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      Prominent features of platelet count, plateletcrit, mean platelet volume and platelet distribution width in pulmonary tuberculosis

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          Abstract

          Background

          We aimed to investigate the relation of platelet count (PLT) and plateletcrit (PCT), mean platelet volume (MPV) and platelet distribution width (PDW) with other acute phase reactants and radiological extent in pulmonary tuberculosis (PTB).

          Methods

          One hundred patients with PTB (Group 1), 50 patients with community-acquired pneumonia (Group 2) and 28 healthy control individuals (Group 3) were included in this analytic study.

          Results

          WBC (White Blood Cell), ESR (Eritrocyte Sedimentation Rate), CRP (C-Reactive Protein), PLT and PCT values were both in Group 1 and Group 2 than in Group 3. PDW values were significantly higher in Group 1 than Group 3. WBC, ESR and CRP values were lower, while PLT and PCT values were higher in the Group 1 compared to Group 2 (p < 0.001). PLT was positively correlated with CRP and ESR values in the tuberculosis group (p < 0.001), while it was not correlated with CRP and ESR in the pneumonia group (p > 0.05). ESR, CRP, PLT and PCT values were found higher in radiological advanced stage (Stage 3) patients with PTB, while hemoglobin (Hb) was found lower (p < 0.05). Higher WBC, ESR, CRP and PCT values as well as radiological advanced stage were more common in PTB patients with thrombocytosis compared to the patients with normal platelet count, whereas Hb was found lower in these patients.

          Conclusions

          This study indicates that reactive thrombocytosis and higher PCT and PDW develop frequently in PTB and there is a relation between thrombocytosis and acute phase reactants, that is the inflammatory response. In addition, tuberculosis with radiological advanced stage is seen more frequently in the patients with thrombocytosis and higher PCT, drawing attention to the possible role of platelets in the cell-based immune process of tuberculosis.

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          Most cited references12

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          Acute-phase response and the hypercoagulable state in pulmonary tuberculosis.

          In our experience, severe pulmonary tuberculosis (PTB) is often complicated by deep venous thrombosis (DVT). Because of the association between inflammation and haemostatic changes that can result in a hypercoagulable state, we have prospectively examined such predisposing factors in representative patients. Sequential analyses in a control group with active PTB showed anaemia, thrombocytosis, elevations in plasma fibrinogen, fibrin(ogen) degradation products (FDP), tissue plasminogen activator (t-PA) and inhibitor (PAI-1) with depressed antithrombin III levels. Age, sex and disease matched individuals with venographically proven DVT had higher FDP (15.8 +/- 14.3 v 3.2 +/- 1.7 micrograms/ml:P < 0.01), t-PA (19.4 +/- 14.9 v 11.3 +/- 0.8 ng/ml:P < 0.01), and functional PAI-1 activity (11.6 +/- 6.3 v 4.2 +/- 4.1:P < 0.01) with lower platelet counts (347 +/- 110 v 563 +/- 230 x 10(9)/1:P < 0.01). Fibrinogen levels in all patients rose during the first 2 weeks of therapy and, together with related disturbances, corrected within 12 weeks. In conclusion, elevated plasma fibrinogen with impaired fibrinolysis coupled with a decrease in antithrombin III and reactive thrombocytosis would appear to favour the development of DVT in PTB.
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            Thrombocytopenia and thrombocytosis at time of hospitalization predict mortality in patients with community-acquired pneumonia.

            Platelets are inflammatory cells with an important role in antimicrobial host defenses. We speculate that an abnormal platelet count may be a marker of severity in patients with community-acquired pneumonia (CAP). The objectives of this study were to evaluate if abnormal platelet count in hospitalized patients with CAP was associated with 30-day mortality and to compare platelet count and leukocyte count as predictors of 30-day mortality. We performed a retrospective cohort study of 500 consecutive patients hospitalized with CAP at the Veterans Hospital of Louisville, Kentucky, between June 2001 and March 2006 to investigate the association of platelet count and leukocyte count with 30-day mortality. Predictor variables were platelet count and leukocyte count. Abnormal platelet count was 400,000/L (thrombocytosis). The outcome variable was 30-day mortality. To control for potential confounding, a propensity score that incorporated 33 variables was used. Platelet count was strongly associated (P = .0009) with 30-day mortality, whereas no association was observed for leukocyte count (P = .5114). High platelet counts resulted in a significantly increased risk of mortality. Thrombocytopenia and thrombocytosis are associated with mortality in patients hospitalized with CAP. When evaluating an initial CBC test in patients with CAP, an abnormal platelet count is a better predictor of outcome than an abnormal leukocyte count.
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              Hemostatic changes in active pulmonary tuberculosis.

              Severe pulmonary tuberculosis (PTB) is sometimes complicated by deep vein thrombosis (DVT). We have searched for possible hemostatic disturbances that are predisposing factors for venous thrombosis in patients with PTB. Coagulation and platelet function tests were studied in 45 patients with active PTB and 20 healthy control volunteers before therapy. Findings were compared with results at 30 days. Analysis in patients with active PTB showed anemia, leucocytosis, thrombocytosis, elevation in plasma fibrinogen, factor VIII, plasminogen activator inhibitor 1 (PAI-1) with depressed antithrombin III (AT III) and protein C (PC) levels. On the 30th day of treatment, anemia, leucocytosis and thrombocytosis were improved. Fibrinogen and factor VIII levels had decreased to normal levels, PC and AT III levels had increased to normal levels, and there was no difference in PAI-1 levels. We found no activated protein C resistance. Platelet aggregation studies demonstrated increased platelet activation. However, DVT was not detected in patients during the follow-up period. Decreased AT III, PC and elevated plasma fibrinogen levels and increased platelet aggregation appear to induce a hypercoagulable state seen in PTB and improve with treatment.
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                Author and article information

                Journal
                Multidiscip Respir Med
                Multidiscip Respir Med
                Multidisciplinary Respiratory Medicine
                BioMed Central
                1828-695X
                2049-6958
                2012
                31 October 2012
                : 7
                : 1
                : 38
                Affiliations
                [1 ]Department of Pulmonology, Yedikule Chest Diseases and Thoracic Surgery Training and Research Hospital, Zeytinburnu/İstanbul, Postal Code: 34760, Turkey
                Article
                2049-6958-7-38
                10.1186/2049-6958-7-38
                3529701
                23114411
                5b1ad11f-5f0f-4412-9e59-6086664ac9ee
                Copyright ©2012 Şahin et al. licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 15 July 2012
                : 16 October 2012
                Categories
                Original Research Article

                Respiratory medicine
                platelet,platelet distribution width,pneumonia,plateletcrit,pulmonary tuberculosis,mean platelet volume,thrombocytosis

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