Six year disease free survival after liver transplantation in a patient with T3 gallbladder carcinoma: case presentation and review of the literature

BACKGROUND: The incidence of gallbladder carcinoma in cirrhotics is unknown. Known risk factors are primary sclerosing cholangitis and polypoid masses. CASE PRESENTATION: A sixty year old with primary sclerosing cholangitis, cirrhosis, and gallbladder polyps underwent liver transplantation. A polypoid lesion measuring 1.5 × 0.5 cm was found on the fundus of the gallbladder. Histological examination revealed moderately differentiated adenocarcinoma with full thickness penetration of the gallbladder encroaching liver parenchyma. Angiolymphatic invasion was noted. The lymph nodes, the cystic duct and the common duct were free of tumor (T3N0M0). Extensive evaluation did not demonstrate metastasis. No chemotherapy was given. He is currently six years post procedure and free of disease. CONCLUSION: "Incidentally" discovered stage IIA gallbladder carcinoma may not negatively affect long term survival after liver transplantation

Extended survival by urgent liver retransplantation after using a first graft with metastasis from initially unrecognized donor sarcoma.

A 58-year-old man underwent orthotopic liver transplantation for polycystic liver disease. Shortly after the procedure, it was discovered that the donor harbored a sarcoma of the aortic arch that had metastasized to the spleen, and bilateral renal cell carcinomas. The two sole organ recipients, our liver recipient and a lung recipient at another institution, were both listed for urgent retransplantation, which they received from the same second donor. The liver explant contained metastatic sarcoma. Twenty-four months survival following lung retransplantation has been previously reported. We report the 76-month disease-free survival in the liver recipient

Inducible left ventricular outflow tract gradient during dobutamine stress echocardiography: an association with intraoperative hypotension but not a contraindication to liver transplantation.

BACKGROUND: Dobutamine stress echocardiography (DSE) is frequently used in the evaluation of cardiac risk prior to orthotopic liver transplantation (OLT). In the general cardiac population, an inducible left ventricular outflow tract gradient (LVOT Delta) during DSE has variable prognostic importance. The purpose of this study was to determine the prevalence and clinical significance of LVOT Delta in patients undergoing OLT during DSE. METHODS: Consecutive medical records of 106 patients who had undergone OLT at our institution from January 1997 until January 2002 were retrospectively analyzed and divided into two groups based on the presence (Group I, LVOT Delta \u3e36 mmHg) or absence (Group II, LVOT Delta\u3c or = 36 mmHg) of a significant LVOT Delta measured during DSE. We determined any outcome differences between these two groups with regard to intraoperative hypotension, cardiac mortality, length of hospital stay, graft function, and renal function post-OLT. RESULTS: Forty-six patients had an LVOT Delta \u3e 36 mmHg (Group I) and 60 patients had LVOT Delta\u3c or = 36 mmHg (Group II). Baseline demographics were similar in both groups. There was no significant overall difference in cardiac mortality between Group I versus Group II patients (0 versus 1 patient, respectively, P=0.57). Intraoperative hypotension occurred in 4 patients in Group I versus 0 patient in Group II (P=0.03). Length of stay, graft function, and postoperative renal function were similar in both groups. CONCLUSION: A significant LVOT Delta \u3e36 mmHg is a frequent finding occurring in 46/106 (43%) of patients who have DSE pre-OLT. Intraoperative hypotension is associated with patients having an LVOT Delta. However, post-OLT patients with significant LVOT Delta have a similar in-hospital outcome compared to patients without significant LVOT Delta

The Significance of Hepatitis G Virus in Serum of Patients With Sporadic Fulminant and Subfulminant Hepatitis of Unknown Etiology

Excluding acute hepatic failure caused by drugs, the etiology of fulminant hepatitis (FH) remains unknown in many patients. There are conflicting data about a possible pathogenic role for the hepatitis G virus (HGV) in patients with cryptogenic fulminant hepatitis (non–A-E FH). We investigated the presence of circulating HGV in 36 patients with well-documented non–A-E fulminant and 5 patients with subfulminant hepatitis from 3 geographic locations in the United States. Serum HGV RNA was determined by reverse transcriptase-polymerase chain reaction using primers from the NS5 region of the HGV genome. HGV RNA was also measured before and after liver transplantation in 5 patients and at different time points in 7 patients. Serum samples were recoded and reanalyzed for HGV RNA using different primer sets to assess the validity of the HGV RNA assay. HGV was present in serum of 14 of the 36 patients (38.8%) with non–A-E fulminant hepatitis. Twenty percent of patients from the Northeast, 11% of the patients from the Southeast, and 50% from the Mid-Atlantic regions of the United States had circulating HGV RNA. The use of therapeutic blood products was significantly associated with the presence of serum HGV RNA (P < .02). Retesting for HGV RNA with different primers was positive in all but 1 case. HGV RNA is not causally related to non–A-E fulminant hepatitis. The finding of HGV RNA in serum from these patients is likely related to the administration of blood product transfusion after the onset of fulminant hepatitis