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L R Fassati

Publications and source records attributed to L R Fassati.

At least 19 recordsLinked to original sources
PubMed2005

Long-term outcome of right split in situ grafts in adults.

In situ split liver transplants represent a technical progression from ex situ split procedures conceived to retrieve grafts for pediatric recipients. The transection line runs along the falciform ligament, so the main artery to the right graft is the right proper artery, whereas the left graft retains the main arterial axis with the celiac trunk. Although the major advantages are for pediatric recipients, due to the expanded pool of grafts available, for adult recipients the results of right split in situ grafts must be compared with whole grafts. We considered two groups of consecutive grafts transplanted since 1993 as first grafts: 20 of the former and 261 of the latter. Groups were comparable for donor gender, recipient age and gender, perfusion solution, ischemia time, and follow-up time, but not for donor age and for the number of arterial anastomoses. Although there were more major surgical complications in the former compared with the latter group (40% vs 25%), the only statistically significant difference was found in retransplantation rate for arterial complications (15% vs 2.2%). No statistical difference was observed in graft or patient actuarial survival rates at 1, 3, or 6 years after transplantation; for right split grafts these were 85%, 69%, and 69% and 95%, 79%, and 79%, respectively.

Adult↗
PubMed2001

Endothelial targeting with C1-inhibitor reduces complement activation in vitro and during ex vivo reperfusion of pig liver.

Tissue damage during cold storage and reperfusion remains a major obstacle to wider use of transplantation. Vascular endothelial cells and complement activation are thought to be involved in the inflammatory reactions following reperfusion, so endothelial targeting of complement inhibitors is of great interest. Using an in vitro model of human umbilical vein endothelial cells (HUVEC) cold storage and an animal model of ex vivo liver reperfusion after cold ischaemia, we assessed the effect of C1-INH on cell functions and liver damage. We found that in vitro C1-INH bound to HUVEC in a manner depending on the duration of cold storage. Cell-bound C1-INH was functionally active since retained the ability to inhibit exogenous C1s. To assess the ability of cell-bound C1-INH to prevent complement activation during organ reperfusion, we added C1-INH to the preservation solution in an animal model of extracorporeal liver reperfusion. Ex vivo liver reperfusion after 8 h of cold ischaemia resulted in plasma C3 activation and reduction of total serum haemolytic activity, and at tissue level deposition of C3 associated with variable level of inflammatory cell infiltration and tissue damage. These findings were reduced when livers were stored in preservation solution containing C1-INH. Immunohistochemical analysis of C1-INH-treated livers showed immunoreactivity localized on the sinusoidal pole of the liver trabeculae, linked to sinusoidal endothelium, so it is likely that the protective effect was due to C1-INH retained by the livers. These results suggest that adding C1-INH to the preservation solution may be useful to reduce complement activation and tissue injury during the reperfusion of an ischaemic liver.

Animals↗
PubMed2000

Unusual peripheral T cell lymphoma presenting as acute liver failure and reappearing in the liver allograft.

A 25-year-old man presented with fulminant hepatic failure from an unusual peripheral T cell lymphoma involving the liver and spleen without lymphadenopathy. He underwent liver transplantation before establishing a definitive diagnosis and 21 days later, died from liver allograft failure because of recurrent lymphoma. In both the native liver and hepatic allograft, the lymphoma presented as a sparse cytologically atypical malignant infiltrate intermixed with numerous reactive macrophages, which showed marked angio- and epitheliotropism and irregular areas of coagulative necrosis. The malignant cells were CD3+/ granzyme B+/TIA1+/CD8-/CD56-/S100-- with variable staining for beta F1, CD5, and CD7. Multiplex polymerase chain reaction (PCR) showed rearrangement of the T cell receptor gamma chain gene in the native and transplanted liver and spleen. Even in the absence of a mass lesion or lymphadenopathy, peripheral T cell lymphoma should be included in the differential diagnosis of fulminant hepatic failure in young patients who show no evidence of viral or autoimmune diseases.

Adult↗
PubMed1998

Pattern and management of recurrent hepatocellular carcinoma after liver transplantation.

A series of 132 patients who underwent liver transplantation for primary liver cancer was collected from three different Italian hospitals and studied for recurrence of hepatocellular carcinoma after liver replacement. Twenty-one patients (15.9%) had a neoplastic recurrence after an average follow-up period of 7.8 months after transplantation (range, 1-25 months); 15 (71%) occurred within the first 18 months after transplant and only two recurred later than 2 years. The sites of recurrence were grafted liver (19%), lung (19%), bone (14%), and other (5%). Eight patients (38%) had multiple organ involvement at the onset. After 1, 2, 3, and 4 years the overall survival rates were 62%, 43%, 29%, and 23%, respectively. The tumor factors related to early cancer recurrence after transplantation were diameter of nodules more than 3 cm (P < 0.05), tumor stage not meeting the "Milan criteria" (P < 0.03), and presence of peri-tumoral capsule (P < 0.05); the number of nodules, TNM stage, presence of vascular invasion, alpha-fetoprotein level more than 150 UI/l, pre-transplant chemoembolization and resectability of cancer deposits did not seem to be related to early recurrence. The prognosis differed in the 7 patients with resectable recurrences (57% 4-year survival) and the 14 patients with unresectable disease (14% 4-year survival) (P < 0.02). Better patient selection and new combined medical strategies could reduce the incidence of and mortality from liver cancer recurrence after transplantation. The role of surgical resection of recurrence should be further investigated.

Adolescent↗
PubMed1998

Post-hepatitis primary disease does not influence 6-year survival after liver transplantation beyond 1 year.

Orthotopic liver transplantation (OLT) is used as a definitive treatment for end-stage liver disease and prolonged posttransplant survival has already been reported. The incidence of late mortality and graft morbidity is, however, not well defined and the role of primary viral disease in the long-term follow-up results is not clear. Data of posttransplant follow-up in 213 patients, 156 adults and 57 children, who survived at least 1 year were reviewed in order to define causes of graft dysfunction, graft loss and death. In 98 patients, 103 persistent graft dysfunctions were found. Thirty-four grafts were later lost [28 deaths and 6 successful retransplantations (re-OLT)]. The results were reviewed grouping patients according to their age and viral hepatitis status at the time of the transplantation. HBV-positive patients (51) showed 4 re-OLT (1 HBV), 3 liver-related deaths (2 HBV), 24 graft dysfunctions (8 HBV, 5 HCV), and 85.2% 6-year survival (based on 100% survival at 1 year). HCV-positive adults (28) showed 1 re-OLT, 3 HCV-related deaths, 24 graft dysfunctions (19 HCV), and 68.8% 6-year survival. HBV-HCV-positive patients (14) showed no graft loss and death, 10 graft dysfunctions (7 HCV, 1 HBV, 2 HBV-HCV), and 81.8% 6-year survival. HBV-HCV-negative adults (63) showed 3 non-hepatitis-related re-OLT, 5 liver-related deaths (2 HCV), 24 graft dysfunctions (6 HCV, 2 HBV), and 83.1% 6-year survival. HBV-HCV-negative children (49) showed no re-OLT, 1 HCV-related death, 14 graft dysfunctions (3 HCV), and 92.6% 6-year survival. HCV-positive children (8) showed 1 HCV-related re-OLT, 2 HCV-related deaths, 4 graft dysfunctions (3 HCV), and 81.3% 6-year survival. The main cause of graft dysfunction was hepatitis (45 HCV and 13 HBV), followed by technical complications (21), rejection (16), recurrent alcoholism (3), HIV infection (1), and unknown causes (4). In this long-term post-transplant follow-up series, viral hepatitis led to graft dysfunction in 58/103 (56.3%) cases, late graft failure was viral hepatitis-related in 11/ 20 (55%) cases, and, as a total, HCV infection was present in 45/58 (77.5%) cases of viral hepatitis-related graft damage. Looking at the timing of hepatitis-related graft failure, in 70% of cases death occurred after the 5th post-transplant year. In our experience, the occurrence of hepatitis, particularly HCV induced, was common and led to abnormal graft function, but the 6-year post-transplant survival (based on 100% survival at 1 year) in patients surviving for at least 1 year did not differ on the basis of the pretransplant viral hepatitis status. This finding may be consistent with the slow progression of the viral damage and longer follow-up results remain to be established. Nevertheless, data from the present study suggest that in long-term liver transplant survivors, the risk of deteriorating liver damage and eventual failure after 5 years remains only in those patients experiencing a viral hepatitis infection.

Adolescent↗
PubMed1998

Rescue FK506 early conversion for refractory rejection after pediatric liver transplantation: experience in 20 children.

Tacrolimus (FK506) is an effective and relatively safe novel immunosuppressant able to revert refractory rejection after pediatric liver transplantation (LTx). Between April 1993 and October 1996, 20 pediatric patients were converted to tacrolimus for biopsy-proven, steroid-resistant liver rejection. The mean follow-up was 18 months. The median time from LTx to switch was 20 days. Tacrolimus was administered per os at a mean dosage of 0.23 mg/kg per day to maintain median blood levels of 10.8 ng/ml at 1 week and 9.2 ng/ml at 1 year from the switch. Of the 20 patients, 15 are alive and they all recovered from rejection without the need of OKT3 after conversion. The major causes of death were: one multiorgan failure, two infections (cytomegalovirus Aspergillus), one bowel perforation, and one posttransplant lymphoproliferative disease. One patient experienced late side effects and was reconverted to cyclosporine when she was already rescued from hepatic allograft rejection. The results confirm that an earlier conversion to tacrolimus should be recommended after pediatric liver transplantation in order to revert hepatic allograft rejection with the best safety profile.

Child, Preschool↗