			Home About us Contact

Requiring Liver Transplantation (requiring + liver_transplantation)

Distribution by Scientific Domains

Medical Sciences	100%

Distribution within Medical Sciences

Transplantation	75%
Hepatology	25%

Selected Abstracts

Nevirapine-Induced Stevens Johnson,Syndrome and Fulminant Hepatic Failure Requiring Liver Transplantation

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 7 2010
J. Jao
We describe a case of nevirapine-induced Stevens,Johnson Syndrome (SJS) and fulminant hepatic failure (FHF) requiring liver transplantation. Five weeks prior to admission, a 57-year-old female with HIV infection had been switched to a nevirapine-based regimen of highly active antiretroviral therapy (HAART) with a CD4 cell count of 695/mm3. Examination of the explanted native liver at initial transplantation revealed massive hepatic necrosis consistent with drug-induced liver injury. Primary graft nonfunction complicated the early postoperative course and liver retransplantation was required. On follow-up 2 years later, she remains in good health with an undetectable viral load on an efavirenz-based regimen of HAART. To our knowledge, this is the first report of successful liver transplantation following SJS and FHF. [source]

Fulminant Wilson's Disease Requiring Liver Transplantation in One Monozygotic Twin Despite Identical Genetic Mutation

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 5 2010
K. M. Kegley
Acute decompensated Wilson's disease (WD) that presents as fulminant hepatic failure carries significant mortality without hepatic replacement. The abnormal gene implicated in WD, ATP7B, has been mapped to chromosome 13, and leads to decreased passage of copper from hepatocytes to bile. Excess copper accumulation exceeds hepatocyte storage capacity resulting in intracellular necrosis, apoptosis and cell death in various organs of the body. The hepatic injury induced by the abnormal accumulation of copper in WD has variable presentation such as acute hepatitis, rapid hepatic deterioration resembling fulminant hepatic failure, or as progressive chronic liver disease in the form of chronic active hepatitis or cirrhosis. There are reports in the literature describing monozygotic (identical) twins with similar hepatic progression requiring liver transplantation, however, with different neurological outcome after transplant. We report a case of one monozygotic twin presenting with acute liver failure requiring emergent liver transplantation while the other twin presented with mild liver disease, when both shared an identical genetic mutation. [source]

Bone disorders in chronic liver disease,

HEPATOLOGY, Issue 4 2007
Jane Collier
Osteomalacia rarely occurs in adult patients with chronic liver disease despite a low serum vitamin D level being reported in up to two-thirds of patients with cirrhosis. In contrast, osteoporosis, which increases the risk of vertebral fractures, occurs in 12%-55% of patients with cirrhosis. Although the prevalence is probably falling, as shown by a fall from 57%-26% in patients with biliary disease requiring liver transplantation over the last 2 decades, it still accounts for significant patient morbidity. Bone density also falls in the first 3 months after liver transplantation, and pretransplant fractures are predictive of posttransplant fractures. Many of the known risk factors for postmenopausal osteoporosis exist in the cirrhotic population, such as excess alcohol intake, steroid use, poor nutrition, and hypogonadism. There is also an increased risk of osteoporosis in patients without cirrhosis, particularly those with hemochromatosis and biliary disease. The diagnosis is made with bone density measurements. The effective treatment is largely based on evidence from postmenopausal osteoporosis as there have been only a few small clinical trials of patients with chronic liver disease. Bisphosphonates are the mainstay of treatment; they have been shown to be effective in biliary disease and are well tolerated. (HEPATOLOGY 2007.) [source]

Subfulminant hepatitis requiring liver transplantation following ibuprofen overdose

LIVER INTERNATIONAL, Issue 1 2000
Article first published online: 24 DEC 200
No abstract is available for this article. [source]

Outcomes of liver transplantation in patients with cirrhosis due to nonalcoholic steatohepatitis versus patients with cirrhosis due to alcoholic liver disease

LIVER TRANSPLANTATION, Issue 12 2009
Vishal Bhagat
Nonalcoholic steatohepatitis (NASH) is becoming a common cause of liver cirrhosis requiring liver transplantation (LT). Cardiovascular complications related to metabolic syndrome and NASH recurrence in the transplanted liver may affect the outcome of LT in these patients. We compared the outcomes of LT for NASH cirrhosis and alcoholic cirrhosis (ETOH) in a large transplant center. A retrospective chart review was performed for all patients who underwent LT for cryptogenic cirrhosis with the NASH phenotype (the NASH group) or ETOH (the ETOH group) at the University of Miami from January 1997 to January 2007. There was no significant difference in survival between the NASH and ETOH groups, despite a trend toward lower survival in the former (P = 0.1699). Sepsis was the leading cause of posttransplant death in both groups, and it was followed by cardiovascular causes in the NASH group (26% versus 7% in the ETOH group, P = 0.21) and malignancies in the ETOH group (29% versus 0% in the NASH group, P = 0.024). Recurrent steatohepatitis (33% versus 0%, P < 0.0001) and acute rejection (41% versus 23%, P < 0.023) were significantly more frequent in the NASH group than in the ETOH group. There was no difference in graft failure between the groups (24% in the NASH group versus 18% in the ETOH group, P = 0.3973). In conclusion, despite a numerical trend favoring the ETOH group, there were no statistically significant differences in posttransplant survival and cardiovascular mortality between the NASH and ETOH groups. Acute rejection and recurrent steatohepatitis were significantly more frequent in the NASH group but did not lead to higher rates of retransplantation. Liver Transpl 15:1814,1820, 2009. © 2009 AASLD. [source]

Outcomes following liver transplantation for seronegative acute liver failure: Experience during a 12-year period with more than 100 patients

LIVER TRANSPLANTATION, Issue 1 2005
Alan J. Wigg
Seronegative hepatitis is a common cause of acute liver failure (ALF) requiring liver transplantation. The primary aim of this study was to examine outcomes following transplantation in this group and to identify factors associated with early (<2 months) mortality. Patients studied were 110 consecutive cases of seronegative ALF transplanted at the Queen Elizabeth Hospital, Birmingham, between January 1992 and January 2004. Univariate analysis of 44 pretransplantation recipient, donor, and operative variables was performed initially to identify factors associated with early posttransplantation mortality. Variables identified as significant or approaching significance were analyzed using stepwise multiple logistic regression analysis. Survival following transplantation for seronegative hepatitis was 83%, 81%, and 73% at 2, 12, and 60 months, respectively. The majority (71%) of deaths occurred within the 1st 2 months and sepsis / multiorgan dysfunction was the most common cause of early death. Univariate analysis revealed 9 variables predicting early death. Subsequent multivariate analysis identified high donor body mass index (BMI; a possible surrogate marker for hepatic steatosis) as the most important predictor of early death (P = .009; odds ratio, 1.2; 95% confidence interval, 1.0-1.3). Recipient age >50 (P = .015; odds ratio, 4.2; 95% confidence interval, 1.3-14.1) and non-Caucasian recipient ethnicity (P = .015; odds ratio, 4.9; 95% confidence interval, 1.2-19.2) were other variables associated with early death on multivariate analysis. This study specifically examined factors that determine the early outcome of transplanted seronegative ALF patients. In conclusion, we found that donor and recipient factors identify patients who have a high chance of early death after transplantation. (Liver Transpl 2005;11:27,34.) [source]