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      Increased In Vivo Thrombin Generation in Patients with Localized Non-Small Cell Lung Cancer Unfit for Surgery

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          Abstract

          Patients with lung cancer face a substantially increased risk of thromboembolic disease. Patients with localized non-small cell lung cancer (NSCLC) who are unfit for surgery due to age or comorbidity have additional thrombotic risk factors. Thus, we aimed to investigate markers of primary and secondary hemostasis, since this could assist in treatment decisions. We included 105 patients with localized NSCLC. Ex vivo thrombin generation was determined by calibrated automated thrombogram and in vivo thrombin generation was determined by measurement of thrombin–antithrombin complex (TAT) levels and prothrombin fragment F1 + 2 concentrations (F1 + 2). Platelet aggregation was investigated by impedance aggregometry. Healthy controls were used for comparison. TAT and F1 + 2 concentrations were significantly higher in NSCLC patients than in healthy controls ( P < .001). The levels of ex vivo thrombin generation and platelet aggregation were not increased in the NSCLC patients. Patients with localized NSCLC considered unfit for surgery had significantly increased in vivo thrombin generation. This finding should be further investigated as it could be relevant for the choice of thromboprophylaxis in these patients.

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          A new method of classifying prognostic comorbidity in longitudinal studies: Development and validation

          Mary Charlson, Peter Pompei, Kathy Ales … (1987)
          The objective of this study was to develop a prospectively applicable method for classifying comorbid conditions which might alter the risk of mortality for use in longitudinal studies. A weighted index that takes into account the number and the seriousness of comorbid disease was developed in a cohort of 559 medical patients. The 1-yr mortality rates for the different scores were: "0", 12% (181); "1-2", 26% (225); "3-4", 52% (71); and "greater than or equal to 5", 85% (82). The index was tested for its ability to predict risk of death from comorbid disease in the second cohort of 685 patients during a 10-yr follow-up. The percent of patients who died of comorbid disease for the different scores were: "0", 8% (588); "1", 25% (54); "2", 48% (25); "greater than or equal to 3", 59% (18). With each increased level of the comorbidity index, there were stepwise increases in the cumulative mortality attributable to comorbid disease (log rank chi 2 = 165; p less than 0.0001). In this longer follow-up, age was also a predictor of mortality (p less than 0.001). The new index performed similarly to a previous system devised by Kaplan and Feinstein. The method of classifying comorbidity provides a simple, readily applicable and valid method of estimating risk of death from comorbid disease for use in longitudinal studies. Further work in larger populations is still required to refine the approach because the number of patients with any given condition in this study was relatively small.
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            Development and validation of a predictive model for chemotherapy-associated thrombosis.

            Alok A. Khorana, Nicole M Kuderer, Eva Culakova … (2008)
            Risk of venous thromboembolism (VTE) is elevated in cancer, but individual risk factors cannot identify a sufficiently high-risk group of outpatients for thromboprophylaxis. We developed a simple model for predicting chemotherapy-associated VTE using baseline clinical and laboratory variables. The association of VTE with multiple variables was characterized in a derivation cohort of 2701 cancer outpatients from a prospective observational study. A risk model was derived and validated in an independent cohort of 1365 patients from the same study. Five predictive variables were identified in a multivariate model: site of cancer (2 points for very high-risk site, 1 point for high-risk site), platelet count of 350 x 10(9)/L or more, hemoglobin less than 100 g/L (10 g/dL) and/or use of erythropoiesis-stimulating agents, leukocyte count more than 11 x 10(9)/L, and body mass index of 35 kg/m(2) or more (1 point each). Rates of VTE in the derivation and validation cohorts, respectively, were 0.8% and 0.3% in low-risk (score = 0), 1.8% and 2% in intermediate-risk (score = 1-2), and 7.1% and 6.7% in high-risk (score >/= 3) category over a median of 2.5 months (C-statistic = 0.7 for both cohorts). This model can identify patients with a nearly 7% short-term risk of symptomatic VTE and may be used to select cancer outpatients for studies of thromboprophylaxis.
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              Role of platelets and platelet receptors in cancer metastasis

              Martin Schlesinger (2018)
              The interaction of tumor cells with platelets is a prerequisite for successful hematogenous metastatic dissemination. Upon tumor cell arrival in the blood, tumor cells immediately activate platelets to form a permissive microenvironment. Platelets protect tumor cells from shear forces and assault of NK cells, recruit myeloid cells by secretion of chemokines, and mediate an arrest of the tumor cell platelet embolus at the vascular wall. Subsequently, platelet-derived growth factors confer a mesenchymal-like phenotype to tumor cells and open the capillary endothelium to expedite extravasation in distant organs. Finally, platelet-secreted growth factors stimulate tumor cell proliferation to micrometastatic foci. This review provides a synopsis on the current literature on platelet-mediated effects in cancer metastasis and particularly focuses on platelet adhesion receptors and their role in metastasis. Immunoreceptor tyrosine-based activation motif (ITAM) and hemi ITAM (hemITAM) comprising receptors, especially, glycoprotein VI (GPVI), FcγRIIa, and C-type lectin-like-2 receptor (CLEC-2) are turned in the spotlight since several new mechanisms and contributions to metastasis have been attributed to this family of platelet receptors in the last years.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Clin Appl Thromb Hemost
                Journal ID (iso-abbrev): Clin Appl Thromb Hemost
                Journal ID (publisher-id): CAT
                Journal ID (hwp): spcat
                Title: Clinical and Applied Thrombosis/Hemostasis
                Publisher: SAGE Publications (Sage CA: Los Angeles, CA )
                ISSN (Print): 1076-0296
                ISSN (Electronic): 1938-2723
                Publication date (Electronic): 19 February 2023
                Publication date Collection: Jan-Dec 2023
                Volume: 29
                Electronic Location Identifier: 10760296231152897
                Affiliations
                [1 ]Department of Clinical Biochemistry, Ringgold 11297, universityAarhus University Hospital; , Aarhus, Denmark
                [2 ]Department of Clinical Medicine, Ringgold 1006, universityAarhus University; , Aarhus, Denmark
                [3 ]Department of Oncology, Ringgold 11286, universityOdense University Hospital; , Odense, Denmark
                [4 ]Academy of Geriatric Cancer Research (AgeCare), Ringgold 11286, universityOdense University Hospital; , Odense, Denmark
                [5 ]Institute of Clinical Research, Ringgold 6174, universityUniversity of Southern Denmark; , Odense, Denmark
                [6 ]Department of Clinical Biochemistry, Ringgold 11286, universityOdense University Hospital; , Odense, Denmark
                [7 ]Faculty of Health, Ringgold 1006, universityAarhus University; , Aarhus, Denmark
                Author notes
                [*]Johanne Andersen Hojbjerg, Department of Clinical Biochemistry, Aarhus University Hospital, Palle Juul-Jensens Boulevard 99, DK-8200 Aarhus N, Denmark. Email: johanand@ 123456rm.dk
                Author information
                https://orcid.org/0000-0002-5604-3451
                Article
                Publisher ID: 10.1177_10760296231152897
                DOI: 10.1177/10760296231152897
                PMC ID: 9941591
                PubMed ID: 36802980
                SO-VID: 16fb4063-84e9-4b9d-912a-3286fe7e2c52
                Copyright © © The Author(s) 2023
                License:

                This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

                History
                Date received : 04 October 2022
                Date revision received : 28 December 2022
                Date accepted : 08 January 2023
                Funding
                Funded by: Academy of Geriatric Cancer Research (AgeCare), Odense University Hospital, Denmark;
                Funded by: Danish Cancer Society Research Center, FundRef https://doi.org/10.13039/100015459;
                Award ID: R247-A14616
                Categories
                Subject: Original Manuscript
                Custom metadata
                typesetter ts19
                cover-date January-December 2023

                Keywords: lung neoplasms,hemostasis,platelet aggregation,thrombin generation
                Data availability:
                Keywords: lung neoplasms, hemostasis, platelet aggregation, thrombin generation

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