Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0341503 (bacterial peritonitis)
 1,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infections in patients with end-stage liver disease (ESLD) are an important cause of morbidity and mortality in these patients. Abnormalities in their natural defense mechanisms, alterations in the enteric flora and the growing utilization of invasive procedures increase the risk of infections in these patients. Common bacterial infections in ESLD patients include spontaneous bacterial peritonitis, urinary tract infections, community-acquired pneumonia, dermatologic infections, and bacteremia. Viral infections such as influenza can have a devastating course in ESLD patients. Hepatitis B and C are now among the most common causes of ESLD. They also present an important therapeutic challenge. As patients with human immunodeficiency virus are surviving longer, ESLD due to hepatitis C is now emerging as a leading cause of morbidity in these patients. Prompt detection of infections, use of appropriate antibiotics for treatment and prophylactic measures such as vaccinations can help improve survival in these patients.
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PMID:Infections in Patients With End-stage Liver Disease. 1741 11

Liver cirrhosis yearly causes 1.2 million deaths worldwide, ranking as the 10th leading cause of death in the most developed countries. High susceptibility to infections along with a significant risk for infection-related mortality justifies the description of liver cirrhosis as the world's most common immunodeficiency syndrome. Liver cirrhosis is an end-stage organic disease hallmarked by a multifaceted immune dysfunction due to deterioration of antimicrobial recognition and elimination mechanisms in macrophages along with an impaired antigen presentation ability in circulating monocytes. Bacterial translocation supports-and is supported by-uncontrolled activation of immune cell responses and/or loss of toll-like receptor (TLR) tolerance, which can turn exaggerated inflammatory responses to systemic inflammation. Lipopolysaccharide (LPS) or endotoxin boosts systemic inflammatory activity through activation of TLR-2- and TLR-4-dependent pathways and facilitate a massive production of cytokines. This, in turn, results into elevated secretion of reactive oxygen species (ROS), which further enhances intestinal hyperpermeability and thus sustains a vicious circle of events widely known as "leaky gut." Albumin can be of particular benefit in cirrhotic patients with spontaneous bacterial peritonitis and/or hepatorenal syndrome type of acute kidney injury (HRS-AKI) due to anti-inflammatory and antioxidative stress as well as volume-expanding properties and endothelial-stabilizing attributes. However, presence of autoantibodies against albumin in patients with liver cirrhosis has been described. Although previous research suggested that these antibodies should be regarded as naturally occurring antibodies (NOA), the origin of the antialbumin immune response is obscure. High occurrence of NAO/albumin complexes in patients with liver disease might reflect a limited clearance capacity due to bypassing portal circulation. Moreover, high burden of oxidized albumin is associated with less favorable outcome in patients with liver cirrhosis. To date, there is no data available as to whether oxidized forms of albumin result in neoepitopes recognized by the immune system. Nevertheless, it is reasonable to hypothesize that these alterations may have the potential to induce antialbumin immune responses and thus favor systemic inflammation.
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PMID:Immune Dysfunction and Albumin-Related Immunity in Liver Cirrhosis. 3093 Jun 89


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