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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. In hepatitis C virus (HCV)-infected patients undergoing liver transplantation (LT), the virus infects the liver graft immediately after transplantation. The main source of HCV infection is circulating virions. Nevertheless, some data suggest that HCV present in extrahepatic compartments may contribute to HCV infection in some cases of hepatitis C recurrence. 2. Studies on early kinetics have shown that HCV replication starts a few hours after transplantation and that HCV-RNA concentrations increase a few hours or days after the procedure, suggesting that HCV has an enormous ability to adapt to the new environment. 3. The quasispecies population may change significantly after transplantation, most likely because of the need to adapt to a new environment. There are no conclusive data supporting the role of HCV quasispecies composition and disease outcomes. 4. Persistence of HCV infection is the rule after transplantation. This is due to immunosuppression and to the immune exhaustion of the previously exposed immune system. 5. In general, HCV is not thought to be directly cytopathic. Thus, it is believed that the immune response against HCV causes liver damage. However, understanding the mechanisms of liver damage in HCV-infected LT recipients is extremely complex because of the existence of a human leukocyte antigen-mismatched organ, the preexisting virus-specific T cells that may be dysfunctional and/or tolerized, and the immunosuppression. 6. Despite the possible effect of immune-mediated liver damage, it is clear that strong immunosuppression is associated with severe forms of hepatitis C recurrence (cholestatic hepatitis, fibrosing cholestatic hepatitis, and accelerated fibrosis progression). Thus, in the absence of a strong anti-HCV immune response, HCV is able to directly (HCV proteins) or indirectly (cytokines) produce liver damage. 7. The activation of stellate cells and accelerated deposition of fibrosis are the final consequences of HCV infection in the graft. There are several mechanisms that may act synergistically to activate and perpetuate stellate cell activation in the setting of LT: ischemia-reperfusion damage, old donor age, HCV proteins, cholestasis, rejection, infection with other viruses (cytomegalovirus), and immune-mediated injury.
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PMID:Virology and pathogenesis of hepatitis C virus recurrence. 1882 23

Cardiac allograft vasculopathy (CAV) remains a life-threatening complication after heart transplantation (HT). Recipients with severe intimal thickening are 10-fold more likely to suffer cardiac events than those without severe hyperplasia. From July 1987 to July 2007, we performed 323 HTs with 5-year actuarial freedom from CAV of 69%, similar to the data reported by the International Society for Heart and Lung Transplantation, namely, 68% at 5 years. Therefore, CAV is not uncommon in Asia. The pathogenesis of CAV is initial endothelial injury followed by intimal hyperplasia and proliferation of vascular smooth muscle cells. It may be caused by both immunological events (involving T or B cells in response to donor major histocompatibility antigens, or natural killer [NK] cell-triggered recruitment of T cells not responsive to donor alloantigen) and nonimmunologic factors, such as older age, ischemia-reperfusion injury, viral infection (particularly cytomegalovirus [CMV] infection), immunosuppressive drugs, and classic risk factors, such as hyperlipidemia, insulin resistance, and hypertension. The therapy for CAV has been disappointing, despite prescriptions of statin lipid-lowering agents, calcium-channel blockers, angiotensin-converting enzyme inhibitors, and antiproliferative drugs. Patients with CAV are often not amenable to successful revascularization (medical or surgical) because of the diffuse obliterative process. Prophylaxis of CAV starts with modification of risk factors: hypertension, hyperlipemia, hyperglycemia, obesity, and smoking, as well as promotion of exercise programs. The HMG-CoA reductase inhibitors and antiproliferative drugs may slow the progression of CAV by various immunologic and nonimmunologic effects. Prevention of CMV infection reduces CAV. Mycophenolate mofetil and signal transduction inhibitors, such as everolimus, reduce intimal thickening and CAV.
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PMID:Treatment and prophylaxis of cardiac allograft vasculopathy. 1892 15

We retrospectively evaluated the use of double-j stent and the incidence of urological complications in 2 groups of patients who received a kidney transplant. From January 2005 to September 2007 we studied 172 patients receiving kidney transplants, 65 and 107 from living and cadaver donors, respectively. From the 172 patients, a total of 34 were excluded due to ureterostomy or Politano-Leadbetter ureterovesical anastomosis. Another 21 patients were excluded from the study due to graft loss due to acute or hyperacute rejection, cytomegalovirus (CMV) infection, or vascular complication. The remaining patients were divided into 2 groups: group A (44 patients) and B (73 patients) with versus without the use of a double-j-stent, respectively. The 2 groups were comparable in terms of donor and recipient gender, ischemia time, and delayed graft function. We failed to observes significant differences between the 2 groups in mean hospital stay (23 +/- 9 and 19 +/- 9), urinary leak (2.3% and 4.1%), and urinary tract infection (20.4% and 19.2%), among groups A and B, respectively. The only difference observed concerned the gravity of the urinary leak; no surgical intervention was needed among the double-j stent group versus 2 patients demanding ureterovesical reconstruction in the nonstent group. In conclusion, our data suggested that the routine use of a double-j stent for ureterovesical anastomosis neither significantly increased urinary tract infection rates, nor decreased the incidence of urinary leaks, but may decrease the gravity of the latter as evidenced by the need for surgical intervention.
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PMID:Impact of double-j ureteric stent in kidney transplantation: single-center experience. 1901 Feb 25

A 56-year-old patient, first diagnosed with an acute cytomegalovirus infection, presented with progressive abdominal pain because of a superior mesenteric vein thrombosis for which he was treated with systemic thrombolysis and heparin in continuous infusion. As this therapy did not have the intended success after 5 days, an interventional radiological procedure was performed with local thrombolysis in the superior mesenteric artery resulting in recanalisation of the vein. Oral anticoagulation was initiated and continued for a period of 6 months. Mesenteric venous thrombosis is a relatively uncommon cause of mesenteric ischemia that can be associated with severe morbidity and significant mortality. With noninvasive techniques, it is possible to establish a diagnosis in the majority of the cases. The importance of an early diagnosis and therapy - not only with anticoagulation, but also thrombolysis in selected cases - is shown with this case and review of the literature.
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PMID:Cytomegalovirus-associated superior mesenteric vein thrombosis treated with systemic and in-situ thrombolysis. 1937 75

The purpose of this study was to determine the effect of donor race on the outcome of black patients with chronic hepatitis C infection who undergo liver transplantation. The records for deceased donor liver transplants that occurred in the United States between January 1998 and December 2007 were obtained from the United Network for Organ Sharing. 26,212 records contained sufficient data to be included in the analysis. Of these, 11,989 (45.7%) records were for patients positive for hepatitis C virus (HCV) and 1292 (4.9%) were for patients both HCV-positive and black. Black recipients with white donors were found to have significantly worse outcomes than all other recipient-donor race combinations (P < 0.001). The crude 5-year survival rate for black recipients who had a black donor was 14% higher than the 5-year survival rate for black recipients who had a white donor. Multivariate regression analysis determined that a graft from a race-unmatched donor was an independent risk factor for graft failure (hazard ratio = 1.41, 95% confidence interval = 1.11-1.79) among HCV-positive black recipients but not among HCV-negative black recipients after adjustments for donor age, recipient age, cold ischemia time, serum creatinine, serum bilirubin, diabetes mellitus, body mass index, and donor cytomegalovirus status. The observation that race-unmatched grafts are a risk factor in HCV-positive black recipients, but not in HCV-negative black recipients, suggests an alteration of the graft-host relationship by HCV. In conclusion, our results suggest that HCV-positive black recipients who undergo liver transplantation can have increased graft survival if their donors are black, with survival rates approaching those of white liver transplant recipients.
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PMID:The effect of donor race on the survival of Black Americans undergoing liver transplantation for chronic hepatitis C. 1971 42

Restorative proctocolectomy with ileal pouch-anal anastomosis (IPAA) is the surgical treatment of choice for the majority of patients with medically refractory ulcerative colitis (UC) or UC with dysplasia, or familial adenomatous polyposis. Various forms of pouchitis frequently occur after surgery. In fact, pouchitis is the most frequent long-term complication of IPAA in patients with UC, with a cumulative prevalence of up to 50%. The etiology and pathogenesis of pouchitis are not entirely clear. It is generally believed that the initiation and development of the disease process of pouchitis is associated with dysbiosis of pouch reservoir, as evidenced by a favorable response to antibiotic therapy. However, the majority of the patients do not show identifiable etiopathogenetic or triggering factors, therefore being labeled to have idiopathic pouchitis. In contrast, a subgroup of patients, particularly those with antibiotic-refractory pouchitis, may have obvious triggering factors for disease flare-up and progression and may be considered to have secondary pouchitis. Therefore, pouchitis can be classified on the basis of etiology into idiopathic and secondary causes. Approximately 20-30% of patients who present with chronic pouchitis have secondary identifiable and triggering factors, including cytomegalovirus or Clostridium difficile infection, ischemia, concurrent immune-mediated disorders, radiation, collagen deposition, and use of nonsteroidal anti-inflammatory drugs. Careful evaluation of these secondary causes of pouchitis that may contribute to resistance to antibiotics should be performed before the introduction of next-line medical therapy.
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PMID:Secondary pouchitis: those with identifiable etiopathogenetic or triggering factors. 1975 72

Biliary strictures (BS), a major complication after orthotopic liver transplantation (OLT), cause morbidity, mortality, graft loss, and increased costs. The virtually unchanged incidence of BS (approximately 10%-25%) suggests that they are not simply "technical" in origin, but probably represent a mucosa ischemic injury inherent in the transplantation procedure. To study risk factors for BS, we analyzed 403 OLTs performed between January 1, 1997 and December 31, 2006, at a single center, excluding cases of regraft or death within 1 month. The average time to the diagnosis of the BS was 253 days (range, 7-1002 days). Upon univariate analysis, the absence of flushing of donor bile ducts, an imported versus a locally procured liver, and rejection were risk factors for BS. In contrast, the following factors were protective: donor cardiac arrest followed by resuscitation (suggesting an ischemic preconditioning effect) as well as addition of epoprostenol to and pressurization of the preservation solution. Patients with higher postoperative peak values of transaminases, bilirubin, alkaline phosphatase, and gamma glutamyl transpeptidase were at greater risk for later development of BS. Donor hypotension, donor age, donor intensive care unit (ICU) stay, type of preservation, positive cross-match, cold and warm ischemia times, sequential versus simultaneous portal/arterial reperfusion, as well as cytomegalovirus (CMV) infection were not risk factors for BS. Upon multivariate analysis, only epoprostenol and pressurization offered protection from BS. In conclusion, this study 2 novel points: (1) patients with high(er) transaminase values and cholestasis early postoperatively are at greater risk to develop later BS and require close monitoring and (2) donor maneuvers for better flushing and preserving peribiliary vascular plexus and biliary mucosa (epoprostenol and pressurization of preservation solution) offer protection from BS.
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PMID:Biliary strictures after liver transplantation: risk factors and prevention by donor treatment with epoprostenol. 1985 57

Gastrointestinal complications (GI) after thoracoabdominal aortic repair can be classified as biliary disease, heptic dysfunction, pancreatitis, GI bleeding, peptic ulcer disease, bowel ischemia, paralytic ileus, and aortoenteric fistula. Theses complications are associated with high post operative morbidity and mortality. Most of the aortoenteric fistulae after thoracoabdominal aortic surgery are found at the duodenum, near the surgical site. These rare complications are caused by an indirect communication with abdominal aorta that originated from an aneursymal formation ruptured into the duodenum. Such aorto-duodenal fistula formation is considered as a result of inflammatory change from secondary infection near the surgical instruments. Herein, we report two cases of massive upper GI bleeding from aorto-duodenal fistulae and spontaneous lower GI perforation related to cytomegalovirus infection after abdominal aortic aneurysmal repair operations.
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PMID:[Cytomegalovirus infection-related spontaneous intestinal perforation and aorto-enteric fistula after abdominal aortic aneurysmal repair]. 2009 69

Use of organs from marginal donors for transplantation is a current strategy to expand the organ donor pool. Its efficacy is universally accepted among data from multicenter studies. Herein, we have reviewed outcomes of double kidney transplantation (DKT) over an 9-year experience in our center. The aim of this study was to evaluate possible important differences between a monocenter versus multicenter studies. Between 1999 and 2008, we performed 59 DKT. Recipient mean age was 63 +/- 5 years. Mean HLA-A, -B, and -DR mismatches were 3.69 +/- 0.922. Donor mean age was 69 +/- 7 years and mean creatinine clearance was 69.8 +/- 30.8 mL/min. Proteinuria was detected in three donors (5%). Mean cold ischemia and warm ischemia times were 1130 +/- 216 and 48 +/- 11 minutes, respectively. The right and left kidney scores were 4.18 +/- 2 and 4.21 +/- 2, respectively. Thirty patients (51%) displayed good postoperative renal function; 22 (37%), acute tubular necrosis with postoperative dialysis; 3 (5%), acute rejection episodes; 4 (7%), single-graft transplantectomy due to vascular thrombosis; 1 (2%), a retransplantation; 5 (8%), a lymphocele; 3 (5%) vescicoureteral reflux or stenosis requiring surgical correction. Cytomegalovirus infection was detected in five patients (8%). In three patients (5%) displayed de novo neoplasia. Three patients showed chronic rejection (5%), whereas we observed a cyclosporine-related toxicity in 7 (12%). Nine patients (15%) developed iatrogenic diabetes. Patient and graft survivals after 3 years from DKT were 93% and 86.3%, respectively. In this study, we applied successfully a widespread score to allocate organs to single kidney transplantation or DKT. In our experience, the score is suitable for the organ allocation but it may be overprotective, excluding potentially suitable organs for a single transplantation.
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PMID:Single-center experience in double kidney transplantation. 2053 35

In a retrospective study, we analyzed 1419 consecutive kidney transplantation procedures performed at a single center to identify potential predictive factors of ureteral stenosis. Only stenosis observed after the first month posttransplantation was considered. The Cox proportional hazard regression model was used to analyze donor age and serum creatinine concentration before procurement, recipient age, cold ischemia time, delayed graft function, number of renal arteries, and presence of a double-J stent. Follow-up evaluation included number and timing of acute rejection episodes, cytomegalovirus infection, acute pyelonephritis, renal function, and patient death. Ureteral stenosis developed in 45 patients (3.17%), and was correlated with donor age older than 65 years (P = .001), kidneys with more than 2 arteries (P = .009), and delayed graft function (P = .02). The data suggest a potential protective role of donor age, number of renal arteries, and delayed graft function in development of ureteral stenosis after kidney transplantation.
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PMID:Late ureteral stenosis after kidney transplantation: a single-center experience. 2053 54


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