assist device (ELAD), was developed by Sussman et al. 6 Cells The objective of this pilot controlled study was to evalderived from a human hepatoblastoma cell line (C3A) are uate the extracorporeal liver assist device (ELAD) in pacultured within the extracapillary space of a dialysis cartients with acute liver failure who were judged to still tridge. Whole blood is used for the perfusion 7 and, unlike the have a significant chance of survival (Ç50%) and in those BAL where plasma perfusion is limited to 6 hours, ELAD who had already fulfilled criteria for transplantation.support can be continued for long periods of time. 8 In early Twenty-four patients were divided into two groups, 17 experimental work in anhepatic dogs, function of the device with a potentially recoverable lesion (group I) and 7 was deduced from the requirement for further anaesthesia, listed for transplantation (group II), and then randomly changes in plasma ammonia level, and length of survival. allocated to ELAD haemoperfusion or control. The meSmall amounts of human albumin were also detected in the dian period of ELAD haemoperfusion was 72 hours circulation which peaked after 7 hours of haemoperfusion. 9 (range 3-168 h). Biocompatibility of the device was good,In further studies performed in a canine model of ALF inwith no acceleration in platelet consumption, and duced by acetaminophen toxicity, 10 80% of treated animals haemodynamic stability was maintained. Two patients survived as compared with none of the controls. 11 In addition were withdrawn from the study because of worsening the extent of liver injury, assessed both histologically and of preexisting disseminated intravascular coagulation from the serum alanine transaminase, appeared to be less in in one case and a hypersensitivity reaction in the other.the haemoperfused animals. 6 An initial case report of the use Deterioration with respect to encephalopathy grade was of the ELAD included one patient who recovered from acute more frequent in the control patients, 7 of 12 (58%), than liver failure secondary to syncytial giant cell hepatitis, 12 and in the ELAD-treated patients, 3 of 12 (25%). In group I in the first clinical series of cases, mental status was imwhere survival for the ELAD cases was 7 of 9 (78%), there proved in 8 of the 11 patients, 4 of whom were transplanted, was a higher than expected survival in the controls, 6although only 1 case survived. 8 of 8 (75%). For group II cases, survival was 1 of 3 (33%)The objective of the present pilot but controlled study was for the ELAD-treated patients, and 1 of 4 (25%) for the to assess use of the ELAD device in two groups of patients, controls. Both of the survivors underwent transplantathose in whom there was judged to be some potential for tion. Assessment of additive function for the device rerecovery and those affected to a greater extent where it is vealed an improvement in galactose elimination capacused as a bridge to transplantation. Particular attention was ity after 6 hours of haemoperfusion. Based on the results d...

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synopsisIn a study of pressuresensitive adhesives prepared from mixtures of natural rubber and three different tackifying resins, it was shown that a tackifying resin may form either one-or two-phase systems with natural rubber. Measurements of the viscoelastic properties of the adhesives show that the effect of tackifying resins is to modify the ' viscoelastic properties so that the adhesive performance in bonding and unbonding is improved. It is suggested that a two-phase system is not necessary for good tack, and a theory based on a two-phase system cannot adequately explain the rate dependence of tack tests. Tack measured by the probe test is shown to be dependent upon a balance between the viscoelastic properties and the transition temperature of the adhesives.This theory is used to explain the effect of contact time, withdrawal speed, and resin 'softening point on the tack of adhesives.

The value of coagulation factor V and VIIIIV levels as prognostic indicators was assessed in 27 patients with fulminant hepatic failure and compared with other predictive indices. Admission factor V levels were significantly reduced in 22 patients with paracetamol induced hepatic failure compared with a healthy control group (median 9*5% v 103%, respectively; p<0001) and with lower values in non-A non-B hepatitis (median 2.7%).Values in the seven patients who died after paracetamol overdose, considered together with the four who underwent liver transplantation (group median 5-1%), were significantly lower than in the 11 who survived (median 11-8%; p<001). Median admission factor VIII was higher in those who died or received a transplant than in those who survived (298% v 162%; p<005), with both results higher than in healthy volunteers (median 104%; p<001) but lower than in non-A non-B hepatitis (median 340%). The ratio of factor VIIIIV on admission was <30 in all patients who survived paracetamol overdose (median 17) with corresponding values >30 in 10 of 11 of those who died (median 39). A factor V result -10% on admission predicted an adverse outcome in 10 of 11 fatal cases, a 91% sensitivity which was greater than for the previously defined indicator of an arterial blood pH <7*30 on admission (sensitivity 82%). Prothrombin time at admission or on day 4 did not usefully predict outcome in our series. Predictive accuracy was 73% and 82% for factor V and admission acidosis respectively and 95% for factor V in conjunction with admission coma grade III or IV and factor VIII (ratio >30). These criteria may be useful in selecting patients with paracetamol induced fulminant hepatic failure for transplantation.Institute of Liver Studies,

The liver is the primary site of synthesis of most coagulation and fibrinolytic proteins, and also plays a role in the clearance of hemostasis factors and their degradation products. In acute liver failure, these functions are severely disturbed, and the risk of hemorrhage is increased. Following a brief summary of the physiology of hemostasis, this review describes the nature and frequency of hemostatic abnormalities in acute liver failure. These abnormalities include quantitative and qualitative platelet defects, impaired synthesis and clearance of the coagulation factors and related inhibitory proteins, and enhanced fibrinolysis. Disseminated intravascular coagulation may also play a role, although this syndrome is difficult to distinguish from changes due to the failure of hepatic synthesis and clearance alone. At present, management options are limited to support with blood products, although pharmacological manipulation of the coagulation and fibrinolytic systems represent a potential area for future study.

The BioLogic-DT sorbent suspension dialyser was developed to remove toxic substances from the blood of patients with liver failure. In the present study a randomised controlled trial was carried out in 10 patients with fulminant hepatic failure who had developed grade 4 encephalopathy to evaluate the safety and biocompatibility of the dialyser in such severely ill patients. A total of 18 treatments were performed in 5 patients. Haemodynamic stability was maintained throughout. There was a significant loss of platelets (163 +/- 34 to 101 +/- 13 x 10(9)/l) and decrease in plasma fibrinogen (0.53 +/- 0.09 to 0.31 +/- 0.08 g/l) with a rise in blood activated clotting time (190 +/- 17 to 223 +/- 22 sec)--not seen in the controls--, which was a result of the dialysis being carried out without the use of heparin as anticoagulant. Removal of metabolites by treatment was limited, with no significant effect on blood ammonia level and further developments of the system will be needed for this very sick group of patients.

Data reported by Bernuau et al. have strongly supported the measurement of coagulation factor V as the best prognostic indicator in fulminant hepatic failure (FHF) and as the test on which selection for urgent liver transplantation should be made. In this study, we have measured plasma factor V in 110 patients with FHF, in grades I-IV coma, in 88 of whom the etiology was acetaminophen overdose. On admission, patients who did not survive had significantly lower factor V levels (median, 5%; range, 1-27; n = 49), compared with those who did (median, 10%; range, 2-70; P < .001). In the 81 patients with acetaminophen-induced FHF who did not receive a transplant, there was no cutoff level of factor V that clearly separated the patients. On statistical analysis, a positive predictive value (the mortality in patients predicted to have a poor prognosis) of 0.49 was calculated for factor V <20% and 0.57 for factor V < 10%. If the prognostic criteria included deep coma (grades III and IV) as well as factor V <20%, a positive predictive value of 0.73 was calculated. This compared with a value of 0.92 for the well-established King's prognostic criteria based on pH, and a combination of international normalized ratio (INR), renal failure, and coma. In the 17 mixed, nonacetaminophen group of patients who did not receive a liver graft, the positive predictive value was 0.85 for a factor V level <20% and 1.00 for factor V <10%, compared with 0.93 for the King's criteria for that etiologic group. This study demonstrates that the predictive accuracy of plasma factor V level is much less effective than the well-validated King's criteria in the selection of patients with acetaminophen-induced FHF needing liver grafting, although it may be useful in patients with FHF due to other causes.