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Systemic Effects in COPD
Abstract
The pathogenesis and clinical manifestations of COPD are not restricted to pulmonary inflammation and structural remodeling. Rather, this disorder is associated with clinically significant systemic alterations in biochemistry and organ function. The systemic aspects of COPD include oxidative stress and altered circulating levels of inflammatory mediators and acute-phase proteins. Indeed, an impaired endogenous oxidant-antioxidant balance has been reported in patients experiencing exacerbations of COPD, and others have observed altered circulating levels of several cytokines and adhesion molecules in patients with stable disease. As in other chronic inflammatory conditions, weight loss, muscle wasting, and tissue depletion are commonly seen in COPD patients. Selective wasting of fat-free mass coupled with impaired respiratory and peripheral muscle function and a reduced capacity for exercise occur in COPD patients. Indeed, weight loss may directly impact poor prognosis in COPD patients. The mechanisms underlying weight loss and muscle wasting are incompletely understood but likely involve an imbalance in ongoing processes of protein degradation and replacement. This may include alterations in the relative levels or activities of endocrine hormones such as insulin, growth hormone, testosterone, and glucocorticoids. Furthermore, chronic systemic inflammation involving cytokines such as interleukin-1 and tumor necrosis factor-alpha may be associated with these hormonal changes an…
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“Classically, circulating TNF-α is reported to be higher in COPD patients than controls and negatively correlated to lean mass [23,24]”
From Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting (2023) · cites this paper as [24]
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“Classically, circulating TNF-α is reported to be higher in COPD patients than controls and negatively correlated to lean mass [23,24], as well as to muscle strength, including upper muscles [25].”
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Metadata
- Authors
- Wouters, E. F. M., Creutzberg, E. C., & Schols, A. M. W. J.
- Affiliations
- Maastricht University Medical Centre (NL)
- Corresponding author
- Wouters, Emil F.M.
- Venue
- Chest
- Publisher
- Elsevier BV
- Published
- 2002-05
- Volume
- 121
- Issue
- 5
- Pages
- 127S-130S
- ISSN
- 0012-3692 (ISSN-L)
- OpenAlex
- W1981878902
- Cited by
- 301
- References
- 33
- Citations by year
- 2026: 3 · 2025: 1 · 2024: 8 · 2023: 8 · 2022: 5 · 2021: 4 · 2020: 5 · 2019: 11 · 2018: 4 · 2017: 13 · 2016: 8 · 2015: 9 · 2014: 11 · 2013: 14 · 2012: 15
- FWCI
- 4.24
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- CHEST Journal (publishedVersion)
- PubMed (publishedVersion)
- Research Publications (Maastricht University) (submittedVersion)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Chronic Obstructive Pulmonary Disease (COPD) Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Physiology (medical) › Nutrition and Health in Aging
- Keywords
- chronic obstructive pulmonary disease, systemic effects, oxidative stress, prooxidant-antioxidant balance, inflammatory mediators, acute phase proteins, COPD exacerbations, weight loss, muscle atrophy, cachexia, skeletal muscle protein metabolism, cytokines, interleukin-1, TNF-α, glucocorticoids, insulin, growth hormone, testosterone, exercise capacity, prognosis
- MeSH terms
- Cachexia, Humans, Muscle Proteins, Prognosis, Tumor Necrosis Factor-alpha, Body Mass Index, Pulmonary Disease, Chronic Obstructive
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