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THROMBOTIC COMPLICATIONS OF PANREATIC CANCER: A CLASSICAL KNOWLEDGE REVISITED

THROMBOTIC COMPLICATIONS OF PANREATIC CANCER: A CLASSICAL KNOWLEDGE REVISITED. D. L . DUMITRASCU, O. SUCIU, C. GRAD, D. GHEBAN 2 ND MEDICAL DEPT. UMPh IULIU HATIEGANU CLUJ ROMANIA. Cluj, Romania. Armand Trousseau (1801­1867).

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THROMBOTIC COMPLICATIONS OF PANREATIC CANCER: A CLASSICAL KNOWLEDGE REVISITED

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  1. THROMBOTIC COMPLICATIONS OF PANREATIC CANCER: A CLASSICAL KNOWLEDGE REVISITED D. L. DUMITRASCU, O. SUCIU, C. GRAD, D. GHEBAN 2ND MEDICAL DEPT. UMPh IULIU HATIEGANU CLUJ ROMANIA

  2. Cluj, Romania

  3. Armand Trousseau (1801­1867)

  4. Looking for this association and its consequences for clinical practice

  5. “In conditions of cachexia, a special state of the blood occurs which predispose to spontaneous coagulation” • Trousseau 1865

  6. Jaundice Pancreas CC Thrombosis of aorta

  7. Pancreatic CC Thrombosis Pancreas

  8. longitudinal and transversal section of popliteal vein: recent thrombosis, complete obstruction of popliteal vein

  9. transversal section of common femural vein at femural bifurcation: recent thrombosis, complet obstruction (duplex color)

  10. Epidemiology • Incidence of thrombosis: • in cancer: 5-60% • 2x higher in cancer pts vs general population • 20% pts DVT have dg cancer

  11. Clinical types of thrombosis: • Superficial migratory thrombophlebitis (Trousseau syndrome) • Idiopathic deep venous thrombosis • Nonbacterial thrombotic endocarditis • Intravascular disseminated coagulation • Thrombotic microangiopathy (thrombocitary thrombocytopenic purpura and the hemolitic-uremic syndrome) • Arterial thrombosis

  12. Localisation of cancer

  13. PathogenesisVirchow’s triad • Alterations in blood flow • Vascular endothelial injury • Alterations in the constituents of the blood • Patients with cancer : hypercoagulable state >> substances with procoagulant activity: tissue factor, cancer procoagulant

  14. Pathogenesis • Hypercoagulability • Abnormal coagulation tests • Thrombine generated in excess • Tumour cells have direct procoagulant effect • Tissue factor activate F IX and FX initiating coagulation • Tumoral procoagulant: a Ca-dependent cistein-protease

  15. Pathogenesis • The factor V Leiden mutation, a mutation of the F5 gene (gene ID: 2153), causes partial resistance of this coagulation factor to the inactivating effects of activated protein C, a protein encoded by the PROC gene (gene ID: 5624) • 5% population RR 3-8

  16. Pathogenesis • The prothrombin 20210A mutation found to be associated with elevated prothrombin levels • 2% population, RR 2.0

  17. Pathogenesis • The endothelial cells may become procoagulant under the influence of proinflammatory cytokinases or other peptides: TNF & IL-1 increase the expression of adhesion molecules for leukocytes, PAF and tissue factor • TNF decreases the endothelial fibrinolytic activity, increases endothelial production of IL-1, increases the expression of thrombomoduline (which diminishes the activation of anticoagulant proteine C).

  18. Other mechanisms • Extrinsec compression • Vascular invasion

  19. TrousseauSyndrome

  20. PANCREATIC CARCINOMA and DVT • N=202 • Venous THROMBOSIS: 108.3 PER 1000 PATIENT-YEARS (~11%) • Thrombosis: 58.6-FOLD INCREASE • CHEMOTHERAPY: 4.8-FOLD • RADIOTHERAPY: 1.0 • POSTOPERATIVE: 4.5-FOLD • METASTASIS: 1.9-FOLD Blom et al Eur. J. Cancer 410, 2006

  21. CANCER IN 1383 CASES OF PHLEBITIS VENOGRAPHY + Nordstrom et al BMJ 1994 <6mo >6 mo • ALL CANCER 66 84 • Oesophagus + stomac: 3 4 • Intestinal 7 10 • Liver 5 3 • Gallbladder 5 1 • PANCREAS 6 2

  22. Sorensen et al NEJM 1998 • 15,348 patients with DVT and 11,305 patients with pulmonary embolism • 1737 cases cancer in the cohort with deep venous thrombosis, compared with 1372 expected cases (standardized incidence ratio, 1.3); • Among the patients with pulmonary embolism, standardized incidence ratio was 1.3, • The risk was substantially elevated only during the first six months of follow-up and declined rapidly • 40% of patients given a diagnosis of cancer within one year after hospitalization for thromboembolism had distant metastases at the time of the diagnosis • Strong associations with cancers: pancreas, ovary, liver (primary hepatic cancer), brain.

  23. Risk of Venous Thrombosis per Type of Malignancy for Patients With a Diagnosis of Malignancy Within 5 Years Before Diagnosis of Venous Thrombosis Bloom et al 2005 Type of Malignancy No. of Patients/No. of Control Odds Ratio (95% CI)/Adjusted Odds Ratio(95% CI) No malignancy 1.00 1.00 Men 1279 /1038 Women 1552/ 1024 Malignancy All hematological cancer 37/ 1 26.2 (3.6-191.4)/ 28.0 (4.0-199.7) Gastrointestinal malignancies Bowel 46/ 2 16.8 (4.1-69.1)/ 16.4 (4.2-63.7) Pancreas 2/ 0 ND ND Stomach 2 /0 ND ND Esophagus 2/ 0 ND ND All gastrointestinal cancer 52/ 2 18.9 (4.6-77.8)/ 20.3 (4.9-83.0)

  24. Risk factors • Advanced age • Caucasians • Comorbidities • History of DVT • Location of cancer • First 6 months after cc dx • Metastasis • Recent surgery, current hospitalization, chemotherapy, central venous catheters, sepsis.

  25. Prognosis • Poorer in pts with cancer (incl. pancreatic cancer + DVT) vs cancer (including pancreatic cancer without DVT (Alcalay et al J Clin Oncol 2006)

  26. Prophylaxis • LMWH 5000 iu once a day (Bergquist et al Br J Surg 1995) • LMWH superior to heparin (Mismetti et al Br J Surg 2001) • Long-term: 4 weeks postop. superior to 1 week (Rasmussen et al Blood 2003)

  27. Conclusions • Pts with pancreatic cancer have higher risk to develop thrombotic events • This contribute to their morbitiy nd mortality • These complications should be actively searched in order to improve life expectancy and qol • Thromboprofilaxis of pts with pancreatic cancer refered to surgery or having catheters is very important

  28. QUESTIONS • Is pancreatic cancer associated with DVT? • YES • NO

  29. Shall we screen pts with DVT (recurrent) for occult malignancy including pancreatic cc? • YES • NO

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