[Laparoscopic downstaging surgery for colorectal cancer with synchronous liver metastases: what value in two-stage hepatectomies?] / La chirurgie laparoscopique de downstaging pour cancer colorectal avec métastases hépatiques synchrones: quel intérêt dans les hépatectomies en deux temps? à propos d'une série de 6 cas.

Bilobar hepatic metastases from colorectal cancer pose a problem in terms of management, with curative surgery often requiring several stages. The purpose of our study was to evaluate laparoscopic approach with portal vein ligation in the first step of two-stage hepatectomy in the treatment of patients with synchronous liver metastases from colorectal cancers (SLMCRC). We conducted a single-center retrospective study from August 2016 to January 2020. It included patients with SLMCRC requiring two-stage curative surgery due to insufficient future liver remnant volume (FRL). The primary endpoint was to evaluate postoperative morbidity and mortality following first step laparoscopy at 30 days. The secondary endpoints were to evaluate conversion rate, FRL hypertrophy following laparoscopic portal vein ligation, postoperative morbidity and mortality of 2nd step of two-stage hepatectomy and finally treatment completion rate. We included six patients (4 men and 2 women) with a mean age of 64 (44-72) years. The first step of surgery consisted of a laparoscopic colonic resection associated with right portal vein ligation in 5 patients and left portal vein ligation in one patient. The postoperative morbimortality was zero. The conversion rate was zero. After portal vein ligation, 5 of the 6 patients had significantly enlarged FRL, with a mean gain in FRL volume of 59.48% (31.02%-68.71%). Two of the six patients had severe morbidity after 2nd step hepatectomy (Clavien IIIb). All patients completed the treatment.

Outcomes of Laparoscopic Combined Surgery for Colorectal Cancer with Synchronous Liver Metastases: A Prospective Comparative Study.

AIM: Combined surgery for colorectal cancer with synchronous liver metastases (CRCSLM) is addressed to selected patients. Technically, by conventional surgery this simultaneous approach raises a problem of adequate access. The purpose of this study is to assess the feasibility and safety of the laparoscopic approach in combined surgery. METHODS: From August 2016 to January 2020 a monocentric prospective comparative study was conducted. Short and long-term outcomes of simultaneous laparoscopic surgery (SLS) were evaluated. Short-term outcomes of SLS were compared to those of laparoscopic colorectal surgery alone (LCRS). RESULTS: Forty patients were included in each arm. In SLS group, the median age was 62.5 years. Hybrid surgery was performed for 60% of patients, down staging laparoscopic surgery for 22.5% of patients and totally laparoscopic surgery for 10% of patients. The conversion rate was 7.5%. Mean operating time was 323 minutes. Overall morbidity rate was 27.5%. Multivariate analysis showed that anemia (p = 0.046) and number of liver resections (p = 0.018) were independent factors of morbidity. Ninety-five percent of colorectal resections were R0, 90% of liver resections were R0. The mean length of hospital stay was 5.1 ± 2.58 days. The recurrence rate was 22.5%. Median diseasefree survival was 27 months. There was no difference in short-term outcomes between the two arms except for operating time which was longer in SLS arm (p < 0.0005). CONCLUSION: Laparoscopy is feasible in combined surgery in selected patients. Minor liver resection may be associated with laparoscopic colorectal surgery without increasing morbidity.

Correlation of adenosine deaminase operating under nitro-oxidative stress with tumor and vascularization in patients with advanced gallbladder carcinoma.

This study investigates serum redox status and adenosine catabolism markers in relation to tumor and angiogenesis, in patients with gallbladder carcinoma (GBC). The level of adenosine deaminase (ADA) and xanthine oxidase (XO) activities, nitrites (NO2-), glutathione (GSH) and malondialdehyde (MDA) were measured in sera of 40 GBC patients and 40 healthy donors. In parallel, 15 tumors at TNM stage IV were scored for CD34 expression and microvessel density (MVD). The results showed that XO and ADA activities, nitrites and MDA levels enhanced by 1.26 (p < 0.01), 2.69, 2.0, and 3.2-fold (p < 0.001), respectively, while those of GSH decreased by 44.6% (p < 0.001). According to receiver operating characteristic (ROC) curve, the optimal cut-off for XO, ADA, MDA, GSH and nitrites were 5.41U/l, 17.02 U/l, 3.72 µM, 36.91 µM and 21.21 µM, respectively. Spearman correlation revealed that ADA activity correlated to nitrites levels (r = 0.3419, p < 0.05) and XO activity (r = 0.5487, p < 0.001). Multivariate binary logistic regression analysis revealed that MDA (OR = 5.78, p < 0.05), ADA (OR = 1.28, p < 0.001) and XO (OR = 2.81, p < 0.05) correlated positively to GBC. CD34 was up expressed in 73.3% of tumors at intermediate to high levels. Multiple regression analysis showed that ADA affected MVD (r = 0.604, p < 0.01). The results suggest that high MDA/GSH ratio is a potential biomarker of GBC. In addition, the oxidative adenosine catabolism indicated that active purine salvage pathway could support tumor progression by sustaining angiogenesis.

Budd-Chiari syndrome: an update on imaging features.

Budd-Chiari syndrome (BCS) is a rare cause of portal hypertension and liver failure. This condition is characterized by an impaired hepatic venous drainage. The diagnosis of BCS is based on imaging, which helps initiate treatment. Imaging findings can be categorized into direct and indirect signs. Direct signs are the hallmarks of BCS and consist of visualization of obstructive lesions of the hepatic veins or the upper portion of the inferior vena cava. Indirect signs, which are secondary to venous obstruction, correspond to intra- and extrahepatic collateral circulation, perfusion abnormalities, dysmorphy and signs of portal hypertension.

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.

Budd-Chiari syndrome: a prospective analysis of hepatic vein obstruction on ultrasonography, multidetector-row computed tomography and MR imaging.

PURPOSE: The goal of this study was to prospectively describe the imaging presentation of hepatic vein (HV) obstruction in patients with Budd-Chiari syndrome (BCS) on duplex and color Doppler ultrasonography (DCD-US), multidetector-row computed tomography (MDCT) and magnetic resonance imaging (MRI). MATERIALS AND METHODS: A total of 176 patients with primary BCS (mean age, 33 years; 101 women) were prospectively included. BCS diagnosis was made by direct visualization of HV and/or upper portion of the inferior vena cava (IVC) obstruction on DCD-US and/or MDCT and/or MRI. Location (right, middle, and left HV), type (thrombus, stenosis, or both), and age (recent vs. long-standing) of HV obstruction were described on each imaging examination. RESULTS: HV obstruction was a constant (100%) finding and associated with IVC abnormalities in 51/176 (28.98%) patients. Obstruction of the three HVs was present in 158/176 (89.77%) patients. The prevalences of right, middle, and left HV thrombus were 151/169 (89.35%), 146/169 (86.39%), and 111/169 (65.68%), respectively. Long-standing HV thrombus was observed in more than 92% of patients on the three imaging methods. Agreement between DCD-US, MDCT, and MRI was perfect in the identification of long-standing HV thrombus (κ = 0.9); this agreement was slight to moderate in revealing the type of HV abnormality (i.e., fibrotic cord and non-visible HV). CONCLUSION: Our results indicate that BCS is a chronic and insidious disease, more often discovered at an advanced stage. These results should warrant further evaluation of screening strategies in patients with risk factors for BCS to identify the disease at an early stage.