1,721,174 research outputs found
Treatment of Chronic Obstructive Pulmonary Disease by Dual Bronchodilation with Coformulation of Indacaterol/Glycopyrronium.
No full textThe potential of biologics for the treatment of asthma
No full textRecent advances in the knowledge of asthma pathobiology suggest that biological therapies that target cytokines can be potentially useful for the treatment of this complex and heterogeneous airway disease. The use of biologics in asthma has been established with the approval of the humanized monoclonal immunoglobulin E-targeted antibody omalizumab (Xolair; Genentech/Novartis) as an add-on treatment for inadequately controlled disease. Furthermore, evidence is accumulating in support of the efficacy of other biologics, such as interleukin-5 (IL-5)- and IL-13-specific drugs. Therefore, these new developments are changing the scenario of asthma therapies, especially with regard to more severe disease. The variability among patients' individual therapeutic responses highlights that it will be necessary to characterize the different asthma subtypes so that phenotype-targeted treatments based on the use of biologics can be implemented
Pharmacotherapeutic strategies for critical asthma syndrome: a look at the state of the art
No full textIntroduction: ‘Critical Asthma Syndrome’ (CAS) is an umbrella term proposed to include several forms of asthma, responsible for acute and life-threatening exacerbations. CAS requires urgent and adequate supportive and pharmacological treatments to prevent serious outcomes. Areas covered: The purpose of this review is to discuss current knowledge on the pharmacotherapeutic strategies for treatment of CAS. Expert opinion: Airflow limitation, airway wall edema, and mucus plugs are the pathophysiological targets of pharmacological therapies. Strategies to achieve these goals are based on the use of various classes of drugs. Inhaled beta2-agonists are the mainstay of the initial therapy of CAS. Inhaled anticholinergic agents may be considered in the treatment of CAS in addition to beta 2 agonists. Systemic corticosteroids should be administered as soon as possible in order to counteract airway inflammation and restore normal airway sensitivity. The effectiveness of pharmacological therapies in CAS is linked not only to the timely use of drugsbut also to the dosage and route of administration. Early recognition and aggressive treatment are essential for the management of CAS; however, prevention is the best cure. Although significant progress has been made, further efforts are needed to implement an optimal exacerbation prevention strategy
VIP: A New Promising Marker for AECOPD - A Fashionable Marker Soon Forgotten?
Full text linkIt is almost impossible to discuss chronic obstructive pulmonary disease (COPD) without making reference to phenotypes or endotypes. Among COPD phenotypes, there is one which is widely recognized for its clinical and economic implications. This is characterized by a high susceptibility to experience acute exacerbations of chronic obstructive pulmonary disease (AECOPD). AECOPD are natural events occurring in the course of COPD, but still remain a major cause of morbidity and mortality associated with this disease [1]. Clinical criteria that define an acute exacerbation are subjective and open for debate. Hence, it is necessary to identify reliable biomarkers that could help in the early identification of AECOPD, also allowing their clinical progression to be measured. This is especially the case when considering the unfavorable outcomes and the socioeconomic costs that acute exacerbations of the disease predict. Several circulating markers are commonly used in clinical practice for the study of patients with AECOPD, such as white blood count (WBC), C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR), although these are nonspecific and not particularly sensitive [2,3]. Furthermore, these clinically available markers are not useful in the early identification of AECOPD, and are therefore not effective in reducing the progression of the disease. Some reports are also available, referring to other new possible markers of AECOPD, such as neutrophil-lymphocyte ratio (NLR) and copeptin [1,4]. Procalcitonin (PCT) has also been proposed as a fashionable marker for AECOPD, although most experts agree that it is not reliable in predicting bacterial infections in AECOPD [5].
In this issue of Respiration, Mandal et al. [6] report the results of their very interesting study about vasoactive intestinal peptide (VIP), properly investigated by these authors and proposed as a promising marker for AECOPD. Indeed, an increased VIP immunoreactivity has been previously found in the airway epithelium and bronchial glands of COPD patients, in comparison to smokers with normal lung function [7]. But are we witnessing the birth of a new clinical tool for the early identification of acute exacerbations of COPD, or will this be the usual fashionable marker that will result in a few publications, but will then be soon forgotten?
The authors of the study detected higher circulating levels of VIP in subjects with AECOPD, when compared to stable COPD patients, and identified a cutoff of 88 pg/ml that could be clinically useful as an indicator of exacerbation. We acknowledge that the results of this study are very stimulating, but we have some questions about the potentiality of VIP as a reliable marker of AECOPD. First, notwithstanding the authors' declaration of a robust performance of VIP in AECOPD diagnosis, how can a single marker be able to identify such different diseases as arthritis, diabetes, cancer, bowel diseases, heart failure, atopic dermatitis and rhinitis [8,9,10,11,12]? The high specificity of VIP in AECOPD diagnosis reported by the authors refers to a small population of 120 COPD patients with acute disease exacerbations, and we believe the study requires at least a solid confirmation on larger patient populations, possibly to be investigated by multidisciplinary studies. A second question is whether VIP would be validated in the near future, and its dosage standardized in clinical practice.
Finally, we recognize that no single biomarker in COPD, as in all other human diseases, is enough to provide a wide acceptance of clinical information. Therefore, we suggest that there is an urgent need to identify a panel of potential biomarkers, such as VIP, which in combination may increase the singular power of each, thus being potentially useful for AECOPD in clinical practice, in order to allow early recognition of this condition, and also to monitor the effects of treatment
Inhaled ultrasonically nebulized distilled water decreases exhaled nitric oxide in asthma.
No full textExhaled nitric oxide (eNO) is increasingly used as a marker of disease
activity in asthma. Inhaled hypertonic saline has been shown to induce
bronchoconstriction and to decrease eNOin asthmatic subjects, whereas the
effects of hypotonic solutions on eNOin these patients have not been studied.
To evaluate the effect of ultrasonically nebulized distilled water (UNDW), an
indirect hypotonic stimulus, on eNO, 17 asthmatic patients were enrolled and
eNOfrom lower airways was measured by chemiluminescence. UNDW significantly
reduced FEV1 ‡ 20% in 9 subjects (UNDW+), but had no effect in
eight patients (UNDW)). Baseline eNOconcentra tion were found to be
51.3 ± 11.1 ppb in UNDW+ and 32.9 ± 7.5 ppb in UNDW) patients, respectively
(p = 0.199, NS). UNDW inhalation significantly decreased eNO
(from 51.3 ± 11.1 ppb to 31.0 ± 7.1 ppb in UNDW+ (p<0.020, n = 9) and
from 32.9 ± 7.5 ppb to 26.2 ± 7.3 ppb in UNDW) subjects (p<0.024,
n = 8), respectively). eNOpe rcentage reduction in UNDW+ patients was
significantly higher compared with UNDW) subjects ()37 ± 4% vs
)23 ± 3%, p = 0.021). There was no correlation between FEV1 changes and
eNOpercent age decreases in both UNDW+ and UNDW) subjects. In
UNDW+ patients, acute bronchodilation induced by salbutamol caused a
recovery in both FEV1 and eNO, though eNO levels remained lower than
baseline values. We concluded that UNDW inhalation can significantly decrease
eNOin asthmatic patients, either responders or nonresponders to this
indirect osmotic challenge; the reduction in eNOlevel s was only partly dependent
on acute changes in airway caliber
Farmacologia clinica dei broncodilatatori e dei glucocorticoidi
No full textAspetti molecolari e clinici dei principali farmaci broncodilatatori e dei glucocorticoidi utilizzati nel trattamento dell'asma bronchiale
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