PubMed Health⌕ Search

Biomedical subjects

L Caccamo

Publications and source records attributed to L Caccamo.

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↗
PubMed2005

A "steroid-free" tacrolimus and low-dose mycophenolate mofetil primary immunosuppression does not prevent early acute rejection after liver transplantation.

To assess the efficacy and safety of a primary immunosuppressive regimen with tacrolimus (Tac) and low-dose mycophenolate mofetil (MMF) without steroids and to determine the exposure to mycophenolic acid (MPA) in the early postoperative period, we performed a single-center, randomized 1:1, open-label, controlled study planned to be 60 liver transplantation patients randomized into 2 groups: group A, tacrolimus + MMF (750 mg orally twice a day); and group B, tacrolimus + MMF (750 mg orally twice a day) + steroids. After an interim analysis by the ethical committee patient enrollment was stopped. Data from 30 patients (12 in group A and 18 in group B with a mean follow-up period of 31 +/- 7 months) showed a patient survival rate of 91.7% in group A and 100% in group B and a graft survival rate of 91.7% and 88.9%, respectively. Nine patients (75%) in group A suffered an acute rejection episode, whereas in group B only 3 patients (16.7%) showed acute rejection (P = .002). All rejection episodes occurred in both groups at 1 week after transplantation. The difference in histological grading was statistically significant (P = .021). The toxicity profiles were similar in both groups. A primary immunosuppressive regimen based on Tac and low-dose MMF without steroids is safe but unable to prevent acute rejection at 1 week after transplantation even if early acute rejection does not affect the outcome in terms of morbidity and graft or patient survival.

Acute Disease↗
PubMed2001

Randomized trial of lamivudine versus hepatitis B immunoglobulin for long-term prophylaxis of hepatitis B recurrence after liver transplantation.

BACKGROUND/AIMS: The long-term prophylaxis of hepatitis B after liver transplantation requires further optimization. In a randomized trial we investigated a regimen where the initially given hepatitis B immunoglobulin (HBIg) is replaced by long-term lamivudine treatment. METHODS: Twenty-four liver transplant recipients (all HBsAg-positive/HBV DNA-negative before transplantation), who had received HBIg for at least 6 months without HBV recurrence, were randomized to receive lamivudine (n = 12) or HBIg (n = 12) for 52 weeks. The efficacy criteria involved seronegativity for HBsAg and undetectable HBsAg/ HBcAg in the liver. RESULTS: Twenty-one of 24 patients completed the study without hepatitis B virus (HBV) recurrence (11 on HBIg, ten on lamivudine), while three patients became HBsAg-positive. Amongst those without HBV recurrence HBV DNA was detectable only by polymerase chain reaction, intermittently in serum and lymphocytes, and in liver specimens from six of eight patients receiving HBIg and five of seven receiving lamivudine. YMDD variant was found in four cases with no viral antigen expression. Eight patients continued lamivudine after the study and during an additional 6-22 months remained HBsAg-negative with normal graft function. CONCLUSIONS: Substitution of HBIg with lamivudine is effective for prevention of HBV recurrence in low-risk liver transplant recipients and offers a convenient and cost-effective alternative for long-term HBV prophylaxis.

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↗
PubMed2001

[Severe mitral insufficiency caused by the rupture of the chordae tendinae in acromegaly. Report of a case].

Cardiovascular disease is a common finding in patients with acromegaly. In such patients, heart failure frequently leads to death. Cardiovascular manifestations of acromegaly include cardiomegaly and very often hypertension, coronary atherosclerosis, and diabetes. Primary valvular disease is less commonly observed. Because it is not clear whether acromegaly-related cardiomyopathy is a specific entity and since there are not many necropsy reports regarding mitral valve prolapse in acromegalic patients, we report the case of severe mitral regurgitation due to rupture of the chordae tendinae in a patient with mitral valve prolapse and acromegaly.

Acromegaly↗
PubMed1999

European collaborative study on factors influencing outcome after liver transplantation for hepatitis C. European Concerted Action on Viral Hepatitis (EUROHEP) Group.

BACKGROUND & AIMS: Liver transplantation for hepatitis C virus (HCV)-related liver disease is characterized by frequent graft infection by HCV. The prognosis and risk factors for morbidity and mortality in this condition were determined. METHODS: A retrospective study of 652 consecutive anti-HCV-positive patients undergoing liver transplantation between 1984 and 1995 in 15 European centers was conducted; 102 patients coinfected with hepatitis B virus (HBV) received immunoglobulin prophylaxis for antibody to hepatitis B surface antigen. RESULTS: Overall, 5-year survival was 72%. Five-year actuarial rates of hepatitis and cirrhosis were 80% and 10%. Genotypes 1b, 1a, and 2 were detected in 214 (80%), 24 (9%), and 24 (9%) of 268 patients analyzed. The only discriminant factor for patient or graft survival was hepatocellular carcinoma as primary indication. Independent risk factors for recurrent hepatitis included the absence of HBV coinfection before transplantation (relative risk [RR], 1.7; 95% confidence interval [CI], 1.2-2.6; P = 0.005), genotype 1b (RR, 2; 95% CI, 1.3-2.9; P = 0.01), and age > 49 years (RR, 1.4; 95% CI, 1.1-1.8; P = 0.01). CONCLUSIONS: The results of transplantation for HCV-related disease are compromised by a significant risk of cirrhosis, although 5-year survival is satisfactory. Genotype 1b, age, and absence of pretransplantation coinfection by HBV are risk factors for recurrent HCV.

Female↗
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↗
PubMed1996

Hepatitis C virus genotypes and reinfection of the graft during long-term follow-up in 35 liver transplant recipients.

To understand the clinical outcome of hepatitis C virus (HCV) recurrence, data from 35 liver transplant recipients who survived more than 6 months were reviewed. The presence of HCV-RNA was evaluated and genotyping was performed. On the basis of alanine aminotransferase (ALT) levels, patients were sorted into four groups. In 20 patients, a chronic elevation in ALT was found; HCV-RNA detection was positive in 17/17 and the following genotypes were found in 15 of them: 1b in ten patients, 2a in four patients, and 3a in one patient. In 11 patients, ALT levels remained normal throughout follow-up; in nine of them HCV-RNA was positive; HCV genotyping was available in eight patients and identified type 1b in two, type 2a in five, and type 3a in another patient. In two patients, ALT fluctuated above and below the upper limits of normality; type 1b HCV-RNA was found in one of them. In two patients, after an initial period of normality, ALT levels showed an abrupt rise; HCV-RNA was positive and type 1b was identified in both patients. Eight patients developed HCV-related deep jaundice and three of them spontaneously recovered. Progressive hepatic injury occurred in eight patients, six with chronic ALT elevation and two showing a late ALT elevation; genotype 1b was present in seven patients while in one, genotype 3a was found; sub-acute graft failure developed in five of them, leading to death in two and retransplantation in the others; the other three patients are alive with recurrent overt cirrhosis. The 1, 3, and 5 year actuarial survivals were 89%, 79%, and 63% respectively. The 1, 3, and 5 year actuarial risks of progressive graft damage were 6%, 7%, and 15%, respectively. In conclusion, HCV reinfection causes a slow decrease in the long-term patients' survival. Persistent elevation of ALT is more frequently observed in patients with genotype 1b infection.

Adolescent↗
PubMed1995

Emergence of hepatitis B virus S gene mutant in a liver transplant recipient.

Immunological and genomic analysis of the "a" determinant was carried out in seven patients with concurrent HBsAg and anti-HBs, four of whom were immunized against hepatitis B virus at liver transplant, two with histologically characterized chronic hepatitis B virus infection, and one HBsAg healthy carrier. The immune reactivity of the HBsAg "a" determinant was evaluated by binding to specific monoclonal antibodies, and the corresponding genomic sequence was studied by differential hybridization in microtiter plates and nucleotide sequence analysis. A double mutation generating an amino acid change (glycine to lysine) at residue 145, able to impair recognition by monoclonal antibodies, was observed in the post-transplant serum from one patient. No significant alteration of the "a" determinant sequence or reactivity was detected in the other patients. Amino acid residue 145 appears therefore to be critical for the recognition by anti-HBs antibodies. A previously undescribed glycine to lysine substitution at this level interferes with the immune reactivity of the "a" determinant.

Amino Acid Sequence↗