Fibrin clot properties are altered in patients with chronic obstructive pulmonary disease

Undas, Anetta; Kaczmarek, Przemysław; Sładek, Krzysztof; Stępień, Ewa; Skucha, Wojciech; Rzeszutko, Marcin; Górkiewicz-Kot, Izabela; Tracz, Wiesława

doi:10.1160/th09-02-0118

Cited by 77 publications

(24 citation statements)

References 33 publications

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“…An electron microscopy study showed that fibrin clots isolated from the plasma of COPD patients are denser and more resistant to lysis than those from control subjects with an equivalent circulating fibrinogen concentration [11]. The same study showed that the fibrin clots from COPD patients became similar to those from subjects without COPD after 3 months of simvastatin treatment.…”

Section: Coagulopathy and Copdmentioning

confidence: 89%

“…In the basal state, COPD patients exhibit abnormally high levels of tissue factor (tissue factor pro-coagulant activity) and Factor VIIa [10], and their fibrin clots are resistant to lysis [11]. After 2 h of artificial hypoxaemia, compared to non-hypoxic controls, COPD patients have abnormally elevated levels of circulating thrombin-antithrombin complex and prothrombin activation fragments, with a parallel elevation in interleukin (IL)-6 [12].…”

Section: Coagulopathy and Copdmentioning

confidence: 99%

See 1 more Smart Citation

Comorbidities of COPD

Cavaillès¹,

Brinchault-Rabin²,

Dixmier³

et al. 2013

European Respiratory Review

407

285

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By 2020, chronic obstructive pulmonary disease (COPD) will be the third cause of mortality. Extrapulmonary comorbidities influence the prognosis of patients with COPD. Tobacco smoking is a common risk factor for many comorbidities, including coronary heart disease, heart failure and lung cancer. Comorbidities such as pulmonary artery disease and malnutrition are directly caused by COPD, whereas others, such as systemic venous thromboembolism, anxiety, depression, osteoporosis, obesity, metabolic syndrome, diabetes, sleep disturbance and anaemia, have no evident physiopathological relationship with COPD. The common ground between most of these extrapulmonary manifestations is chronic systemic inflammation.All of these diseases potentiate the morbidity of COPD, leading to increased hospitalisations and healthcare costs. They can frequently cause death, independently of respiratory failure. Comorbidities make the management of COPD difficult and need to be evaluated and treated adequately. @ERSpublications Extrapulmonary comorbidities are common in COPD and influence prognosis; we propose an exhaustive comorbidities review

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Section: Coagulopathy and Copdmentioning

confidence: 89%

Section: Coagulopathy and Copdmentioning

confidence: 99%

Comorbidities of COPD

Cavaillès¹,

Brinchault-Rabin²,

Dixmier³

et al. 2013

European Respiratory Review

407

285

View full text Add to dashboard Cite

show abstract

“…The most common diseases related to thrombosis are inflammatory by nature. Reduced clot permeability and susceptibility to lysis have been observed in rheumatoid arthritis [30], chronic obstructive pulmonary disease [31], and inflammatory bowel disease [32]. Binding of C-reactive protein (CRP) with fibrinogen and fibrin [33] is likely to contribute to the prothrombotic clot phenotype as evidenced by correlations of CRP with plasma clot permeability and lysis [30–32].…”

Section: Modifiers Of Fibrin Clot Propertiesmentioning

confidence: 99%

Prothrombotic Fibrin Clot Phenotype in Patients with Deep Vein Thrombosis and Pulmonary Embolism: A New Risk Factor for Recurrence

Undas

2017

BioMed Research International

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Prothrombotic fibrin clot phenotype, involving faster formation of dense meshwork composed of thinner and highly branched fibers that are relatively resistant to plasmin-induced lysis, has been reported in patients with not only myocardial infarction or stroke, but also venous thromboembolism (VTE), encompassing deep vein thrombosis (DVT), and/or pulmonary embolism (PE). Prothrombotic fibrin clot phenotype, in particular prolonged clot lysis time, is considered a novel risk factor for VTE as well as venous thrombosis at unusual location, for example, cerebral sinus venous thrombosis, retinal vein obstruction, and Budd-Chiari syndrome. Growing evidence from observational studies indicates that abnormal fibrin clot properties can predict recurrent DVT and PE and they are involved in serious complications of VTE, for example, thromboembolic pulmonary hypertension and postthrombotic syndrome. The purpose of this article is to review our current understanding of the role of fibrin clot structure and function in venous thrombosis with emphasis on clinical issues ranging from prognosis to therapy.

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“…This could be explained by their pleiotropic effects, including anti-inflammatory and immunomodulatory effects, which was demonstrated by the significant decrease in systemic inflammation markers such as C-reactive protein and IL-6 [53, 54]. Additionally, statins were demonstrated to regulate the balance between Th1 and Th2 cells by inhibiting the Th1 development but augmenting the Th2 development of CD4 + cells [55].…”

Section: Therapeutic Implications Of Targeting Kv13-channels In the mentioning

confidence: 99%

Lymphocyte Kv1.3-channels in the pathogenesis of chronic obstructive pulmonary disease: novel therapeutic implications of targeting the channels by commonly used drugs

Kazama

Tamada

2016

Allergy Asthma Clin Immunol

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In patients with chronic obstructive pulmonary disease (COPD), over-activated T-lymphocytes produce pro-inflammatory cytokines and proliferate in situ in the lower airways and pulmonary parenchyma, contributing substantially to the pathogenesis of the disease. Despite our understanding of the molecular mechanisms by which lymphocytes are activated, we know little about the physiological mechanisms. T-lymphocytes predominantly express delayed rectifier K+-channels (Kv1.3) in their plasma membranes and these channels play crucial roles in inducing the lymphocyte activation and proliferation. In the pathogenesis of chronic inflammatory diseases, such as chronic kidney disease (CKD) or inflammatory bowel disease (IBD), these channels, which are overexpressed in proliferating lymphocytes within the inflamed organs, are responsible for the progression of the diseases. Since the over-activation of cellular immunity is also mainly involved in the pathogenesis of COPD, this disease could share similar pathophysiological features as those of CKD or IBD. From a literature review including ours, it is highly likely that the Kv1.3-channels are overexpressed or over-activated in T-lymphocytes isolated from patients with COPD, and that the overexpression of the channels would contribute to the development or progression of COPD. The involvement of the channels leads to novel therapeutic implications of potentially useful Kv1.3-channel inhibitors, such as calcium channel blockers, macrolide antibiotics, HMG-CoA reductase inhibitors and nonsteroidal anti-inflammatory drugs, in the treatment of COPD.

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Fibrin clot properties are altered in patients with chronic obstructive pulmonary disease

Cited by 77 publications

References 33 publications

Comorbidities of COPD

Comorbidities of COPD

Prothrombotic Fibrin Clot Phenotype in Patients with Deep Vein Thrombosis and Pulmonary Embolism: A New Risk Factor for Recurrence

Lymphocyte Kv1.3-channels in the pathogenesis of chronic obstructive pulmonary disease: novel therapeutic implications of targeting the channels by commonly used drugs

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