**3. Conclusions**

40 Deep Vein Thrombosis

inhibitor-1 activity or by increasing tissue plasminogen activator activity. Their data suggest that external pneumatic compression devices do not prevent deep venous thrombosis by fibrinolytic enhancement; effective prophylaxis is achieved only when the devices are used in a manner that reduces lower extremity venous stasis. Jacobs et al., 1996; reported that sequential gradient intermittent pneumatic compression induces prompt, but short-lived, alterations in both fibrinolytic function, and the values quickly reverted to baseline on termination of compression. Okuda et al., 2002; reported that intermittent compression boot did not prevent increased intravascular thrombogenesis and platelet activation through significant increases of plasma D-dimmer and β-thromboglobulin after laparoscopic cholecystectomy. Killewich et al., 2002; also reported that enhanced regional fibrinolysis in the lower extremities could not be detected with the use of external pneumatic compression devices, as measured with tissue plasminogen activator and plasminogen activator inhibitor-1 activity in common femoral venous blood samples in patients undergoing abdominal surgery. On the other hand, Comerota et al., 1997; reported that external pneumatic compression devices induced a significant decrease in plasminogen activator

In our study, the IPC used alone during laparoscopic fundoplication, did not prevent increased intravascular thrombogenesis through significant increases of plasma F1+2 and

Giddings et al.,1999; reported that IPC led to highly significant falls in factor VIIa, associated with increased levels of tissue factor pathway inhibitor in non-smoking volunteers. Chouhan et al., 1999; investigated the effect of IPC on the tissue factor pathway in 6 normal subjects and 6 patients with postthrombotic venous disease. Their study results demonstrated that IPC results in an increase in plasma TFPI and decline in FVIIa in both groups. Authors speculated that inhibition of tissue factor pathway, the initiating mechanism of blood coagulation, is a possible mechanism for the antithrombotic effect of IPC. Our study results demonstrate that IPC used alone did not increase TFPI in plasma and

Most circulating TFPI is bound to lipoproteins. TFPI is also found in platelet α-granules and on the endothelium cell surface. TFPI bound to the endothelium is released with therapeutic doses of heparin or low molecular weight heparin, suggesting that TFPI binds to

Our clinical data suggest that LMWH, administered 1 h before operation, together with IPC induce more favorable hypocoagulation profile compared with LMWH alone. However, clinical data, comparing the rate of DVT between these two prophylactic methods are still lacking. On the other hand, alone LMWHs have been evaluated in a large number of randomized clinical trials and have been shown to be safe and effective for the prevention

Our recommendation is LMWH, administered 1 h before operation, together with IPC against postoperative venous tromboembolism in laparoscopic operations. Of course, this recommendation has to be proved in future prospective randomized clinical trials,

didn't produce hypocoagulation effect during laparoscopic fundoplication.

endogenous glycosaminoglycans on the endothelium wall surface.

and treatment of venous thrombosis in laparoscopic or in open surgery.

comparing the incidence of DVT between these two prophylactic methods.

inhibitor-1 activity in normal volunteers.

TAT during and after laparoscopic fundoplication.


#### **4. References**


**3** 

*1,2Italia* 

**Vena Cava Malformations** 

*1Azienda Ospedaliero-Universitaria Pisana, 2Istituto di Fisiologia Clinica del CNR* 

 **as an Emerging Etiologic Factor for** 

Massimiliano Bianchi1, Lorenzo Faggioni1, Virna Zampa1, Gina D'Errico1, Paolo Marraccini2 and Carlo Bartolozzi1

 **Deep Vein Thrombosis in Young Patients** 

Deep venous thrombosis (DVT) is an illness of clinical interest, due to the associated morbidity and mortality and its social and health care consequences. The etiology in young patients has shown it frequently associated with congenital coagulation abnormalities and

Homozygous C677T mutation in the methylenetetrahydrofolate reductase gene

**1. Introduction** 

**Inherited**  Common

Rare

Very rare

**Acquired**

Older age Cancer

Antitrombin deficiency Protein C deficiency Protein S deficiency

Dysfibrinogenemia

Probably inherited

Surgery and trauma Prolonged immobilization

Previous thrombosis

Homozygous homocystinuria

Myeloproliferative disorders

Pregnancy and the puerperium

acquired/inherited risk factors (table I) (a,b).

G169A mutation in the factor V gene (factor V Leiden) G20219A mutation in the protrombin (factor II) gene

Increased levels of factor VII, IX, XI or fibrinogen

Use of contraceptives or hormone-replacement therapy

