Increased nitric oxide excretion in patients with severe acute pancreatitis: evidence of an endotoxin mediated inflammatory response?

Background and aims: Nitric oxide represents a potential key mediator of the local and systemic manifestations of acute pancreatitis (AP) in experimental models but its role in human disease is uncertain. We therefore sought to assess if systemic nitric oxide (NO) production is elevated in severe AP...

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Bibliographic Details
Published in:Gut 2003-02, Vol.52 (2), p.270-274
Main Authors: Rahman, S H, Ammori, B J, Larvin, M, McMahon, M J
Format: Article
Language:English
Subjects:
Acute Disease
acute pancreatitis
Acute Physiology and Chronic Health Evaluation score II
Adult
Aged
APACHE-II
Bacterial infections
bacterial translocation
Bacterial Translocation - physiology
Biological and medical sciences
Biomarkers - urine
C reactive protein
C-Reactive Protein - analysis
CRP
Disease
EndoCAb
endotoxin core antibody
Endotoxins - metabolism
Female
Gastroenterology. Liver. Pancreas. Abdomen
Humans
Immunoglobulin G - analysis
Immunoglobulin M - analysis
Immunoglobulins - analysis
Infections
Intestinal Mucosa - metabolism
intestinal permeability
lipopolysaccharide
Liver. Biliary tract. Portal circulation. Exocrine pancreas
LPS
Lymphatic system
Male
Medical sciences
Metabolites
Middle Aged
Mortality
MOSF
multiorgan system failure
Necrosis
Nitric oxide
Nitric Oxide - urine
nitric oxide synthase
Nitrites - urine
NOS
Other diseases. Semiology
Pancreatic Disease
Pancreatitis - metabolism
Pancreatitis - microbiology
Pancreatitis - pathology
PEG
Permeability
Polyethylene glycol
Rodents
Signal transduction
SIRS
Studies
systemic inflammatory response syndrome
total urine nitrite
TUN
urinary nitrite excretion
Urine
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Summary:Background and aims: Nitric oxide represents a potential key mediator of the local and systemic manifestations of acute pancreatitis (AP) in experimental models but its role in human disease is uncertain. We therefore sought to assess if systemic nitric oxide (NO) production is elevated in severe AP and determine whether this is a reflection of biochemical severity or endotoxin exposure. Patients and methods: Patients were recruited within 72 hours of pain onset. NO derived nitrite excretion determined from a 24 hour sterile urine collection was correlated with intestinal macromolecular permeability (polyethylene glycol excretion ratio), markers of systemic endotoxin exposure (IgG:IgM endotoxin core antibody (EndoCAb) ratio), disease severity, and the magnitude of systemic inflammation (peak C reactive protein (CRP) and Acute Physiology and Chronic Health Evaluation score II (APACHE-II)). Results: In patients with a severe attack (n=20), nitrite excretion was increased significantly compared with patients with a mild attack (n=45, 20.6 μg v 15.65 μg; p
ISSN:0017-5749
1468-3288
1458-3288
DOI:10.1136/gut.52.2.270