Geert Maleux

Value of carbon dioxide wedged venography and transvenous liver biopsy in the definitive diagnosis of Abernethy malformation.

We report a 25-year-old man who presented with congenital absence of the portal vein, or Abernethy malformation, a rare congenital disorder in which the mesenteric and splenic venous drainages bypass the liver and directly drain into the inferior vena cava through an extrahepatic portosystemic shunt. Magnetic resonance imaging, which showed multiple nodular lesions in both liver lobes that were associated with an absence of intrahepatic portal venous branches, strongly suggested the diagnosis of the Abernethy malformation. Carbon dioxide wedged venography and transvenous liver biopsy, which were performed in the same session by a right jugular approach, confirmed these findings. This technique can be considered a valuable alternative diagnostic tool to catheter arteriography and percutaneous transhepatic liver biopsy.

682 APPARENT DIFFUSION COEFFICIENT DETERMINED TARGET RESPONSE AT DIFFUSION-WEIGHTED MRI IS AN INDEPENDENT PREDICTOR OF OUTCOME IN HEPATOCELLULAR CANCER PATIENTS TREATED WITH TRANSARTERIAL CHEMOEMBOLIZATION

Patients and Methods: Two hundred pairs of patients with cirrhosis and HCC and unrelated patients with cirrhosis alone were enrolled. Polymorphisms of TNFa −238, TNFa −308, and lymphotoxin (LT)a +252 were genotyped by the polymerase chain reaction with direct sequencing or restriction fragmented length polymorphism. TNF haplotypes were also analyzed. From routine laboratory data, the following surrogate markers associated with hepatic fibrosis were measured: platelet count, aspartate aminotransferase/alanine aminotransferase ratio, aspartate aminotransferase/platelet ratio index, Pohl score, and cirrhosis discriminant score. These fibrosis surrogate markers were analyzed with polymorphisms and haplotypes of TNF locus. Results: The frequencies of the variant genotypes and alleles of LTa +252 and TNFa −308 in patients with HCC were significantly higher than those in patients with cirrhosis alone. There was no such a difference in the TNFa −238 polymorphisms. Univariate analysis indicated that LTa +252 G/G genotype (odds ratio (OR) = 2.31) and TNFa −308 G/A genotype (OR=2.31) were significantly associated with HCC. Multivariate analysis indicated that LTa +252 G/G (OR=2.05, 95% confidence interval (CI), 1.20– 3.51), TNFa −308 G/A (OR=1.77, 95%CI, 1.02–3.07), and TNF haplotypes (AGA, OR=5.69; 95%CI, 1.90–17.10; GGA, OR=2.07; 95%CI, 1.18–3.63; and GGG, OR=1.51, 95%CI, 1.11–2.04) were independent risk factors for HCC. Among patients with cirrhosis and HCC, significant hepatic fibrosis was found between 71.4% and 93.5% of patients with variant TNF genotypes and between 54.4% and 86.8% of patients harboring TNF haplotypes (AGA, GAG and GGG). Multivariate analysis showed that factors associated with variant genotypes included cirrhosis with Child–Pugh C (OR=8.85; 95%CI, 3.08–35.64), serum a-fetoprotein >100ng/ml (OR=2.50; 95%CI, 1.23–5.06), and thrombocytopenia (OR=3.26; 95%CI, 1.14– 9.30). Conclusions: Patients with cirrhosis who carry the TNF genetic variants were correlated with advanced fibrosis and severe liver damage, which may contribute to a higher risk to HCC.