Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Most patients with hepatocellular carcinoma (HCC) also have cirrhosis, an independent cause of death. We considered an alternative definition of tumor-related death in patients with HCC and attempted to validate our definition. Two hundred thirty-seven HCC patients were diagnosed, followed, and died over a 12-year period and were evaluated every 2 months, including their last 6 months of life. We defined death by cancer if there was, in the last 6 months of life, a CT scan increase of >25% in the sum of tumor index lesions' cross-sectional areas or new onset of, or increase in, either vascular invasion or metastatic disease (Group 1). Patients with stable cancer were considered to have died from any other cause (Group 2). We found that 135 (57%) patients died from cancer progression (Group 1), whereas 102 (43%) patients did not (Group 2). There was a statistically significant difference between Group 1 and Group 2 patients in percentage with bilobar disease (P = 0.03), more than one tumor (P = 0.01), an increase in AFP (P = 0.04), vascular invasion (P = 0.001), and the presence of metastases (P = 0.01). We conclude that 57% of patients with unresectable HCC died as a direct result of cancer progression, but 43% did not. The latter died from complications of their cirrhosis, including sepsis, GI bleeds, and renal failure.
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PMID:Causes of death in patients with unresectable hepatocellular carcinoma. 1743 87

Living donor liver transplantation of the right lobe might offer the possibility to extend the eligibility criteria of patients with hepatocellular carcinoma (HCC) in cirrhosis without penalizing patients who are waiting for a graft from a deceased donor. From 1988 to 2005, surgical treatment of HCC was performed in 580 patients (187 transplantation, 393 resection) in a European center. In the transplantation group, 21 patients with HCC in cirrhosis underwent LDLT (11% of all transplantations for HCC; 22% of 96 LDLT). Solitary HCC were accepted irrespective of their diameter unless vascular invasion was detectable. Multiple HCC nodes were considered acceptable up to a diameter of the largest node of 6 cm and a total tumor diameter of 15 cm. The median follow-up period was 26 months (range, 1-65 months). Vascular invasion had occurred in 12 patients (57%). One patient (4.8%) died within 60 days after transplantation from sepsis. Rates of 3-year survival and 3-year recurrence-free survival were 68% and 64%, respectively. Overall 3-year survival rates in patients with HCC in cirrhosis not meeting the Milan criteria (n = 13) or the San Francisco criteria (n = 8) were 62% and 53%, respectively. LDLT is a safe procedure. However, small sample sizes do not yet permit a definitive comparison to be made between the former results obtained after cadaveric donation. So far, the outcome of the patients is in favor of a careful extension of the selection criteria for HCC in cirrhosis.
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PMID:Living donor liver transplantation of the right lobe for hepatocellular carcinoma in cirrhosis in a European center. 1753 94

As part of the multifactorial role of liver in protein synthesis, many coagulation factors, natural anticoagulants, and compounds of the fibrinolytic system are produced in the liver. A prolonged liver disease, either biliary obstruction or parenchymal liver disease, is consecutively accompanied by abnormal clotting. In the present paper we review the haemostasis impairment in obstructive jaundice with special reference to the hepatic cirrhosis and failure, to systemic inflammation and sepsis that develops in cholestatic diseases, and finally in some other benign or malignant diseases including pancreatic adenocarcinoma, acute pancreatitis, cholangiocarcinoma, and hepatocellular carcinoma. Finally, a special reference to the possible therapeutic interventions has been made. The aim of the present review is to collect the current concepts concerning the haemostasis impairment in obstructive jaundice and provide practical guidelines for the diagnostic and therapeutic strategies. Understanding the pathophysiology of haemostatic changes in patients with cholestasis, and, more generally, liver disease, is the hallmark of accurate diagnosis and treatment.
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PMID:Haemostasis impairment in patients with obstructive jaundice. 1759 68

The clinical course of cryoglobulinemic syndrome (CS) is usually slow; however, fast aggravations have been frequently reported in recent years. In these cases vasculitic ischemic tissue damage accounts for glomerular involvement, neuropathy, cutaneous ulcers, ischemic heart disease, lung or jejunal impairment and stroke. Other critical events in CS may be represented by sepsis, liver insufficiency, hepatocellular carcinoma and non-Hodgkin's lymphomas. Sometimes emergency can not be controlled and the evolution is fatal. Long-term follow up, emergency outcome and cause of death have not been considered in controlled studies, in large series. Here we report a 53-year old woman affected by IgG-IgMk type II HCV-related mixed cryoglobulinemia, who presented several critical events over the course of the disease, which required therapeutical emergency interventions. The latter consisted of plasma exchange, cytotoxic agents, corticosteroids, intravenous immunoglobulin, antihypertensive drugs, antibiotics, and rituximab. Eventually no therapy was effective and the patient died from a catastrophic-like syndrome. This case is relevant because it enables us to consider some important steps in the treatment of emergency in CS.
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PMID:Emergency in cryoglobulinemic syndrome: what to do? 1793 11

Biliary complications after liver transplantation (LT) using organs retrieved from donors after cardiac death are not well characterized. The aim of this study was to evaluate the severity of biliary complications and outcomes after donation after cardiac death liver transplantation (DCD-LT). A retrospective evaluation of 20 DCD-LTs from 1997-2006 was performed. The recipient age was 53+/-8.7, and the donor age was 35+/-11 years. The warm ischemia time, cold ischemia time, peak alanine aminotransferase level, and peak aspartate aminotransferase level were 33+/-12 minutes, 8.7+/-2.7 hours, 1757+/-1477 U/L, and 4020+/-3693 U/L, respectively. The bilirubin and alkaline phosphatase levels at hospital discharge after LT were 3.2+/-5.4 mg/dL and 248+/-200 U/L, respectively. During a median follow-up of 7.5 months (range: 1-73), 5 patients (25%; 1 death after re-LT) died (3 from sepsis, 1 from recurrent hepatocellular carcinoma at 4 months, and 1 from a cardiac event at 46 months), and additionally, 4 patients (20%) required re-LT (1 because of hepatic artery thrombosis, 1 because of primary graft nonfunction, and 2 because of biliary strictures). Twelve (60%) developed biliary complications, and of these, 11 (55%) had serious biliary complications. The biliary complications were as follows: a major bile leak for 2 patients (10%; both eventually underwent retransplantation), anastomotic strictures for 5 patients (25%), hilar strictures for 7 patients (35%), extrahepatic donor duct strictures for 9 patients (45%), intrahepatic strictures for 10 patients (50%), stones for 1 patients (5%), casts for 7 patients (35%), and debris for 2 patients (10%). More than 1 biliary complication was seen in most patients, and these were unpredictable and required multiple diagnostic or therapeutic procedures. Serious biliary complications are common after DCD-LT, and research should focus on identifying donor and recipient factors that predict and prevent serious biliary complications.
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PMID:Biliary complications and outcomes of liver transplantation from donors after cardiac death. 1804 64

Pemetrexed has demonstrated activity in hepatocellular carcinoma (HCC) cell lines, and has a manageable toxicity profile in clinical trials, suggesting its potential as a treatment for HCC patients. A multicenter, Phase II community-based study was conducted to assess the response rate and toxicity profile of single-agent pemetrexed in first-line patients with advanced or metastatic HCC. Patients premedicated with folic acid, vitamin B(12), and dexamethasone were administered pemetrexed 600 mg/m(2) IV on day 1 of each 21-day cycle until disease progression. This nonrandomized study employed Simon's 2-stage design, enrolling 21 eligible patients in the first stage, stopping accrual if < or =2 responders were observed. Responses were four stable disease, 14 progressive disease, and three not evaluable: two had early toxicities (renal/liver failure, sepsis) and one was noncompliant. The most common grade 3 hematological toxicities were neutropenia 6 of 21 (29%) and thrombocytopenia 3 of 21 (14%); with no grade 4 toxicities. Thirteen patients died on-study: 12 PD and one liver failure; none were drug-related. The median survival was 5.2 months (range, <1-12.2). The planned second stage was cancelled, and the trial was closed owing to lack of response. While pemetrexed was tolerated in this patient population, it was not active.
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PMID:A phase II study of pemetrexed in patients with advanced hepatocellular carcinoma. 1830 99

With the accumulation of orthotopic liver transplantation (OLT) recipients, an increased number of patients with graft failure need retransplantation (re-OLT). This study was undertaken to examine our clinical experience of re-OLT for patients with poor graft function after primary transplantation at a single center. We analyzed retrospectively, the clinical data of 32 re-OLTs in 31 patients at our center from January 2004 to February 2007, including indications and causes of death, timing of retransplantation, and surgical techniques. The indications included bile leak (2 cases), biliary stricture (16 cases), recurrence of hepatocellular carcinoma (HCC) (5 cases), hepatic artery stenosis (4 cases), hepatic artery thrombosis (HAT) (2 cases), and hepatitis B recurrence (3 cases). The rate of re-OLT was 4.29%. All patients underwent modified piggyback liver transplantations with cadaveric allografts. No intraoperative mortality and acute rejection occurred. Overall, 17 of 31 patients (54.8%) died after re-OLT with survival times ranging from 2 weeks to 28 months. Another 14 patients were cured with survival times of 4 to 32 months. The perioperative mortality rate of patients who underwent re-OLT between 8 and 30 days after their initial transplantation was highest (66.7%). The most common cause of death after re-OLT was sepsis (47.1%), multiple-organ failure (17.6%), and recurrence of HCC (17.6%), whereas the majority of deaths posttransplantation were sepsis-related (54%) within 1 year. Re-OLT is the only therapeutic option for a failing liver graft. Proper indications and optimal operative time, advanced surgical procedures, reasonable individual immunosuppression regimens, and effective perioperative anti-infection treatments contribute to the improved survival of patients after re-OLT.
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PMID:A single-center experience of retransplantation for liver transplant recipients with a failing graft. 1858 34

Liver transplantation is an excellent therapeutic option for terminal liver disease. During the last decades the results of liver transplantation have improved significantly with a patient survival rate of nearly 90% at one year and 80% at 5 years of follow-up. The main indications for liver transplantation include: end-stage liver disease associated to cirrhosis, acute liver failure, and hepatic tumors (mainly hepatocarcinoma). The absolute contraindications for a transplant are less frequent than in the past, and include: severe co-morbidity (cardiac or pulmonary), sepsis, advanced HIV disease and extra-hepatic malignancy. This document presents a Consensus of the main groups performing liver transplantation in Chile, about its indications and contraindications. It also reviews general aspects of liver transplantation, including the selection and referral of liver transplant candidates, allocation of organs and the evaluation of severity of liver disease.
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PMID:[General considerations, indications and contraindications for liver transplantation in Chile: a multicenter consensus development document]. 1939 35

Melioidosis is endemic in Taiwan. It is caused by infection with Burkholderia pseudomallei. A prolonged course of oral eradication therapy to avoid relapse after an intensive intravenous therapy is recommended to treat melioidosis. Melioidosis with cardiac involvement is rare and is often combined with septicemia, for which the mortality rate is 20-60%. The initial clinical presentations of melioidosis mimic Mycobacterium tuberculosis infection, which is the most common etiology of bacterial pericarditis in Taiwan. We present a case of non-septicemic melioidosis that presented as non-suppurative cardiac tamponade and left subcarinal lymphadenopathy. Underlying diseases included hepatitis B-related liver cirrhosis and hepatocellular carcinoma. The patient was successfully treated with 2 weeks of intravenous ceftazidime and 12 weeks of oral doxycycline, trimethoprim-sulfamethoxazole, and amoxicillin/clavulanate. Melioidosis-related pericarditis should be considered in the differential diagnoses of bacterial pericarditis in Taiwan.
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PMID:Non-septicemic melioidosis presenting as cardiac tamponade. 1878 43

Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are created in normal hepatocytes and are critical for normal physiologic processes, including oxidative respiration, growth, regeneration, apoptosis, and microsomal defense. When the levels of oxidation products exceed the capacity of normal antioxidant systems, oxidative stress occurs. This type of stress, in the form of ROS and RNS, can be damaging to all liver cells, including hepatocytes, Kupffer cells, stellate cells, and endothelial cells, through induction of inflammation, ischemia, fibrosis, necrosis, apoptosis, or through malignant transformation by damaging lipids, proteins, and/or DNA. In Part I of this review, we will discuss basic redox biology in the liver, including a review of ROS, RNS, and antioxidants, with a focus on nitric oxide as a common source of RNS. We will then review the evidence for oxidative stress as a mechanism of liver injury in hepatitis (alcoholic, viral, nonalcoholic). In Part II of this review, we will review oxidative stress in common pathophysiologic conditions, including ischemia/reperfusion injury, fibrosis, hepatocellular carcinoma, iron overload, Wilson's disease, sepsis, and acetaminophen overdose. Finally, biomarkers, proteomic, and antioxidant therapies will be discussed as areas for future therapeutic interventions.
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PMID:Nitric oxide and redox regulation in the liver: part II. Redox biology in pathologic hepatocytes and implications for intervention. 2040 Jan 12


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