Thrombocytosis in adults: analysis of 777 patients

Santhosh-Kumar, C.R.; Yohannan, M. D.; Higgy, Kamal E.; Al-Mashhadani, Shihab A.

doi:10.1111/j.1365-2796.1991.tb00383.x

Cited by 80 publications

(50 citation statements)

References 10 publications

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“…Inflammatory reactions involving cytokines take place in patients with active IBD [8], and it has been demonstrated that interleukin-6 (IL-6), which is a mediator of inflammation, is associated with activation of the coagulation pathway [7]. IL-6 stimulates the release of thrombopoietin and induces thrombocytosis in patients with inflammatory disease [8], and reactive thrombocytosis is a typical feature in IBD [14]. Infusion of recombinant IL-6 stimulates coagulation activation [7] and is associated with a decreased capacity of the anticoagulant system in patients who suffered an acute stroke [15].…”

Section: Introductionmentioning

confidence: 99%

Platelets and Anticoagulant Capacity in Patients with Inflammatory Bowel Disease

Larsen

Nielsen²,

Fredholm³

et al. 2002

Pathophysiol Haemos Thromb

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Patients with inflammatory bowel disease (IBD) are susceptible to thromboembolic complications. Several mechanisms can be responsible, including abnormal regulation of coagulation activity, disturbances of fibrinolysis, inflammatory reactions and thrombocytosis. The aim of this study was to assess hemostatic alterations in these parameters during exacerbation of disease. We studied disease activity in 99 IBD patients receiving anti-inflammatory therapy, in relation to: procoagulant markers, i.e. prothrombin fragment F1 + 2 (F1 + 2), D-dimer and platelet count, anticoagulant markers, i.e. protein C, protein S and antithrombin, and a mediator of inflammation (IL-6). Coagulation activity and platelet count were increased during active disease in IBD patients compared with those in a state of remission. The IL-6 concentrations were positively correlated with disease activity and thrombocytosis in patients with ulcerative colitis, but no association with the anticoagulant capacity could be demonstrated except for a decrease in protein C during high disease activity.

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Section: Introductionmentioning

confidence: 99%

Platelets and Anticoagulant Capacity in Patients with Inflammatory Bowel Disease

Larsen

Nielsen²,

Fredholm³

et al. 2002

Pathophysiol Haemos Thromb

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“…Thrombocytosis has been shown to be associated with infectious disease, tissue damage, and chronic inflammatory disorders [5]. In malignant disease, thrombocytosis is thought to be secondary to an increased rate of platelet production with no alteration in platelet survival [6].…”

Section: Introductionmentioning

confidence: 99%

Tumor Anemia and Thrombocytosis in Patients with Vulvar Cancer

et al. 2000

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The aim of our study was to determine the prevalence of tumor anemia and thrombocytosis in patients with vulvar cancer, and to evaluate the prognostic value or pretreatment hemoglobin (Hb) and platelet count regarding disease-free and overall survival of patients with vulvar cancer. We measured pretreatment Hb and platelet count in 62 patients with squamous cell vulvar cancer. The results were correlated to clinical data. Median Hb and platelet count in patients with vulvar cancer were 13.1 g/dl (range 8.3–16.2) and 268,500/μl (range 88,000–778,000), respectively. Cut-off levels of 12 g/dl and 300,000/μl were selected for tumor anemia and tumor thrombocytosis, respectively according to published criteria. Tumor anemia and tumor thrombocytosis were present in 30.6 and 27.4% of patients with vulvar cancer, respectively. In a univariate analysis tumor stage and tumor thrombocytosis were significantly associated with a shortened disease-free (log-rank test, p < 0.001 and p = 0.003, respectively) and overall survival (log-rank test, p < 0.001 and p < 0.001, respectively). Tumor anemia was not associated with a shortened disease-free, but with a shortened overall survival of patients with vulvar cancer (log-rank test, p = 0.1 and p = 0.002, respectively). A multivariate Cox regression model considering tumor stage, tumor anemia, and tumor thrombocytosis showed, however, that pretreatment Hb and platelet count did not confer additional prognostic information to that already obtained by the established prognosticator tumor stage on disease free (multivariate Cox regression model, p = 0.8, p = 0.2, and p = 0.003, respectively) and overall survival (multivariate Cox regression model, p = 0.4, p = 0.5, and p = 0.04, respectively). Pretreatment tumor anemia and tumor thrombocytosis were associated with a poor prognosis, but were not an independent predictor of outcome in patients with vulvar cancer.

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“…Whereas primary thrombocytosis is observed in myeloproliferative syndromes, secondary or reactive thrombocytosis is noted in numerous clinical situations, 1 especially in association with inflammatory states of either infectious or noninfectious origin such as trauma and malignancy. 2,3 The extent to which mediators of the immune or hematopoietic system are involved in the regulation of the circulating platelet count in these conditions is insufficiently understood.Interleukin-6 (IL-6) plays a prominent role in inflammatory and neoplastic diseases. 4-6 Accordingly, mice deficient in IL-6 show a severely impaired acute-phase response.…”

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confidence: 99%

Interleukin-6 stimulates thrombopoiesis through thrombopoietin: role in inflammatory thrombocytosis

Kaser

Brandacher

Steurer

et al. 2001

Blood

555

390

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Baseline platelet production is dependent on thrombopoietin (TPO). TPO is constitutively produced and primarily regulated by receptor-mediated uptake by platelets. Inflammatory thrombocytosis is thought to be related to increased interleukin-6 (IL-6) levels. To address whether IL-6 might act through TPO to increase platelet counts, TPO was neutralized in vivo in C57BL/10 mice treated with IL-6, and hepatic TPO mRNA expression and TPO plasma levels were studied. Transcriptional regulation of TPO mRNA was studied in the hepatoblastoma cell line HepG2. Furthermore, TPO plasma levels were determined in IL-6-treated cancer patients. It is shown that IL-6-induced thrombocytosis in C57BL/10 mice is accompanied by enhanced hepatic TPO mRNA expression and elevated TPO plasma levels. Administration of IL-6 to cancer patients results in a corresponding increase in TPO plasma levels. IL-6 enhances TPO mRNA transcription in HepG2 cells. IL-6-induced thrombocytosis can be abrogated by neutralization of TPO, suggesting that IL-6 induces thrombocytosis through TPO. A novel pathway of TPO regulation by the inflammatory mediator IL-6 is proposed, indicating that the number of platelets by themselves might not be the sole determinant of circulating TPO levels and thus of thrombopoiesis. This regulatory pathway might be of relevance for the understanding of reactive thrombocytosis. IntroductionThrombocytosis can be classified into primary and secondary forms. Whereas primary thrombocytosis is observed in myeloproliferative syndromes, secondary or reactive thrombocytosis is noted in numerous clinical situations, 1 especially in association with inflammatory states of either infectious or noninfectious origin such as trauma and malignancy. 2,3 The extent to which mediators of the immune or hematopoietic system are involved in the regulation of the circulating platelet count in these conditions is insufficiently understood.Interleukin-6 (IL-6) plays a prominent role in inflammatory and neoplastic diseases. 4-6 Accordingly, mice deficient in IL-6 show a severely impaired acute-phase response. 7 Administration of IL-6 to humans has been associated with an increase in circulating platelet counts. [8][9][10][11][12][13][14] Furthermore, serum levels of IL-6 were significantly higher in patients with reactive thrombocytosis than in control patients. 15,16 Whether the thrombopoietic effect of IL-6 in vivo is caused by direct stimulation of hematopoietic progenitor cells or is indirectly mediated is unknown.Thrombopoietin (TPO), the ligand of the c-mpl proto-oncogene, is the primary regulator of proliferation and differentiation of megakaryocyte progenitors. [17][18][19][20][21][22][23] Mice rendered deficient in TPO or TPO receptor by gene targeting show severe thrombocytopenia, with platelet counts reduced by approximately 90%. 22,24 Treatment of mice, nonhuman primates, and humans with recombinant TPO or recombinant megakaryocyte growth and development factor, which constitutes a truncated, biologically active form of TPO, results in sig...

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Thrombocytosis in adults: analysis of 777 patients

Cited by 80 publications

References 10 publications

Platelets and Anticoagulant Capacity in Patients with Inflammatory Bowel Disease

Platelets and Anticoagulant Capacity in Patients with Inflammatory Bowel Disease

Tumor Anemia and Thrombocytosis in Patients with Vulvar Cancer

Interleukin-6 stimulates thrombopoiesis through thrombopoietin: role in inflammatory thrombocytosis

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