Impact of donor, recipient, and graft features on the development of primary dysfunction in liver transplants.

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 Ramón 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.

[Gaucher's disease type I: an infrequent cause of portal hypertension]. / Enfermedad de Gaucher tipo I: una causa infrecuente de hipertensión portal.

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.

Caroli's disease: study of six cases, including one with epithelial dysplasia.

Six cases of Caroli's Disease are reviewed. Three of the patients had an associated form of the disease, one of which had a congenital hepatic fibrosis, another a cystic dilatation of extrahepatic bile duct and the last one suffered both the above mentioned associated anomalies. Three patients presented with the simple form which was initially described by Caroli. The distribution of the biliary lesions was a bilobar one in four cases and monolobar in two. One patient presented areas of biliary ectasia partially lined by dysplastic epithelium. Surgical treatment was used in four cases, a left hepatectomy being carried out in two of them and an internal biliary drainage by Roux-Y hepaticojejunostomy in the other two. This is a rare disease, frequently associated with congenital hepatic fibrosis, possibly pre-malignant and whose treatment of choice is hepatic resection.

Nodular regenerative hyperplasia of the liver in rheumatic diseases: report of seven cases and review of the literature.

Nodular regenerative hyperplasia (NRH) of the liver is an uncommon pathologic finding associated, in most cases, with rheumatic and hematologic diseases. Although its pathogenesis remains unclear, NRH probably results from liver regeneration to maintain its functional capacity after ischemia-induced injury. An intrahepatic microvascular occlusive mechanism has been considered most likely pathogenetically. NRH may lead to portal hypertension. Thus, the diagnosis of Felty's syndrome must be considered with caution in patients with rheumatoid arthritis (RA) and NRH of the liver. We report seven additional cases of NRH in patients with rheumatic disorders and review the literature to determine the patterns of clinical presentation and natural history of this condition. We also report four patients (three systemic lupus erythematosus [SLE] and one primary antiphospholipid syndrome [PAPS]) in whom antiphospholipid antibodies may have played a role in the genesis of NRH.

Purification of a liver DNA-synthesis promoter from plasma of partially hepatectomized rats.

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.

Laparoscopic findings in seven patients with nodular regenerative hyperplasia of the liver.

We describe the laparoscopic findings in seven patients with nodular regenerative hyperplasia of the liver. This unusual condition is characterized by nodules of hyperplastic hepatocytes diffusely distributed throughout the liver parenchyma, without fibrous septa between the nodules. In all patients, the diagnosis was made by liver biopsy under laparoscopic control. Laparoscopy revealed the presence of portal hypertension, nonnodular undulated liver surface, recognizable lobular pattern, and a hepatic consistency softer than normal to palpation. All of these findings indicated a diagnosis of nodular regenerative hyperplasia. Definitive diagnosis was established from biopsy specimens.