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      Effects of cigarette smoking on coagulation screening tests and platelet counts in a Sudanese male adults population

      research-article
      , MD, PhD
      Saudi Medical Journal
      Saudi Medical Journal

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          Abstract

          Objectives:

          To study the effects of heavy cigarette smoking on coagulation (CGG) screening tests and platelet counts (PLTs) in a Sudanese male adults population.

          Methods:

          A case control study was conducted at both Kosti and Gabalein towns, Sudan, during October 2016 to May 2017. A 100 adult cigarette smokers were selected and another 100 matched non-smokers were selected as healthy controls. Blood samples were collected in trisodium citrate anti-coagulant for prothrombin time (PT), partial thromboplastin time (PTT), and international normalized ratio (INR), analyzed using standard methods (co-agulometer machine) and Ethylenediaminetetraacetic acid for the platelet counts, using an automated haematology analyzer (Sysmex, Tokoyo, Japan).

          Results:

          The results showed that the mean platelet counts were significantly lower in the smokers (183x10 3/cmm±64x10 3/cmm) versus (244x10 3/cmm±38x10 3/cmm) in non-smokers, ( p<0.000). Pearson correlation analysis suggested a weak negative correlation between platelet counts with the duration of smoking (r= -0.289, p<0.004) and the age of the smokers (r= -0.238, p<0.017). The mean PT and INR were also significantly lower in smokers (12.9±1.2 seconds) compared with the non-smokers (13.7±1.04 seconds, p<0.000), for PT and (0.95±0.09 versus 1.01±0.08, p<0.000) for INR. In contrast, PTT had no significant variation in smokers (30.5±3.8 seconds) and the non-smokers (37.9±4.6 seconds). A p-value>0.05 was considered significant.

          Conclusion:

          Cigarette smokers tend to have lower platelet counts, shorter PT, and INR values, compared to non-smokers. Therefore, smoking might be associated with bleeding disorders but further investigations are needed.

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          Most cited references20

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          The biology behind the atherothrombotic effects of cigarette smoke.

          Cigarette smoke is an aerosol that contains >4,000 chemicals, including nicotine, carbon monoxide, acrolein, and oxidant compounds. Exposure to cigarette smoke induces multiple pathological effects in the endothelium, several of which are the result of oxidative stress initiated by reactive oxygen species, reactive nitrogen species, and other oxidant constituents of cigarette smoke. Cigarette-smoke exposure interferes adversely with the control of all stages of plaque formation and development and pathological thrombus formation. The reactive oxygen species in cigarette smoke contribute to oxidative stress, upregulation of inflammatory cytokines, and endothelial dysfunction, by reducing the bioavailability of nitric oxide. Plaque formation and the development of vulnerable plaques also result from exposure to cigarette smoke via the enhancement of inflammatory processes and the activation of matrix metalloproteases. Moreover, exposure to cigarette smoke results in platelet activation, stimulation of the coagulation cascade, and impairment of anticoagulative fibrinolysis. Many cigarette-smoke-mediated prothrombotic changes are quickly reversible upon smoking cessation. Public health efforts should urgently promote our understanding of current cigarette-smoke-induced cardiovascular pathology to encourage individuals to reduce their exposure to cigarette smoke and, therefore, the detrimental consequences of associated atherothrombotic disease.
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            Mechanisms of coronary thrombosis in cigarette smoke exposure.

            Acute rupture or erosion of a coronary atheromatous plaque and subsequent coronary artery thrombosis cause the majority of sudden cardiac deaths and myocardial infarctions. Cigarette smoking is a major risk factor for acute coronary thrombosis. Indeed, a majority of sudden cardiac deaths attributable to acute thrombosis are in cigarette smokers. Both active and passive cigarette smoke exposure seem to increase the risk of coronary thrombosis and myocardial infarctions. Cigarette smoke exposure seems to alter the hemostatic process via multiple mechanisms, which include alteration of the function of endothelial cells, platelets, fibrinogen, and coagulation factors. This creates an imbalance of antithrombotic/prothrombotic factors and profibrinolytic/antifibrinolytic factors that support the initiation and propagation of thrombosis.
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              • Record: found
              • Abstract: found
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              Is Open Access

              Novel proteolytic microvesicles released from human macrophages after exposure to tobacco smoke.

              Cigarette smoking damages the extracellular matrix in a variety of locations, leading to atherosclerotic plaque instability and emphysematous lung destruction, but the underlying mechanisms remain poorly understood. Here, we sought to determine whether exposure of human macrophages, a key participant in extracellular matrix damage, to tobacco smoke extract (TSE) induces the release of microvesicles (MVs; or microparticles) with proteolytic activity; the major proteases involved; and the cellular mechanisms that might mediate their generation. We found that MVs released from TSE-exposed macrophages carry substantial gelatinolytic and collagenolytic activities that surprisingly can be predominantly attributed to a single transmembrane protease of the matrix metalloproteinase (MMP) superfamily (namely, MMP14). Flow cytometric counts revealed that exposure of human macrophages to TSE for 20 hours more than quadrupled their production of MMP14-positive MVs (control, 1112 ± 231; TSE-induced, 5823 ± 2192 MMP14-positive MVs/μL of conditioned medium; means ± SEM; n = 6; P < 0.01). Our results indicate that the production of these MVs by human macrophages relies on a series of regulated steps that include activation of two mitogen-activated protein kinases (MAPKs, i.e., the Jun N-terminal kinase and p38 MAPK), and then MAPK-dependent induction and maturation of cellular MMP14, a remarkable accumulation of MMP14 into nascent plasma membrane blebs, and finally caspase- and MAPK-dependent apoptosis and apoptotic microvesicle generation. Proteolytically active MVs induced by tobacco smoke may be novel mediators of clinical important matrix destruction in smokers.
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                Author and article information

                Journal
                Saudi Med J
                Saudi Med J
                Saudi Medical Journal
                Saudi Medical Journal (Saudi Arabia )
                0379-5284
                September 2018
                : 39
                : 9
                : 897-901
                Affiliations
                [1] From the Collage of Health Sciences, The Saudi Electronic University, Riyadh, Kingdom of Saudi Arabia, and from the Faculty of Medical laboratory Sciences, El Imam El Mahdi University, Kosti, Sudan
                Author notes
                Address correspondence and reprint request to: Dr. Ahmed M. Elkhalifa, The Saudi Electronic University, Riyadh, Kingdom of Saudi Arabia, E-mail: ahmedelnour2003@ 123456yahoo.com ORCID ID: orcid.org/0000-0002-2660-5054
                Article
                SaudiMedJ-39-897
                10.15537/smj.2018.9.22630
                6201005
                30251733
                4d6b3fb2-c47a-4265-a5de-44a43b9e0520
                Copyright: © Saudi Medical Journal

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 22 May 2018
                : 08 August 2018
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