[Activation of coagulation in patients with lung cancer]. / Activation de la coagulation chez des patients atteints du cancer du poumon.

The aim of this study is to evaluate the anomalies of coagulation (by assaying the factor VIII, fibrinogen, D-dimer and resistance to activated protein C) in patients with lung cancer. METHODS: 101 patients newly diagnosed with lung cancer before treatment and 72 control blood donors were included in the study after informed consent. All coagulation tests were performed on Stago STA-Compact. Statistical analyses were performed using the SPSS software version 22. RESULTS: The study of the coagulation showed that plasma levels of all coagulation parameters were significantly higher in patients compared to controls. Coagulation was not influenced by the age of patients. No significant difference was found between the histological types in terms of coagulation. Factor VIII level was significantly elevated in stage IV patients compared to stage I + II + III patients. At the cut-off value of 6.22 g/L, the elevation of fibrinogen had a significant statistical relationship with thromboembolic disease (p=0.014) giving an hazard ratio of 3.868, confidence interval [1.358-11.012]. In multivariate analysis the hazard ratio doubled to 6.398, confidence interval [1,970-20,778]. DISCUSSION: Lung cancer patients showed an increase in coagulation factors that resulted in a state of hypercoagulability that was independent of the histology of lung cancer. The elevation of fibrinogen was predictive of thromboembolic disease at the early diagnosis of lung cancer before any therapy.

Aetiological factors of Budd-Chiari syndrome in Algeria.

AIM: To study the clinical presentation of Budd-Chiari syndrome (BCS) and identify the aetiologies of this disease in Algeria. METHODS: Patients with BCS, hospitalised in our unit from January 2004 until June 2010 were included and the aetiological factors were assessed. Patients presenting a BCS in the setting of advanced-stage cirrhosis or a liver transplantation were excluded from the study. The diagnosis was established when an obstruction of hepatic venous outflow (thrombosis, stenosis or compression) was demonstrated. We diagnosed myeloproliferative disease (MPD) by bone marrow biopsy and V617F JAK2 mutation. Anti-phospholipid syndrome (APLS) was detected by the presence of anticardiolipin antibodies, anti-ß2 glycoprotein antibodies and Lupus anticoagulant. We also detected paroxysmal nocturnal haemoglobinuria (PNH) by flow cytometry. Celiac disease and Behçet disease were systematically investigated in our patients. Hereditary anticoagulant protein deficiencies were also assessed. We tested our patients for the G20210A mutation at Beaujon Hospital. Imaging procedures were performed to determine a local cause of BCS, such as a hydatid cyst or a liver tumour. RESULTS: One hundred and fifteen patients were included. Mean follow up: 32.12 mo. Mean age: 34.41 years, M/F = 0.64. Chronic presentation was frequent: 63.5%. The revealing symptoms for the BCS were ascites (74.8%) and abdominal pain (42.6%). The most common site of thrombosis was the hepatic veins (72.2%). Involvement of the inferior vena cava alone was observed in 3 patients. According to the radiological investigations, BCS was primary in 94.7% of the cases (n = 109) and secondary in 5.2% (n = 6). An aetiology was identified in 77.4% of the patients (n = 89); it was multifactorial in 27% (n = 31). The predominant aetiology of BCS in our patients was a myeloproliferative disease, observed in 34.6% of cases. APLS was found in 21.7% and celiac disease in 11.4%. Other acquired conditions were: PNH (n = 4), systemic disease (n = 6) and inflammatory bowel disease (n = 5). Anticoagulant protein deficiency was diagnosed in 28% of the patients (n = 18), dominated by protein C deficiency (n = 13). Secondary BCS was caused by a compressing hydatic cyst (n = 5) and hepatocellular carcinoma (n = 1). CONCLUSION: The main aetiologic factor of BCS in Algeria is MPD. The frequency of celiac disease justifies its consideration when BCS is diagnosed in our region.