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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Non-O1 Vibrio cholerae are gram-negative rods that can cause sporadic gastroenteritis, bacteraemia, and extraintestinal infections, primarily following the consumption of raw seafood or exposure of damaged skin to contaminated saltwater during the summer months. Bacteraemic necrotizing fasciitis caused by non-O1 V. cholerae has rarely been reported. Liver cirrhosis, haemochromatosis, and immunosuppression are important factors contributing to the severity of the infections and outcome. This report describes a case of liver cirrhosis in which right lower leg compartment syndrome and acute renal failure presented as the initial symptoms of bacteraemic necrotizing fasciitis. The organisms growing in the wound and blood cultures were identified as non-O1 V. cholerae. After antibiotic therapy, fasciotomy, right above-knee amputation, repeat debridement of the left lower leg and split-thickness skin grafts, the patient was eventually discharged in a stable condition.
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PMID:Bacteraemic necrotizing fasciitis with compartment syndrome caused by non-O1 Vibrio cholerae. 1711 24

Patients with cirrhosis have altered immune defenses and are considered immunocompromised individuals. Changes in gut motility, mucosal defense and microflora allow for translocation of enteric bacteria into mesenteric lymph nodes and the blood stream. Additionally, the cirrhotic liver is ineffective at clearing bacteria and associated endotoxins from the blood thus allowing for seeding of the sterile peritoneal fluid. Thus, hospitalised cirrhotic patients, particularly those with gastrointestinal hemorrhage, are at high risk of developing bacterial infections, the most common being spontaneous bacterial peritonitis. Given the significant morbidity and mortality associated with spontaneous bacterial peritonitis and the fact that half of the cases are community acquired, all hospitalised cirrhotic patients should have a diagnostic paracentesis to exclude infection. Those admitted with gastrointestinal bleed and a negative paracentesis require short-term prophylaxis with norfloxacin. A third generation cephalosporin is the treatment of choice for spontaneous bacterial peritonitis and, once the acute infection is resolved, secondary prophylaxis with oral norfloxacin is warranted. Patients who develop renal dysfunction at the time of active infection have the highest mortality and require adjunctive albumin therapy. This article reviews the pathogenesis of SBP, the evidence behind the antibiotics used, the rationale for adjunctive albumin therapy in the setting of acute renal failure, and the role of prophylactic antibiotics in specific high-risk populations.
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PMID:Prevention and treatment of infections in patients with cirrhosis. 1722 98

In patients with cirrhosis, acute renal failure is due to prerenal failure (a result of decreased renal perfusion) and tubular necrosis. There are 3 main causes of prerenal failure: 'true hypovolemia' (which complicates hemorrhage, gastrointestinal or renal fluid losses), sepsis, and type 1 hepatorenal syndrome (HRS). Prerenal failure may also be due to the administration of non-steroidal antiinflammatory drugs, or intravascular radiocontrast agents. Prerenal failure is reversible after restoration of renal blood flow. Treatments target the cause of hypoperfusion, and fluid replacement is used to treat 'non-HRS' prerenal failure. In patients with type 1 HRS with very low short-term survival rate, liver transplantation is the ideal treatment. Systemic vasoconstrictor therapy with terlipressin (combined with intravenous human albumin), noradrenaline (combined with albumin and furosemide) or midodrine (combined with octreotide and albumin) may improve renal function in patients with type 1 HRS waiting for liver transplantation. MARS (for Molecular Adsorbent Recirculating System) and the transjugular intrahepatic portosystemic shunt may also improve renal function in these patients. In patients with cirrhosis, acute tubular necrosis is mainly due to an ischemic insult to the renal tubules. Studies are needed on the natural course and treatment (e.g., renal-replacement therapy) of acute tubular necrosis in patients with cirrhosis.
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PMID:Diagnosis and treatment of acute renal failure in patients with cirrhosis. 1722

The role of urinary biomarkers of kidney injury in the prediction of adverse clinical outcomes in acute renal failure (ARF) has not been well described. The relationship between urinary N-acetyl-beta-(D)-glucosaminidase activity (NAG) and kidney injury molecule-1 (KIM-1) level and adverse clinical outcomes was evaluated prospectively in a cohort of 201 hospitalized patients with ARF. NAG was measured by spectrophotometry, and KIM-1 was measured by a microsphere-based Luminex technology. Mean Acute Physiology, Age, Chronic Health Evaluation II (APACHE II) score was 16, 43% had sepsis, 39% required dialysis, and hospital mortality was 24%. Urinary NAG and KIM-1 increased in tandem with APACHE II and Multiple Organ Failure scores. Compared with patients in the lowest quartile of NAG, the second, third, and fourth quartile groups had 3.0-fold (95% confidence interval [CI] 1.3 to 7.2), 3.7-fold (95% CI 1.6 to 8.8), and 9.1-fold (95% CI 3.7 to 22.7) higher odds, respectively, for dialysis requirement or hospital death (P < 0.001). This association persisted after adjustment for APACHE II, Multiple Organ Failure score, or the combined covariates cirrhosis, sepsis, oliguria, and mechanical ventilation. Compared with patients in the lowest quartile of KIM-1, the second, third, and fourth quartile groups had 1.4-fold (95% CI 0.6 to 3.0), 1.4-fold (95% CI 0.6 to 3.0), and 3.2-fold (95% CI 1.4 to 7.4) higher odds, respectively, for dialysis requirement or hospital death (P = 0.034). NAG or KIM-1 in combination with the covariates cirrhosis, sepsis, oliguria, and mechanical ventilation yielded an area under the receiver operator characteristic curve of 0.78 (95% CI 0.71 to 0.84) in predicting the composite outcome. Urinary markers of kidney injury such as NAG and KIM-1 can predict adverse clinical outcomes in patients with ARF.
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PMID:Urinary N-acetyl-beta-(D)-glucosaminidase activity and kidney injury molecule-1 level are associated with adverse outcomes in acute renal failure. 1726 47

Bacteremia has rarely been reported in patients receiving treatment for hepatitis C virus (HCV) infection. We describe the features and investigation of four cases of Staphylococcus aureus bacteremia occurring between 3 November 2004 and 10 January 2005 in patients on therapy for chronic HCV infection. The unusual occurrence of S. aureus bacteremia in a series of patients led to an epidemiologic investigation and molecular typing methods were employed to assess the relatedness of cases. The mean time of bacteremia onset was week 10 of HCV treatment. No patient had neutropenia previously. The average duration of bacteremia was 2.6 days and complications included acute renal failure (2/4), disseminated intravascular coagulopathy (DIC) with sepsis syndrome (1/4), septic arthritis (1/4), spinal epidural abscess (1/4) and endocarditis (1/4). Two patients were in the same weight class for dosing, but no other epidemiologic links were found. One patient admitted to intravenous drug use (IVDU) and a second was suspected of IVDU. The two other patients were cirrhotic, but had no further identifiable risk factors. All bacterial isolates were methicillin-susceptible. By pulsed-field gel electrophoresis, two cases were found to have identical bacterial strains. However, fluorescent-based amplified fragment-length polymorphism analysis demonstrated distinct band patterns in all four cases. The epidemiologic data and molecular analysis of this cluster of S. aureus bacteremia cases among patients receiving combination therapy for treatment of chronic HCV infection suggest that these cases were not related. Additionally, IVDU and cirrhosis, but not neutropenia, are identified as potential risk factors for this uncommon complication of HCV therapy.
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PMID:Staphylococcus aureus bacteremia in patients receiving pegylated interferon-alpha and ribavirin for chronic hepatitis C virus infection. 1765 Feb 90

Patients with liver cirrhosis undergoing gastrointestinal surgery still suffer from high operative morbid-mortality despite advancements in surgical critical care. The objective of this study is to see if this same relationship applies to patients undergoing esophagectomy for cancer. From 1993 to 2003, sixteen esophageal cancer patients with liver cirrhosis were operated on. They were all male with a mean age of 51.5 years. According to the Child-Pugh classification, 10 patients were Child 'A', 4 patients Child 'B' and Child 'C' in 2 patients. The surgical procedure was through an Ivor-Lewis esophagogastrectomy with intra-thoracic anastomosis. Major morbidity included: 4 respiratory failure, 2 acute renal failure, 3 pneumonia, and one in each of the patients with gastrointestinal bleeding and hepatic failure. The mean follow up among the survivors was 19.1 months. The hospital mortality was 25% (4/16). Using the rate according to Child classification, the mortality rates were: A: 1/10 (10%), B: 2/4 (50%) and C: 2/2 (100%). We conclude that patients with liver cirrhosis in Child-Pugh A could tolerate esophagectomy with an acceptable risk. However, patients with a more advanced state of liver dysfunction are at higher risk for esophagogastrectomy. Careful patient selection and meticulous peri-operative care is warranted in those embarking on surgical resection.
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PMID:Is it safe to perform esophagectomy in esophageal cancer patients combined with liver cirrhosis? 1767 Apr 48

A 47-year-old man underwent liver transplantation for cirrhosis secondary to hepatitis C and alcoholism. This was complicated by primary donor liver dysfunction and acute renal failure requiring dialysis. Gadolinium magnetic resonance cholangiopancreatography was performed 2 weeks post transplant, and a second successful liver transplant was performed 1 week later. Shortly after this, the patient developed rapidly progressive erythematous plaques over his abdomen, lower and upper limbs. There was marked oedema and skin induration. Fibrosis severely limited his mobility, leaving him wheelchair-bound. An abdominal plaque biopsy revealed increased dermal mucin and cellularity, with proliferation of spindled fibroblastic cells. Paraprotein was not detected in the serum. Facial sparing, the absence of serum paraprotein and the histopathological findings confirmed the diagnosis of nephrogenic systemic fibrosis. Immunohistochemical stains revealed CD34-positive spindle-shaped cells, and electron microscopy did not detect free gadolinium. Following improvement in renal function and various treatments, his plaques softened, fibrosis slowed and mobility partially improved. Gadolinium magnetic resonance cholangiopancreatography was performed following this improvement. Six weeks later, further progression of nephrogenic systemic fibrosis occurred despite normal renal function.
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PMID:Nephrogenic systemic fibrosis associated with liver transplantation, renal failure and gadolinium. 1818 50

Postoperative acute renal failure is a frequent and serious medical complication following orthotopic liver transplant. Here, we report our experiences with liver transplant recipients who developed acute renal failure in the early period following orthotopic liver transplant. Among 100 liver transplants performed between April 1993 and January 2004, we retrospectively analyzed 91 patients (mean age, 29.9 +/- 14.0 years) who had undergone orthotopic liver transplant. The underlying causes of liver failure were cryptogenic liver cirrhosis (n=27), viral hepatitis (n= 21) (hepatitis-B-related liver cirrhosis [n=13], hepatitis-C-related liver cirrhosis [n=7], and hepatitis-B- and C-related liver cirrhosis [n=1]), autoimmune hepatitis (n=18), Wilson's disease (n=10), primary sclerosing cholangitis (n=8), biliary atresia (n=3), Budd-Chiari syndrome (n=2), and primary biliary cirrhosis (n=2). The immunosuppressive regimen included mycophenolate mofetil (azathioprine for 10 patients), cyclosporine, and steroids. Six patients received a combination of tacrolimus and steroids. Ten patients (10.9%) experienced acute renal failure, 7 (70%) were men, and none of them required renal replacement therapy and/or died. Four patients were diagnosed as having cryptogenic liver cirrhosis; 2 with hepatitis-C-related liver cirrhosis, 2 with autoimmune liver cirrhosis; 1 with primary biliary cirrhosis; and 1 hepatitis-B-related liver cirrhosis. Six patients were Child-Pugh's classification C, and the others were B. The rate of postoperative acute renal failure in our patients was relatively low when compared with other series, and our outcomes were good.
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PMID:Acute renal failure in the first 100 orthotopic liver transplant patients in Southern Iran. 1819 28

Hepatorenal syndrome (HRS) is a functional renal failure that frequently develops in patients with advanced cirrhosis and severe impairment in systemic circulatory function. Traditionally it has been considered to be the consequence of a progression of the splanchnic arterial vasodilation occurring in these patients. However, recent data indicate that a reduction in cardiac output also plays a significant role. There are two different types of HRS. Type-2 HRS consists of a moderate and steady or slowly progressive renal failure. It represents the extreme expression of the circulatory dysfunction that spontaneously develops in patients with cirrhosis. The main clinical problem in these patients is refractory ascites. Type-1 HRS is a rapidly progressive acute renal failure that frequently develops in closed temporal relationship with a precipitating event, commonly spontaneous bacterial peritonitis. In addition to renal failure, patients with type-1 HRS present deterioration in the function of other organs, including the heart, brain, liver, and adrenal glands. Type-1 HRS is the complication of cirrhosis associated with the worst prognosis. However, effective treatments of HRS (vasoconstrictors associated with intravenous albumin, transjugular intrahepatic portacaval shunt, albumin dialysis) that can improve survival have recently been introduced.
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PMID:Pathogenesis and treatment of hepatorenal syndrome. 1829 79

A lot of patients suffering from liver cirrhosis show a decreased renal perfusion and glomerular filtration rate. An impaired renal function is the result of complex e.g. hemodynamic disturbances, resulting of the chronic liver disease. This explains its disposition to renal dysfunction and the higher incidence of acute renal failure in liver cirrhosis. In the case of renal failure hepatorenal syndrome, apart from prerenal, renal and postrenal causes, should be included in the differential diagnosis especially when signs of portal hypertension are apparent regarding its high mortalityand fatal prognosis requiring an immediate therapeutically approach. Special attention must be due to preventive strategies to avoid renal deterioration. This includes simple steps e.g. a careful election of medication but also an adequate therapy of infection-associated complications in patients with liver cirrhosis.
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PMID:[Acute renal failure in patients with liver cirrhosis--what to do? An update]. 1854 Mar 28


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