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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

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

slide5
“In conditions of cachexia, a special state of the blood occurs which predispose to spontaneous coagulation”
    • Trousseau

1865

slide6

Jaundice

Pancreas CC

Thrombosis of aorta

slide7

Pancreatic CC

Thrombosis

Pancreas

slide8
longitudinal and transversal section of popliteal vein: recent thrombosis, complete obstruction of popliteal vein
slide9
transversal section of common femural vein at femural bifurcation: recent thrombosis, complet obstruction (duplex color)
epidemiology
Epidemiology
  • Incidence of thrombosis:
    • in cancer: 5-60%
  • 2x higher in cancer pts vs general population
  • 20% pts DVT have dg cancer
clinical types of thrombosis
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
pathogenesis virchow s triad
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
pat h ogene sis
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
pathogenesis
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
pathogenesis1
Pathogenesis
  • The prothrombin 20210A mutation found to be associated with elevated prothrombin levels
  • 2% population, RR 2.0
pathogenesis2
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).
other mec h anism s
Other mechanisms
  • Extrinsec compression
  • Vascular invasion
pancreatic carcinoma and dvt
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

cancer in 1383 cases of phlebitis venography nordstrom et al bmj 1994
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
sorensen et al nejm 1998
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.
slide23
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)

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

conclusions
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
questions
QUESTIONS
  • Is pancreatic cancer associated with DVT?
  • YES
  • NO
shall we screen pts with dvt recurrent for occult malignancy including pancreatic cc
Shall we screen pts with DVT (recurrent) for occult malignancy including pancreatic cc?
  • YES
  • NO
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