Clinico-roentogenologic findings in hepatocellular carcinoma fed by the right inferior phrenic artery at the initial chemoembolization.

BACKGROUND/AIMS: The purpose of this study was to investigate factors that may predict the development of the right inferior phrenic artery (RIPA) as a feeding artery in hepatocellular carcinoma (HCC) at the initial (first session) chemoembolization. METHODOLOGY: From January 1997 to June 2002, 538 patients with HCC were treated with a first session of transcatheter arterial chemoembolization (TACE). Twenty-six of these patients underwent TACE via both the Hepatic artery (HA) and RIPA at the initial TACE. We retrospectively analyzed the Child-Pugh's classification, macroscopic tumor type, location and size of the tumor, past history of intervention, complications and outcome in these 26 patients with HCC fed by the RIPA. RESULTS: The incidence of HCC fed by both the HA and RIPA at the initial TACE was 4.8% (26/538 patients). No hepatic arterial occlusion or attenuation was found in any of these 26 patients. All of the tumors abutted the diaphragm and were located at the surface of the liver. All of the tumors that were larger than 5 cm in diameter protruded from the surface of the liver. Seven of the 9 patients with HCC smaller than 5 cm in diameter had a defect in the liver capsule induced by previous intervention for the treatment of a different tumor, such as hepatic resection or percutaneous ablation therapy. There were no serious complications after TACE. CONCLUSION: The RIPA can be an extrahepatic feeding artery for HCC even at the initial TACE. A high incidence of HCC fed by the RIPA was recognized in cases in which a large tumor protruded from the surface of the liver, and when the liver capsule was damaged due to previous intervention such as hepatic resection or in ruptured HCC even at the initial TACE.

Genetic basis of tissue specificity of vasculitis in MRL/lpr mice.

OBJECTIVE: To clarify the mode of inheritance of the tissue distribution of vasculitis in MRL/Mp-lpr/lpr (MRL/lpr) lupus-prone mice and to identify the susceptibility loci. METHODS: Vasculitis in individual MRL/lpr, C3H/HeJ-lpr/lpr (C3H/lpr), (MRL/lpr x C3H/lpr)F(1), and (MRL/lpr x C3H/lpr)F(2) intercross mice was analyzed by histopathologic grading of main branches of the aorta and of medium-sized arteries in the lower limbs. Genomic DNA samples from F(2) intercross mice were examined by simple sequence-length polymorphism analysis, and the polymorphic microsatellite markers highly associated with vasculitis in each tissue were determined as vasculitis susceptibility loci. RESULTS: A susceptibility locus with significant linkage to vasculitis of main branches of the aorta was mapped on chromosome 4 at D4Mit213 (map position 13.3cM) selectively in males, while vasculitis of medium-sized arteries in the lower limbs was mapped to different chromosomes: at D8Mit31 on chromosome 8 (map position 33.0) selectively in females and at D5Mit36 on chromosome 5 (map position 65.0). All of these were different from the previously defined loci governing susceptibility to vasculitis involving the kidneys. CONCLUSION: Systemic vasculitis in MRL/lpr mice is genetically controlled with cumulative effects of multiple gene loci, each of which has tissue specificity.