3
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      The Significance of iron deficiency and anemia in a real-life COPD cohort

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background: Current evidence suggests an increased prevalence of iron deficiency (ID) and anemia in chronic obstructive pulmonary disease (COPD). ID and subsequent anemia can be due to iron losses via bleeding resulting in absolute ID or inflammation-driven retention of iron within macrophages resulting in functional ID and anemia of inflammation.

          Methods: This is a retrospective analysis of 204 non-exacerbated COPD patients in outpatient care. Current definitions of absolute and functional ID were applied to determine the prevalence of ID and to analyze associations to disease severity in terms of lung function parameters and clinical symptoms.

          Results: The studied cohort of COPD patients demonstrated a high prevalence of ID, ranging from 30 to 40% during the observation time. At the initial presentation, absolute or functional ID was found in 9.3% to 12.3% of COPD individuals, whereas combined forms of absolute and functional ID were most prevalent (25.9% of all individuals). The prevalence of ID increased during longitudinal follow-up (37 ± 15 months), and especially combined forms of ID were significantly related to anemia. Anemia prevalence ranged between 14.2% and 20.8% during the observation period and anemia was associated with lower FEV1, DLCOc, and CRP elevation. Accordingly, ID was associated with decreased FEV1, DLCOc, and an elevation in CRP.

          Conclusion: ID is common in COPD patients, but a uniform definition for accurate diagnosis does not exist. Prevalence of functional ID and anemia increased during follow-up. The associations of ID and anemia with reduced functional lung capacity and elevated inflammation may reflect a more severe COPD phenotype.

          Related collections

          Most cited references24

          • Record: found
          • Abstract: found
          • Article: not found

          Oxidative stress in COPD.

          Oxidative stress is now recognized as a major predisposing factor in the pathogenesis of COPD. Existing therapies for COPD are ineffective at halting disease progression, with bronchodilators being the mainstay of pharmacotherapy, providing symptomatic relief only. It is, therefore, important for a better understanding of the underlying mechanisms by which oxidative stress drives disease pathogenesis to develop novel and more effective therapies. Antioxidant capacity in COPD is substantially reduced as a result of cigarette smoking and exacerbations, with oxidative stress persisting long after the cessation of cigarette smoking or exacerbation, due to the continued production of reactive oxygen species from endogenous sources. We discuss (1) how oxidative stress arises in the lung, (2) how it is neutralized, (3) what genetic factors may predispose to the development of COPD, and (4) how this impacts inflammation and autoimmunity in the development of emphysema and small airways disease. Finally, various strategies have been considered to neutralize the increased oxidative burden present in COPD. This review highlights why current antioxidant strategies have so far failed and what promising alternatives are on the horizon. Moreover, a number of studies have shown that there is no single "magic bullet" to combat oxidative stress, but instead a combination therapy, targeting oxidative stress in the various subcellular compartments, may prove to be more effective in COPD.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: found
            Is Open Access

            Involvement of cigarette smoke-induced epithelial cell ferroptosis in COPD pathogenesis

            Ferroptosis is a necrotic form of regulated cell death (RCD) mediated by phospholipid peroxidation in association with free iron-mediated Fenton reactions. Disrupted iron homeostasis resulting in excessive oxidative stress has been implicated in the pathogenesis of chronic obstructive pulmonary disease (COPD). Here, we demonstrate the involvement of ferroptosis in COPD pathogenesis. Our in vivo and in vitro models show labile iron accumulation and enhanced lipid peroxidation with concomitant non-apoptotic cell death during cigarette smoke (CS) exposure, which are negatively regulated by GPx4 activity. Treatment with deferoxamine and ferrostatin-1, in addition to GPx4 knockdown, illuminate the role of ferroptosis in CS-treated lung epithelial cells. NCOA4-mediated ferritin selective autophagy (ferritinophagy) is initiated during ferritin degradation in response to CS treatment. CS exposure models, using both GPx4-deficient and overexpressing mice, clarify the pivotal role of GPx4-regulated cell death during COPD. These findings support a role for cigarette smoke-induced ferroptosis in the pathogenesis of COPD.
              Bookmark
              • Record: found
              • Abstract: not found
              • Article: not found

              Iron deficiency

                Bookmark

                Author and article information

                Journal
                Int J Med Sci
                Int J Med Sci
                ijms
                International Journal of Medical Sciences
                Ivyspring International Publisher (Sydney )
                1449-1907
                2020
                19 August 2020
                : 17
                : 14
                : 2232-2239
                Affiliations
                [1 ]Department of Internal Medicine II, Infectious Diseases, Pneumology, Rheumatology, Medical University of Innsbruck, Innsbruck, Austria.
                [2 ]Christian Doppler Laboratory for Iron Metabolism and Anemia Research, Medical University of Innsbruck, Austria.
                Author notes
                ✉ Corresponding authors: Judith Löffler-Ragg and Günter Weiss, E-mail: judith.loeffler@ 123456i-med.ac.at (J.L.); guenter.weiss@ 123456i-med.ac.at (G.W). Medical University of Innsbruck, Department of Internal Medicine II, Anichstraße 35, A-6020, Innsbruck, Austria. Phone: + 43 (0) 512-504-23251; Fax: +43 (0) 512-504-23317.

                *These authors contributed equally to this manuscript.

                Competing Interests: The authors have declared that no competing interest exists.

                Article
                ijmsv17p2232
                10.7150/ijms.46163
                7484656
                32922186
                919c13d5-fbf3-48e2-b579-afae18d5ca9f
                © The author(s)

                This is an open access article distributed under the terms of the Creative Commons Attribution License ( https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.

                History
                : 19 March 2020
                : 12 July 2020
                Categories
                Research Paper

                Medicine
                copd,obstructive pulmonary disease,anemia,iron deficiency,inflammation
                Medicine
                copd, obstructive pulmonary disease, anemia, iron deficiency, inflammation

                Comments

                Comment on this article