Physical and Functional Impairment During and After Hospitalization in Subjects With Severe COPD Exacerbation

Torres‐Sánchez, Irene; Cabrera‐Martos, Irene; Díaz-Pelegrina, Ana; Valenza-Demet, Gerald; Moreno-Ramírez, Maria Paz; Valenza, Marie Carmen

doi:10.4187/respcare.04597

Cited by 24 publications

(23 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Therapeutic strategies to prevent ICU-acquired or COPD exacerbation-associated muscle wasting are currently lacking, and restoration of lost muscle mass and function following recovery from critical illness or COPD exacerbation is challenging and often incomplete [ 30 , 31 ]. Pulmonary inflammation often accompanies these conditions and is sufficient to induce muscle atrophy, but the intracellular mechanisms governing the net loss of muscle protein have not completely been identified.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary inflammation-induced loss and subsequent recovery of skeletal muscle mass require functional poly-ubiquitin conjugation

et al. 2018

View full text Add to dashboard Cite

BackgroundPulmonary inflammation in response to respiratory infections can evoke muscle wasting. Increased activity of the ubiquitin (Ub)-proteasome system (UPS) and the autophagy lysosome pathway (ALP) have been implicated in inflammation-induced muscle atrophy. Since poly-Ub conjugation is required for UPS-mediated proteolysis and has been implicated in the ALP, we assessed the effect of impaired ubiquitin conjugation on muscle atrophy and recovery following pulmonary inflammation, and compared activation and suppression of these proteolytic systems to protein synthesis regulation.MethodsPulmonary inflammation was induced in mice by an intratracheal instillation of LPS. Proteolysis (UPS and ALP) and synthesis signaling were examined in gastrocnemius muscle homogenates. Ub-conjugation-dependency of muscle atrophy and recovery was addressed using Ub-K48R (K48R) mice with attenuated poly-ubiquitin conjugation, and compared to UBWT control mice.ResultsPulmonary inflammation caused a decrease in skeletal muscle mass which was accompanied by a rapid increase in expression of UPS and ALP constituents and reduction in protein synthesis signaling acutely after LPS. Muscle atrophy was attenuated in K48R mice, while ALP and protein synthesis signaling were not affected. Muscle mass recovery starting 72 h post LPS, correlated with reduced expression of UPS and ALP constituents and restoration of protein synthesis signaling. K48R mice however displayed impaired recovery of muscle mass.ConclusionPulmonary inflammation-induced muscle atrophy is in part attributable to UPS-mediated proteolysis, as activation of ALP- and suppression of protein synthesis signaling occur independently of poly-Ub conjugation during muscle atrophy. Recovery of muscle mass following pulmonary inflammation involves inverse regulation of proteolysis and protein synthesis signaling, and requires a functional poly-Ub conjugation.Electronic supplementary materialThe online version of this article (10.1186/s12931-018-0753-8) contains supplementary material, which is available to authorized users.

show abstract

Section: Discussionmentioning

confidence: 99%

Pulmonary inflammation-induced loss and subsequent recovery of skeletal muscle mass require functional poly-ubiquitin conjugation

et al. 2018

View full text Add to dashboard Cite

show abstract

“…AECOPD reduces the physical activity of patients [ 148 ]. Hospitalization due to AECOPD leads to physical and functional impairment [ 149 ] with loss of quadriceps muscle strength [ 150 ], exercise tolerance [ 151 ] and health status [ 152 ]. The role of PR during hospitalization may thus be justified.…”

Section: Pulmonary Rehabilitationmentioning

confidence: 99%

Management of severe acute exacerbations of COPD: an updated narrative review

Crisafulli

Barbeta

Ielpo

et al. 2018

Multidiscip Respir Med

View full text Add to dashboard Cite

BackgroundPatients with chronic obstructive pulmonary disease (COPD) may experience an acute worsening of respiratory symptoms that results in additional therapy; this event is defined as a COPD exacerbation (AECOPD). Hospitalization for AECOPD is accompanied by a rapid decline in health status with a high risk of mortality or other negative outcomes such as need for endotracheal intubation or intensive care unit (ICU) admission. Treatments for AECOPD aim to minimize the negative impact of the current exacerbation and to prevent subsequent events, such as relapse or readmission to hospital.Main bodyIn this narrative review, we update the scientific evidence about the in-hospital pharmacological and non-pharmacological treatments used in the management of a severe AECOPD. We review inhaled bronchodilators, steroids, and antibiotics for the pharmacological approach, and oxygen, high flow nasal cannulae (HFNC) oxygen therapy, non-invasive mechanical ventilation (NIMV) and pulmonary rehabilitation (PR) as non-pharmacological treatments. We also review some studies of non-conventional drugs that have been proposed for severe AECOPD.ConclusionSeveral treatments exist for severe AECOPD patients requiring hospitalization. Some treatments such as steroids and NIMV (in patients admitted with a hypercapnic acute respiratory failure and respiratory acidosis) are supported by strong evidence of their efficacy. HFNC oxygen therapy needs further prospective studies. Although antibiotics are preferred in ICU patients, there is a lack of evidence regarding the preferred drugs and optimal duration of treatment for non-ICU patients. Early rehabilitation, if associated with standard treatment of patients, is recommended due to its feasibility and safety. There are currently few promising new drugs or new applications of existing drugs.

show abstract

“…Exacerbation is the most important issue in patients with COPD as it is related to their quality of life and progression of the disease and patient disability . In this study, patients with high P‐A ratio had greater risks of exacerbations which indicate the importance of the relative diameter of the pulmonary artery in determining the risk and prognosis of the disease in COPD patients.…”

Section: Discussionmentioning

confidence: 61%

The pulmonary artery‐aorta ratio: Is it related to quality of life in chronic obstructive pulmonary disease?

Ghobadi

Janbazi

Matin

et al. 2018

Clinical Respiratory J

View full text Add to dashboard Cite

show abstract

Physical and Functional Impairment During and After Hospitalization in Subjects With Severe COPD Exacerbation

Abstract: Hospitalization due to COPD exacerbation leads to physical and functional impairment in patients; impairment is greater at 1-month follow-up. It would be interesting to conduct physical therapy interventions to prevent the impairment.

Cited by 24 publications

References 42 publications

Pulmonary inflammation-induced loss and subsequent recovery of skeletal muscle mass require functional poly-ubiquitin conjugation

Pulmonary inflammation-induced loss and subsequent recovery of skeletal muscle mass require functional poly-ubiquitin conjugation

Management of severe acute exacerbations of COPD: an updated narrative review

The pulmonary artery‐aorta ratio: Is it related to quality of life in chronic obstructive pulmonary disease?

Contact Info

Product

Resources

About