Transjugular intrahepatic portosystemic shunt as bridge-to-surgery in refractory gastric antral vascular ectasia

Gastric antral vascular ectasia(GAVE) may cause gastrointestinal bleeding(GIB). The treatment of GAVE relies on endoscopic approaches such as electrocoagulation(argon plasma coagulation, laser therapy, heater probe therapy, radiofrequency ablation), cryotherapy, and band ligation. In refractory cases, antrectomy may be considered. In the event of an associated cirrhosis and portal hypertension, it has been suggested that antrectomy could be an option, provided the mortality risk isn't considered too great. We report the case of a 67-year-old cirrhotic patient who presented with GAVE related GIB, unresponsive to multiple endoscopic treatments. The patient had a good liver function(model for end-stage disease 10). After a multidisciplinary meeting, a transjugular intrahepatic portosystemic shunt(TIPS) procedure was performed, in order to treat the cirrhosis associated ascites. The outcome was successful. An antrectomy was then performed, with no recurrence of GIB and no transfusion need during three months of follow up. In this case, the TIPS procedure achieved a complete ascites regression, allowing a safer surgical treatment of the GAVE-related GIB.

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 V617 F JAK2 mutation. Anti-phospholipid syndrome(APLS) was detected by the presence of anticardiolipin antibodies, anti-β2 glycoprotein antibodies and Lupus anticoagulant. We also detected paroxysmal nocturnal haemoglobinuria(PNH) by flow cytometry. Celiac disease and Behcet disease were systematically investigated in our patients. Hereditary anticoagulant protein deficiencies were also assessed. We tested our patients for the G20210 A 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.