleviating nasal congestion secondary to allergic rhinitis. However, few studies have assessed the effect of topical corticosteroids on daytime fatigue and sleep. In 20 patients with allergic rhinitis and symptoms of daytime sleepiness, flunisolide significantly improved sleep quality and congestion but daytime sleepiness was not significantly improved. A similar study with fluticasone propionate showed improvement in nasal congestion and sleep but there was no significant change in objective sleep measurements recorded on polysomnography. Further research involving objective measures of sleep quality is necessary to determine the efficacy of medications in the treatment of allergic rhinitis associated with fatigue and daytime somnolence.
    American journal of respiratory medicine: drugs, devices, and other interventions 06/2012; 1(3).
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    ABSTRACT: Obstructive sleep apnea (OSA) is a common condition of childhood, and is associated with significant morbidity. Prevalence of the condition peaks during early childhood, due in part to adenoidal and tonsillar enlargement within a small pharyngeal space. The lymphoid tissues regress after 10 years of age, in the context of ongoing bony growth, and there is an associated fall in the prevalence of OSA. Obstruction of the nasopharynx by adenoidal enlargement promotes pharyngeal airway collapse during sleep, and the presence of large tonsils contributes to airway obstruction. Administration of systemic corticosteroids leads to a reduction in the size of lymphoid tissues due to anti-inflammatory and lympholytic effects. However, a short course of systemic prednisone has been demonstrated not to have a significant effect on adenoidal size or the severity of OSA, and adverse effects preclude the long-term use of this therapy. Intranasal corticosteroids are effective in relieving nasal obstruction in allergic rhinitis, and allergic sensitization is more prevalent among children who snore than among those who do not snore. Intranasal corticosteroids have also been demonstrated to reduce adenoidal size, independent of the individual’s atopic status. There is preliminary evidence of an improvement in the severity of OSA in children treated with intranasal corticosteroids, but further studies are needed before such therapy can be routinely recommended. Prescribing clinicians should take into account the potential benefits to the patient, the age of the child, the presence of comorbidities such as allergic rhinitis, the agent used, and the dose and duration of treatment when considering such therapy.
    American journal of respiratory medicine: drugs, devices, and other interventions 06/2012; 1(3).
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    ABSTRACT: Management of recurrent malignant pleural effusion, a common complication of malignancy, poses a challenge to clinicians. Although almost one century has elapsed since the introduction of the pleurodesis procedure, the ideal approach and best agent are still to be defined. Optimally, pleurodesis should be done at the bedside with a minimally invasive procedure, and suitable agents to achieve pleural symphysis should be inexpensive, available worldwide and free of adverse effects. To date, no substance completely fulfills these requirements. Silver nitrate should be considered for pleurodesis because of its low cost and ease of handling. Although talc has been used most frequently to induce pleurodesis, reports of death due to acute respiratory failure have raised concerns about the safety of this agent. Tetracycline, an effective alternative used in the past, is no longer commercially available. This agent has been substituted with derivatives of tetracycline, such as minocycline and doxycycline with success rates similar to those with tetracycline. Several antineoplastic agents have been injected into the pleural space with the aim of producing pleural symphysis, the most representative of this group being bleomycin. Recent knowledge of the molecular mechanisms involved in pleural inflammation has brought into focus new substances, such as transforming growth factor β and vascular endothelial growth factor, which may be used as pleurodesis agents in the future. Nevertheless, more studies are necessary to better define the potential of these substances in the induction of pleural symphysis. Ideally, a sclerosing agent should be cost-effective, available worldwide and easily administered. Talc will probably stand as the preferred agent to be used for pleurodesis in malignant pleural effusion because of its efficacy, easy manipulation and handling. However, further investigation is necessary to minimize adverse effects related to talc.
    American journal of respiratory medicine: drugs, devices, and other interventions 06/2012; 2(3).
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    ABSTRACT: Eosinophilic bronchitis is a common and treatable cause of chronic cough. The major pathological feature is eosinophilic airway inflammation, similar to that seen in asthma. However, the associated airway dysfunction is quite different, with evidence of heightened cough reflex sensitivity, but no variable airflow obstruction or airway hyperresponsiveness. Recent evidence suggests that the differences in functional association are related to differences in localization of mast cells in airway wall, with airway smooth muscle infiltration occurring in asthma and epithelial infiltration in eosinophilic bronchitis. Diagnosis is usually made with induced sputum analysis after exclusion of other causes for chronic cough on clinical, radiological and lung function assessment. The cough responds well to inhaled corticosteroids but dose and duration of treatment remain unclear. Little is known about the natural history of this condition. However, some patients with COPD without a history of previous asthma have sputum eosinophilia, so one possibility is that some cases of eosinophilic bronchitis may develop fixed airflow obstruction. Further study of this interesting condition will increase our understanding of airway inflammation and airway responsiveness, leading to novel targets for therapeutics for both eosinophilic bronchitis and asthma.
    American journal of respiratory medicine: drugs, devices, and other interventions 04/2012; 2(2).
  • American journal of respiratory medicine: drugs, devices, and other interventions 04/2012; 2(2).
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    ABSTRACT: Children and adolescents experiencing acute exacerbations of asthma benefit from the use of β2-adrenoceptor agonists (β2-agonists) and systemic corticosteroids. However, there have been conflicting reports regarding the efficacy of inhaled anticholinergic agents. This article summarizes the evidence provided by randomized controlled trials studying the efficacy of adding inhaled anticholinergic agents to β2-agonists in nonhospitalized children and adolescents with acute exacerbations of asthma. This systematic review of randomized controlled trials suggests that the addition of inhaled anticholinergic agents to β2-agonists is beneficial in children and adolescents, particularly those with severe exacerbations of asthma. When given in repeated doses, the addition of inhaled anticholinergic agents to β2-agonists improves lung function and reduces the risk of hospital admission by 25%. Several treatment regimens, namely ipratropium bromide (250 or 500μg per dose) every 20–60 minutes for two to three doses have been tested with similar beneficial effects. The addition of a single dose of an inhaled anticholinergic agent to β2-agonists improves lung function but does not prevent hospital admission. The review did not identify any beneficial effects of anticholinergic agents in children with nonsevere asthma. Use of anticholinergic agents was not associated with increase in the incidence of nausea, vomiting or tremor. In conclusion, the addition of repeated doses of an inhaled anticholinergic agent to inhaled β2-agonist is indicated in the emergency room management of children and adolescents with acute asthma, particularly those with severe exacerbations.
    American journal of respiratory medicine: drugs, devices, and other interventions 04/2012; 2(2).
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    ABSTRACT: Adenosine, an endogenous signaling nucleoside that modulates many physiological processes has been implicated in playing an ever increasingly important role in the pathogenesis of asthma and chronic obstructive pulmonary disease (COPD). All cells contain adenosine and adenine nucleotides and the cellular production of adenosine is greatly enhanced under conditions of local hypoxia as may occur in inflammatory conditions such as asthma and COPD. In 1983, it was first reported that inhaled adenosine causes dose-related bronchoconstriction in patients with both allergic and non-allergic asthma but not in healthy volunteers. This hyperresponsiveness was also reported in patients with COPD, with those patients who smoked exhibiting a significantly greater response. This bronchoconstrictor effect of adenosine is orchestrated through the stimulation of specific cell membrane receptors and involves an important inflammatory cell, the mast cell. There is substantial evidence which suggests that mast cell activation is central to this unique response to adenosine. Mast cell mediator release makes a significant contribution towards airflow obstruction and the consequent symptoms in patients with asthma. Over the last two decades, researchers have investigated the effect of mast cell inhibitors as well as mast cell mediator receptor antagonists and their role in attenuating the bronchoconstrictor response to inhaled adenosine 5′-monophosphate (AMP). Promising results have been shown using mast cell stabilizers, histamine H1 receptor antagonists, selective cysteinyl leukotriene-1 receptor antagonists and inhibitors of 5-lipoxygenase and cyclo-oxygenase. Through these findings, the mast cell has been recognized as being a critical inflammatory cell in the adenosine-induced response in patients with asthma and COPD. To date, four subtypes (A1, A2A, A2B, A3) of adenosine receptors have been cloned each with a unique pattern of tissue distribution and signal transduction. Activation of these receptors has pro- and anti-inflammatory consequences making the development of agonists and/or antagonists at these receptor sites a novel approach in the treatment of patients with asthma and COPD. This review highlights the importance of adenosine in the pathophysiology of asthma and COPD, the critical role of the mast cell and the potential to target the adenosine receptor subtype in patients with asthma and COPD. The complete characterization of these adenosine receptor subtypes in terms of their distribution in humans and the development of selective agonists and antagonists, holds the key to our complete understanding of the role of this important mediator in asthma and COPD.
    American journal of respiratory medicine: drugs, devices, and other interventions 04/2012; 1(2).
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    ABSTRACT: Chronic fatigue syndrome (CFS) is a recognized clinical illness of unknown cause and pathophysiologic mechanisms. Immunizing patients against influenza would seem to be a prudent strategy since infection has been associated with symptom exacerbation. However, patients with CFS have demonstrated variable abnormalities in the immune system, the clinical significance of which is unclear. Anecdotal information has suggested that, due to the etiologic uncertainty surrounding CFS, many patients reject immunization, fearful of untoward effects. This article attempts to clarify the situation by reviewing immunologic findings in CFS and influenza vaccines in current use. Results from a recent survey of perceptions of patients with CFS regarding immunization revealed that 31% felt immunization was neither safe nor beneficial. This opinion was universal in those patients who had never received influenza vaccine. Among patients who had received vaccine and experienced an adverse effect, 26% felt the vaccine was safe and 28% felt it was beneficial. Among those who had received vaccine without an adverse effect, 45% believed the vaccine was safe, and 55% felt it was effective. CFS patients as a group expressed concern that influenza vaccine would alter an already dysfunctional immune system, or worsen CFS symptoms. Significantly more patients with CFS who had never received influenza vaccine voiced this opinion than did patients who had received immunization for influenza in the past. Contrary to the opinions expressed by the sample, clinical trials in CFS have yet to find that any type of immunization has produced a deleterious effect on symptoms or functioning. Moreover, patients with CFS in a randomized, placebo-controlled, double-blind trial of influenza immunization produced an antibody titer in the protective range to inactivated trivalent influenza vaccine, although the geometric mean titer was slightly blunted compared with healthy vaccinees. Although patients with CFS in placebo and active groups reported four times the number of post-injection adverse effects of healthy vaccinees, data re-analysis revealed that this finding was related to the overlap of common, post-influenza immunization symptoms and CFS constitutional symptoms. CFS is a poorly understood illness and some patients may believe in causal theories that lead to the rejection of disease prevention strategies such as immunization. However, influenza immunization appears to provide protective antibody levels without worsening CFS symptoms or causing excessive adverse effects. Efforts to motivate patients with CFS to obtain annual influenza immunization should take into account illness perceptions and concentrate on education based on placebo-controlled trials.
    American journal of respiratory medicine: drugs, devices, and other interventions 02/2012; 1(1).
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    ABSTRACT: For several years there has been discussion of whether first-line pharmacological treatment of allergic rhinitis should be antihistamines or intranasal corticosteroids. No well documented, clinically relevant differences seem to exist for individual nonsedating antihistamines in the treatment of allergic rhinitis. Likewise, the current body of literature does not seem to favor any specific intranasal corticosteroid. When comparing efficacy of antihistamines and intranasal corticosteroids in allergic rhinitis, present data favor intranasal corticosteroids. Interestingly, data do not support antihistamines as superior in treating conjunctivitis associated with allergic rhinitis. Safety data from comparative studies in allergic rhinitis do not indicate differences between antihistamines and intranasal corticosteroids. Combining antihistamines and intranasal corticosteroids in the treatment of allergic rhinitis does not provide additional beneficial effects to intranasal corticosteroids alone. Considering present data, intranasal corticosteroids seem to offer superior relief in allergic rhinitis, when compared with antihistamines.
    American journal of respiratory medicine: drugs, devices, and other interventions 02/2012; 2(1).
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    ABSTRACT: Second-generation histamine H1 receptor antagonists are recognized as being highly effective treatments for allergic-based disease and are among the most frequently prescribed drugs in the world. The newer antihistamines represent a heterogeneous group of compounds with markedly different chemical structures, a spectrum of antihistaminic properties, adverse effects, half-life, tissue distribution, metabolism and varying degrees of anti-inflammatory effects. Histamine is an important mast cell- and basophil-derived mediator that has been implicated in the pathogenesis of asthma, resulting in smooth muscle contraction, mucus hypersecretion, and increased vascular permeability leading to mucosal edema. Antihistamines should never be used as monotherapy for asthma but there is evidence that these drugs give a measure of protection in histamine-induced bronchoconstriction. Furthermore, several studies have demonstrated that the use of second-generation antihistamines, as adjunct therapy, may benefit those patients whose allergic asthma co-exists with allergic rhinitis. Indeed, many patients present with both allergic rhinitis and asthma. The link between the upper and lower respiratory airways is now well established and there is increasing evidence that allergic rhinitis is a risk factor for the development of asthma. More recently, a number of novel antihistamines have been developed which are either metabolites of active drugs or enantiomers and there is emerging evidence that at least one of these drugs, desloratadine, may give significant symptomatic benefit in some types of asthma. It is of interest to note that cetirizine provides a primary pharmacological intervention strategy to prevent the development of asthma in specifically-sensitized high risk groups of infants. Moreover, the documented anti-inflammatory activities of antihistamines may provide a novel mechanism of action for the therapeutic control of virus-induced asthma exacerbations by inhibiting the expression of intercellular adhesion molecule-1 (ICAM-1) by airway epithelial cells. Finally, several well-conducted studies suggest that combination therapy with antihistamines and anti-leukotrienes may be as effective as corticosteroid use in patients with allergic asthma and seasonal allergic rhinitis.
    American journal of respiratory medicine: drugs, devices, and other interventions 02/2012; 1(1).
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    ABSTRACT: Emotional factors are an obstacle in the diagnosis and management of asthma. This review discusses three problem patterns: negative emotions in relatively normal patients with asthma; patients presenting possible functional symptoms and; patients presenting asthma in conjunction with psychiatric deviations. Negative emotions influence the symptoms and management of asthma, even in relatively normal patients. Psychogenic symptoms appear normal, but culminate in functional symptoms in a minority of patients. Diagnosing and treating asthma in patients with comorbid asthma and psychiatric symptoms is very difficult. On the one hand, treating asthma may often be just treating the emotions. On the other hand, negative emotions make the treatment of asthma guesswork. Physicians should estimate emotional influences in their patients’ symptoms for an optimal evaluation of medication efficacy. Assessment and analysis of emotional factors surrounding exacerbations seems essential, e.g. emotional precipitants of asthma and asthma-evoked negative emotions. Moreover, patients should be informed about stress-induced breathlessness and the consequences of overuse of bronchodilators. When patients present with atypical symptoms, or do not properly respond to asthma medication, functional symptoms should be suspected. Psychiatric analysis may often lead to the conclusion that symptoms have a functional basis. In patients with comorbid asthma and anxiety disorders, asthma should be the focus for treatment since difficult-to-control asthma often causes anxiety problems in the first place. Moreover, panic-like symptoms in asthma are often related to sudden onset asthma exacerbations. However, in patients with comorbid asthma and depression, depression should become the focus of treatment. The reason is that optimal treatment of depressive asthmatics is probably impossible. Special issues include specific problems with children, compliance problems, and physicians’ dilemmas regarding the simultaneous treatment of asthma and psychiatric symptoms.
    American journal of respiratory medicine: drugs, devices, and other interventions 02/2012; 2(1).