Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

For the last decade, numerous experimental studies have demonstrated that the main part of liver injury caused by low or no flow states does not occur at the time of hypoxia, but during reperfusion. These experimental studies have a crucial clinical impact, because ischemia/reperfusion injury is involved in situations such as temporary vascular exclusion during liver surgery for trauma or tumors, preservation injury before liver transplantation, and liver cell necrosis observed in hypoxic (ischemic) hepatitis. The aim of the present review is to clarify the sequence of pathophysiological events responsible for ischemia/reperfusion injury of the liver, and to examine the potential contribution of liver ischemia/reperfusion injury to the syndrome of human hypoxic hepatitis.
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PMID:Ischemia/reperfusion injury of the liver: pathophysiologic hypotheses and potential relevance to human hypoxic hepatitis. 1123 16

The mesenteric hemodynamic response to circulatory shock is characteristic and profound; this vasoconstrictive response disproportionately affects both the mesenteric organs and the organism as a whole. Vasoconstriction of post-capillary mesenteric venules and veins, mediated largely by the alpha-adrenergic receptors of the sympathetic nervous system, can effect an "autotransfusion" of up to 30% of the total circulating blood volume, supporting cardiac filling pressures ("preload"), and thereby sustaining cardiac output at virtually no cost in nutrient flow to the mesenteric organs. Under conditions of decreased cardiac output caused by cardiogenic or hypovolemic shock, selective vasoconstriction of the afferent mesenteric arterioles serves to sustain total systemic vascular resistance ("afterload"), thereby maintaining systemic arterial pressure and sustaining the perfusion of non-mesenteric organs at the expense of mesenteric organ perfusion (Cannon's "flight or fight" response). This markedly disproportionate response of the mesenteric resistance vessels is largely independent of the sympathetic nervous system and variably related to vasopressin, but mediated primarily by the renin-angiotensin axis. The extreme of this response can lead to gastric stress erosions, nonocclusive mesenteric ischemia, ischemic colitis, ischemic hepatitis, ischemic cholecystitis, and/or ischemic pancreatitis. Septic shock can produce decreased or increased mesenteric perfusion, but is characterized by an increased oxygen consumption that exceeds the capacity of mesenteric oxygen delivery, resulting in net ischemia and consequent tissue injury. Mesenteric organ injury from ischemia/reperfusion due to any form of shock can lead to a triggering of systemic inflammatory response syndrome, and ultimately to multiple organ dysfunction syndrome. The mesenteric vasculature is therefore a major target and a primary determinant of the systemic response to circulatory shock.
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PMID:The mesenteric hemodynamic response to circulatory shock: an overview. 1133 91

Apoptosis, or programmed cell death, and the elimination of apoptotic cells are crucial factors in the maintenance of liver health Apoptosis allows hepatocytes to die without provoking a potentially harmful inflammatory response In contrast to necrosis, apoptosis is tightly controlled and regulated via several mechanisms, including Fas/Fas ligand interactions, the effects of cytokines such as tumor necrosis factor alpha (TNF-alpha) and transforming growth factor beta (TGF-beta), and the influence of pro- and antiapoptotic mitochondria-associated proteins of the B-cell lymphoma-2 (Bcl-2) family. Efficient elimination of apoptotic cells in the liver relies on Kupffer cells and endothelial cells and is thought to be regulated by the expression of certain cell surface receptors. Liver disease is often associated with enhanced hepatocyte apoptosis, which is the case in viral and autoimmune hepatitis, cholestatic diseases, and metabolic disorders. Disruption of apoptosis is responsible for other diseases, for example, hepatocellular carcinoma. Use and abuse of certain drugs, especially alcohol, chemotherapeutic agents, and acetaminophen, have been associated with increased apoptosis and liver damage. Apoptosis also plays a role in transplantation-associated liver damage, both in ischemia/reperfusion injury and graft rejection. The role of apoptosis in various liver diseases and the mechanisms by which apoptosis occurs in the liver may provide insight into these diseases and suggest possible treatments.
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PMID:Apoptosis in diseases of the liver. 1134 18

Cholestasis is a common finding after liver transplantation and usually signifies graft dysfunction. The most important factor in the evaluation of patients with cholestasis is an awareness of the disorders that commonly arise along a time continuum post-transplant. Therefore, the approach to cholestasis requires a systematic review of biochemical, histological, and radiographic data. This article considers the causes of cholestasis in liver transplant recipients, excluding those associated with biliary anastomotic stricturing. These causes include conditions as diverse as ischemia reperfusion injury, ABO blood group incompatibility, hepatic arterial thrombosis, cytomegalovirus infection, fibrosing cholestatic hepatitis secondary to hepatitis B and C viruses, recurrent primary sclerosing cholangitis, recurrent primary biliary cirrhosis, and chronic rejection. Also examined are management issues pertinent to these conditions and strategies used in preventing or diminishing the effects of cholestasis once established.
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PMID:Cholestatic diseases of liver transplantation. 1135 20

Xanthine oxidase (XO) is a highly versatile flavoprotein enzyme, ubiquitous among species (from bacteria to human) and within the various tissues of mammals. The enzyme catalyses the oxidative hydroxylation of purine substrates at the molybdenum centre (the reductive half-reaction) and subsequent reduction of O(2) at the flavin centre with generation of reactive oxygen species (ROS), either superoxide anion radical or hydrogen peroxide (the oxidative half-reaction). Many diseases, or at least symptoms of diseases, arise from a deficiency or excess of a specific metabolite in the body. For an example of an excess of a particular metabolite that produces a disease state is the excess of uric acid which can led to gout. Inhibition of XO decreases the uric acid levels, and results in an antihyperuricemic effect. Allopurinol, first synthesised as a potential anticancer agent, is nowadays a clinically useful xanthine oxidase inhibitor used in the treatment of gout. There is overwhelming acceptance that xanthine oxidase serum levels are significantly increased in various pathological states like hepatitis, inflammation, ischemia-reperfusion, carcinogenesis and aging and that ROS generated in the enzymatic process are involved in oxidative damage. Thus, it may be possible that the inhibition of this enzymatic pathway would be beneficial. In this review the State of the Art will be presented, which includes a summary of the progress made over the past years in the knowledge of the structure and mechanism of the enzyme, associated pathological states, and in the efforts made towards the development of new xanthine oxidase inhibitors.
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PMID:Progress towards the discovery of xanthine oxidase inhibitors. 1186 Mar 55

Distinctive arthritic patterns, some of which may parallel or even precede intestinal disease activity, are seen in inflammatory bowel disease. Some spondyloarthropathies are associated with transient ileocolic inflammation. Vasculitis frequently affects the gastrointestinal tract, predominantly manifesting with abdominal pain. In severe cases, intestinal ischemia and perforation may occur. Various arthritides are thought to be associated with other gastrointestinal diseases, such as celiac disease and hepatitis. The association between intestinal disease and arthritis is still being investigated. Interactions between the inflammatory intestinal cells and inflamed synovial cells have been demonstrated. Certain intestinal bacteria such as Klebsiella pneumoniae are suspected to play a role as triggers for the development of arthropathies. Genetic factors, especially human leukocyte antigen associations, are also being increasingly investigated for better characterization of the types of arthritis and possible prognostic implications. Various therapies, including nonsteroidal anti-inflammatory drugs, used to treat rheumatologic diseases have the potential to cause gastrointestinal complications.
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PMID:Gastrointestinal issues in children with rheumatologic disease. 1242 59

Live donor renal transplantation offers significant advantages over cadaveric renal transplantation. It yields significantly better patient and graft survival on both short-term and long-term follow-up. Laparoscopic donor nephrectomy minimizes the morbidities associated with the surgical procedure and allows a speedy return to normal daily activities. The operation also provides an atraumatic kidney subjected to minimal warm ischemia time and with adequate length of artery and vein, resulting in immediate functioning of the kidney after transplantation with a low rate of ureteral complications. A 37-year-old man was referred as a kidney donor for his brother. Both donor and recipient were hepatitis-B surface antigen carriers. Cross-matching and human leukocyte antigen test showed good compatibility. Left donor nephrectomy was performed successfully by hand-assisted laparoscopy. The warm ischemic time was 4.5 minutes and the graft kidney functioned immediately after transplantation. The donor was discharged from the hospital on postoperative Day 3 with good recovery.
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PMID:Hand-assisted laparoscopic live donor nephrectomy: a case report. 1251 7

Severe congestive heart failure is associated with two distinct forms of liver dysfunction: jaundice that is related to passive congestion and acute hepatocellular necrosis that is caused by impaired perfusion. Cardiac cirrhosis (fibrosis) may result from prolonged recurrent congestive heart failure. Ischemic hepatitis (shock liver) usually manifests as asymptomatic elevation of the serum aminotransferase levels after an episode of hypotension, although the clinical presentation may mimic that of acute viral hepatitis. In most cases, ischemic hepatitis is of little clinical consequence and is self-limited. Acute liver failure may occur in patients with preexisting cirrhosis, severe chronic heart failure, or sustained hepatic ischemia.
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PMID:The liver in heart failure. 1251 1

OBJECTIVES: To determine risk factors of mortality in the preoperative, perioperative, and immediate postoperative period of a pediatric population that has undergone orthotopic liver transplantation for fulminant hepatic failure in a pediatric intensive care unit. DESIGN: Retrospective review of medical records. SETTING: A pediatric intensive care unit in a children's hospital. PATIENTS: Sixty patients with fulminant hepatic failure who fulfilled King's College criteria for liver transplantation. INTERVENTION: Orthotopic liver transplantation was performed according to standard techniques. Before transplantation, patients were admitted to a pediatric intensive care unit when intensive care was required, and patients were always admitted to a pediatric intensive care unit after the operation. Measurements: A total of 20 variables were studied via univariate and multivariate analysis; statistical significance was accepted when p </=.05. MAIN RESULTS: A total of 70 orthotopic liver transplantations were performed in 60 children (mean age, 64.11 +/- 40.97 months; range, 11 months to 14 yrs) for fulminant hepatic failure. Fulminant hepatic failure was caused by hepatitis A virus in 60% of cases, and non-A non-B non-C hepatitis was responsible in 40% of cases. Univariate analysis showed that the complications of infectious, hemodynamic, renal, and gastrointestinal bleeding are significant variables. Posttransplant respiratory support was also a significant variable. When the same variables were calculated with a multivariate analysis, no significant results were obtained. Multivariate analysis showed that mortality risk factors in this population were: etiology of liver failure (p <.002), liver size (p <.014), ischemia time (p <.041), ventilatory support before transplantation (p <.048), neurologic complications after orthotopic liver transplantation (p <.003), and acute rejection (p <.021). CONCLUSIONS: Hepatitis A virus is the major cause of fulminant liver failure in Argentina, but non-A non-B non-C hepatitis is an independent risk factor of mortality. Reduced-size graft, longer ischemia time, ventilatory support before orthotopic liver transplantation, neurologic complications, and acute rejection after transplantation are independent predictive factors of mortality. Better sanitary conditions and universal immunization for hepatitis A virus should reduce hepatitis A virus and hepatitis A virus-induced fulminant hepatic failure.
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PMID:Mortality risk factors of a pediatric population with fulminant hepatic failure undergoing orthotopic liver transplantation in a pediatric intensive care unit. 1278 Sep 61

Non-anastomotic biliary stricture (NAS) formation is a major complication of liver transplantation. We prospectively determined the time to development of responsiveness to treatment, and clinical outcomes following NAS formation. In addition, an extensive analysis of the association of recipient, donor, and clinical variables with NAS formation was performed. A total of 749 consecutive patients was studied in a prospective, protocol-based fashion. Seventy-two patients (9.6%) developed NAS at a mean of 23.6 +/- 34.2 weeks post-transplantation. Non-anastomotic biliary stricture formation resolved in only 6% of affected patients. Although patient survival was not affected, retransplantation and graft loss rates were significantly greater in recipients who developed NAS. In contrast to previous reports, a pretransplant diagnosis of HCV was associated with a low frequency of NAS formation. The incidence of NAS was independently associated with pretransplant diagnoses of PSC and autoimmune hepatitis. Hepatic artery thrombosis, and prolonged warm and cold ischemia times were also independent risk factors for NAS formation. We conclude that NAS developed in approximately 10% of primary liver transplant recipients. A pretransplant diagnosis of autoimmune hepatitis has been identified as a novel independent risk factor for NAS formation. Development of NAS significantly attenuates graft but not patient survival.
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PMID:Risk factors for and clinical course of non-anastomotic biliary strictures after liver transplantation. 1281 81


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