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Objectives To establish the utility of eight anatomic/pathologic suboptimal and 9 others graft features, versus in 20 donor versus 14 recipient characteristics to predict primary transplant dysfunction. Patients and methods We reviewed 248 consecutive liver transplants performed at the Hospital Ramon y Cajal, Madrid, in 206 patients over a 79-month period. At least one biopsy specimen was obtained from 169 grafts (68.1%). Recipients were classified as showing primary function or dysfunction, the latter group being subdivided into primary failure and inadequate initial function. The primary function and inadequate initial function groups were defined in terms of transaminases less or more than 2000 IU and prothrombin activity over or under 50%, respectively during posttransplant days 2 to 7. Results The following graft-related rates were recorded: arteriopathy 6.5%, steatosis 29.4% (macrovesicular 26.4%, microvesicular 4.7%, or both 1.7%), hepatocyte vacuolization 14.2%, sinusoidal ectasia 12.4%, hepatocellular necrosis 44.7%, and neutrophilic infiltration 24.4%. The only significant factors in the multivariate analysis were cause of donor death other than cranioencephalic trauma (P = .032) and moderate steatosis (30%–60% affected hepatocytes); (P = .012). Conclusions The only factors that seem to influence the development of primary liver dysfunction were a moderate degree of graft steatosis and a cause of brain death other than cranioencephalic trauma.

Portal hypertension associated to Gaucher's disease type I with non cirrhotic liver involvement is a very in-equent finding. We report a case of Gaucher's disease type I without cirrhosis in which portal hypertension is the main manifestation. The mechanism of the portal hypertension is discussed in our report and can be related to an elevation in hepatic fluid resistance due to the Gaucher's cells compression on sinusoids.

A protein was isolated from plasma of partially (70%) hepatectomized rats that, injected in mice, increases the uptake of [3H]thymidine by liver DNA by 200-300% over that by injected control saline. The purification procedure consists essentially of three chromatography steps, employing Sephadex G-75, DEAE-cellulose and hydroxyapatite. The hepatic promoter (HP) preparation shows a single band in SDS/polyacrylamide (15%)-gel electrophoresis (silver stained), with an Mr of 64 000; its activity is suppressed by trypsin or pepsin and is unaffected by deoxyribonuclease or ribonuclease. On injection into mice (150 ng/mouse), it increases the mitotic index of the liver. It shows organ-specificity, acting on liver but not on spleen, kidney, lung or brain. In primary liver cultures, it produces an increase in uptake of [3H]thymidine into DNA in the range 1-10 ng/ml. In this system in vitro, it increases the uptake of 22Na+ immediately after addition.