“Correct Use of Inhaled Corticosteroids in Chronic Obstructive Pulmonary Disease”: A Consensus Document

Alcázar, Bernardino; Casanova, Ciro; Miravitlles, Marc; Lucas, Pilar de; Riesco, Juan Antonio; González-Moro, José Miguel Rodríguez

doi:10.1016/j.arbr.2015.02.002

Cited by 20 publications

(9 citation statements)

References 28 publications

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“…In contrast, one third of ACOS patients and half of the frequent exacerbators did not receive ICS after diagnosis. A recent consensus document on the use of ICS has agreed on the indication of ICS in exacerbator and ACOS patients as well as in the withdrawal of ICS in patients that do not fulfil these criteria [22].…”

Section: Discussionmentioning

confidence: 99%

Treatment patterns in COPD patients newly diagnosed in primary care. A population-based study

Barrecheguren

Monteagudo

Ferrer

et al. 2016

Respiratory Medicine

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Section: Discussionmentioning

confidence: 99%

Treatment patterns in COPD patients newly diagnosed in primary care. A population-based study

Barrecheguren

Monteagudo

Ferrer

et al. 2016

Respiratory Medicine

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“…While ICS have become a key element in the treatment of asthma, their role in patients with stable COPD remains unclear, and may be beneficial only for a specific subset of ICS responders, but not for everyone [Alcázar Navarrete et al 2015]. Taking into consideration that an elevated risk of pneumonia with ICS use has been repeatedly found in studies of various designs, this safety concern should be balanced with the available evidence on efficacy, with particular emphasis on reduction of exacerbations and survival.…”

Section: Discussionmentioning

confidence: 99%

Inhaled corticosteroids and the increased risk of pneumonia: what’s new? A 2015 updated review

Iannella

Luna

Waterer

2016

Ther Adv Respir Dis

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There is a considerable amount of evidence that supports the possibility of an increased risk of pneumonia associated with prolonged use of inhaled corticosteroids (ICS) in patients with chronic obstructive pulmonary disease (COPD). However, as yet, no statistically significant increase in pneumonia-related 30-day mortality in patients on ICS has been demonstrated. The lack of objective pneumonia definitions and radiological confirmations have been a major source of bias, because of the similarities in clinical presentation between pneumonia and acute exacerbations of COPD. One of the newer fluticasone furoate studies overcomes these limitations and also provides an assessment of a range of doses, suggesting that the therapeutic window is quite narrow and that conventional dosing has probably been too high, although the absolute risk may be different compared to other drugs. Newer studies were not able to rule out budesonide as responsible for pneumonia, as previous evidence suggested, and there is still need for evidence from head-to-head comparisons in order to better assess possible intra-class differences. Although the exact mechanisms by which ICS increase the risk of pneumonia are not fully understood, the immunosuppressive effects of ICS on the respiratory epithelium and the disruption of the lung microbiome are most likely to be implicated. Given that COPD represents such a complex and heterogeneous disease, attempts are being made to identify clinical phenotypes with clear therapeutic implications, in order to optimize the pharmacological treatment of COPD and avoid the indiscriminate use of ICS. If deemed necessary, gradual withdrawal of ICS appears to be well tolerated. Vaccination against pneumococcus and influenza should be emphasized in patients with COPD receiving ICS. Physicians should keep in mind that signs and symptoms of pneumonia in COPD patients may be initially indistinguishable from those of an exacerbation, and that patients with COPD appear to be at increased risk of developing pneumonia as a complication of ICS therapy.

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“…Currently, the majority of lung-targeting drugs are delivered through inhalation 11–13 , such as inhaled corticosteroid. Drugs administered by inhalation may be effective to treat respiratory tract disease, but may be ineffective for pulmonary diseases that involve alveoli and interstitium, such as interstitial lung disease 14,15 .…”

Section: Introductionmentioning

confidence: 99%

Identification of a nanobody specific to human pulmonary surfactant protein A

He¹,

Wang

Yin³

et al. 2017

Sci Rep

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Nanobody (Nb) is a promising vector for targeted drug delivery. This study aims to identify an Nb that can specifically target the lung by binding human pulmonary surfactant protein A (SP-A). Human lung frozen tissue sections were used for 3 rounds of biospanning of our previously constructed Nb library for rat SP-A to establish a sub-library of Nb, which specifically bound human lung tissues. Phage-ELISA was performed to screen the sub-library to identify Nb4, which specifically bound human SP-A. The binding affinity Kd of Nb4 to recombinant human SP-A was 7.48 × 10−7 M. Nb4 (19 kDa) was stable at 30 °C–37 °C and pH 7.0–7.6 and specifically bound the SP-A in human lung tissue homogenates, human lung A549 cells, and human lung tissues, whereas didn’t react with human liver L-02 cells, kidney 293T cells, and human tissues from organs other than the lung. Nb4 accumulated in the lung of nude mice 5 minutes after a tail vein injection of Nb4 and was excreted 3 hours. Short-term exposure (one month) to Nb4 didn’t cause apparent liver and kidney toxicity in rats, whereas 3-month exposure resulted in mild liver and kidney injuries. Nb4 may be a promising vector to specifically deliver drugs to the lung.

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“Correct Use of Inhaled Corticosteroids in Chronic Obstructive Pulmonary Disease”: A Consensus Document

Cited by 20 publications

References 28 publications

Treatment patterns in COPD patients newly diagnosed in primary care. A population-based study

Treatment patterns in COPD patients newly diagnosed in primary care. A population-based study

Inhaled corticosteroids and the increased risk of pneumonia: what’s new? A 2015 updated review

Identification of a nanobody specific to human pulmonary surfactant protein A

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