Non-neoplastic portal vein thrombosis (PVT) is an increasingly recognized complication of liver cirrhosis. It is often diagnosed fortuitously and can be either partial or complete. The clinical significance of PVT is not obvious except in some situations such as when patients are on the waiting list for liver transplantation. The only known therapy is anticoagulation which has been shown to permit the disappearance of thrombosis and to prevent further extension. Anticoagulation is a challenging therapy in individuals with liver cirrhosis because of the well-recognized coagulation abnormalities observed in that setting and because of the increased risk of bleeding, especially from gastrointestinal tract caused by portal hypertension. We herein review the current knowledge on that topic in order to highlight the advantages and disadvantages of the currently proposed therapeutic attitudes in face of the diagnosis of PVT in individuals with cirrhosis.
Close to one-quarter of the ITx recipients had advanced liver fibrosis. In the current era of improved PN management, our data suggests that previously reported risk factors for IFALD, such as extreme short gut syndrome and PN duration, may have a lesser impact on development of liver fibrosis. A prolonged duration of bilirubin elevation may be associated with advanced liver fibrosis in patients with IFALD, but this requires validation in a larger cohort.
Recipients of solid organ transplants take life-long immunosuppressive agents to prevent rejection. In Canada, an estimated 3000 transplant procedures are performed annually and 40 000 people are living with a transplant. Early studies from Europe and the United States suggested that transplant recipients were at greater risk of severe COVID-19, with a two-to fivefold greater mortality than the general population. [1][2][3] It is unclear whether the increased risk is owing to multiple comorbidities, immunosuppression or a combination of both factors. Initial trials of therapeutics for SARS-CoV-2, including remdesivir, dexamethasone and tocilizumab, did not formally include transplant recipients. [4][5][6] Similarly, pivotal studies of the SARS-CoV-2 vaccines did not include immunocompromised populations. 7,8 Therefore, the use of COVID-19 therapeutics and SARS-CoV-2 vaccines in the transplant population has been extrapolated from the general population. Commonly used COVID-19 therapies such as dexamethasone and tocilizumab may place transplant recipients at risk of overimmunosuppression,
Paired Bx in the SB and the colon are usually in agreement regarding the presence or the absence of ACR. However, colonic Bx alone may not suffice to exclude ACR following ITx. With minor modifications, the histopathological criteria of the SB may be adaptable to the colonic allograft.
Invasive fungal infections (IFI) are an important infectious complication after orthotopic liver transplantation (OLT), occurring in 4.7% of all OLT recipients (OLTr). 1 Invasive candidiasis (IC) accounts for about 68%-79% of all IFI while invasive aspergillosis (IA) accounts for up to 8%-11%. 2 While rare, IA is particularly dreaded among OLTr as it is associated with severe disseminated disease, central nervous system involvement, and high mortality ranging between 60% and 90%. [3][4][5][6][7][8][9] While several risk factors have been associated with the development of IA, those associated with highest risk for aspergillosis among OLTr include: dialysis, retransplantation, 10-12 acute liver failure, 13 and pre-transplant colonization with Aspergillus. 6
BACKGROUND: Liver transplantation (LT) is the only curative treatment for cirrhosis. However, the presence of complications can impact outcomes following LT. Sarcopenia, or muscle mass loss, is highly prevalent in patients with cirrhosis and is associated with longer hospitalization stays and a higher infection rate post-surgery. We aimed to identify patients at higher risk of early sarcopenia post-LT. METHODS: This retrospective study included 79 cirrhotic patients who underwent LT. Muscle mass was evaluated using the third lumbar spine vertebra skeletal muscle mass index (SMI) and sarcopenia was defined using established cut-off values. Computerized tomography (CT) scans performed within six-month peri-operative period (three months pre- and post-LT) were included in the study. Complications and comorbidities were collected and correlated to SMI post-LT and predictive models for SMI post-LT were constructed. RESULTS: The overall prevalence of sarcopenia was 46% and 62% before and after LT, respectively. Newly developed sarcopenia was found in 42% of patients. Post-LT sarcopenia was associated with longer hospital stays (54±37 vs 29±10 days, p = 0.002), higher number of infection (3±1 vs 1±2, p = 0.027), and greater number of complications (5±2 vs 3±2, p <0.001) compared to absence of sarcopenia. Multivariate analyses showed that the SMI post-LT was independently associated with pre-LT renal function markers, the glomerular filtration rate (GFR) and creatinine (Model 1, GFR: β = 0.33; 95% CI = 0.04–0.17; p = 0.003; Model 2, Creatinine: β = –0.29; 95% CI = –0.10 to –0.02; p = 0.009). CONCLUSIONS: The present study highlights the potential role of renal dysfunction in the development and persistence of sarcopenia after LT.
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