To assess the efficacy and adverse effects of preoperative transcatheter chemoembolization (CE) on surgical resection, postoperative outcome, and recurrence of hepatocellular carcinoma. Design: A before-after trial comparing a group of patients undergoing liver resection after CE (CE group) with a group of patients undergoing liver resection without prior CE (control group), matched for tumor size and underlying liver disease. Setting: A tertiary care university hospital in a metropolitan area. Patients: Twenty-four patients in each group, treated between 1986 and 1992. Interventions: A mean of 1.6±0.2 preoperative CE procedures were performed per patient in the CE group. Tumorectomies, segmentectomies, and major liver resections were performed with a comparable frequency in each group. Results: Overall, CE was not associated with a significant reduction of tumor size (7.8±1 cm prior to CE vs 7.1±1 cm after CE) or ␣-fetoprotein levels (2560±2091 µg/L prior to CE vs 1788±1270 µg/L after the last CE). Chemoembolization promoted tumor necrosis but did not influence tumor encapsulation, invasion of the capsule, venous permeation, presence of daughter nodules, or surgical margins. Liver resection was rendered more difficult by preoperative CE as a result of pediculitis and gallbladder lesions in 37% of patients, but the postoperative course was not altered. Disease-free survival (33%±12% vs 32%±12% at 3 years) and overall survival were comparable. Conclusions: Convincing evidence is lacking to support systematic preoperative CE in patients with initially resectable hepatocellular carcinoma. Further studies should aim to identify the subgroup of patients who may benefit from this neoadjuvant treatment.

A retrospective study was made of 34 patients who underwent major liver resection with a single period of vascular occlusion exceeding 60 min. The liver remnant was normal in all cases. Vascular occlusion was achieved by continuous portal triad clamping (15 patients), hepatic vascular exclusion (15) or a sequential combination of both procedures (four). Liver cooling was not used. The mean (s.e.m.) duration of continuous normothermic liver ischaemia was 73.6 (2.5) (range 60-127) min. The mean (s.e.m.) amount of blood transfused during operation was 5.3(0.8) units packed red cells. There were no deaths after surgery and the postoperative course was uneventful, or limited to asymptomatic pleural effusion, in 18 patients. Three patients suffered postoperative bleeding necessitating further surgery and one of these required reintervention for a prolonged bile leak. Four patients had transient liver failure that resolved spontaneously within 15 days. There was a 13-fold increase in serum transaminase activities and the proaccelerin level was 45 per cent that of normal on day 1 after operation. These changes were returning to normal levels within 15 days. Continuous vascular occlusion during major liver resection is a useful manoeuvre that may be performed safely on normal hepatic parenchyma for up to 90 min.

AHXR is invariably associated with increased circulating anti-non-Gal antibodies. These antibodies are not observed in recipients without AHXR, and five of six recipients with AHXR were adequately depleted of anti-Gal antibodies by maintenance GAS914. This indicates that anti-non-Gal antibodies play a significant role in the pathogenesis of AHXR. Also, the assessment of these antibodies could be used as an early monitor of AHXR.

HAR of hDAF solid organs could be ascribed to high levels of anti-pig antibodies. It is hypothesized that the hDAF transgene shows a threshold in efficacy, above which an overwhelming attack by antibodies and complement activation cannot be modulated to prevent HAR. HAR does not occur when animals with lower levels are used, or when antibodies are effectively depleted from the circulation by GAS914 treatment.

The inclusion of TP10 in the immunosuppressive protocol does not clearly lead to improved xenograft survival. Despite effective neutralization of anti-Gal antibodies and effective inhibition of systemic complement activity, AHXR was apparent in four of six animals under chronic TP10 treatment, including deposits of complement activation products in the graft. Apparently, effective systemic complement inhibition by TP10 in combination with local complement regulation by the hDAF transgene product does not necessarily result in effective inhibition of complement activation at locations in the xenograft upon binding of anti-porcine antibodies to the grafted endothelium.