Abstract
Primary pancreatic injury that occurs in acute pancreatitis leads to necrosis of pancreatic cells and is accompanied by the development systemic inflammatory response of varying severity. Systemic inflammatory response, in turn, can lead to the development of multiple organ dysfunction syndrome and death of patients. The release of damage-associated molecular patterns into the extracellular space is the trigger pathological mechanism underlying these processes. The released patterns exert their effects via Toll-like receptors (TLR). These findings suggest that TLR can be considered a new target for therapeutic intervention in acute pancreatitis. We studied mRNA expression of TLR2 and TLR4 in the peripheral blood mononuclear cells from the patients with acute pancreatitis and showed a decrease in the examined parameters associated with lornoxicam treatment. Anti-mediator therapy decreased mortality in these patients.
Publication types
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Randomized Controlled Trial
MeSH terms
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Adult
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Aged
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Anti-Inflammatory Agents, Non-Steroidal / pharmacology*
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Anti-Inflammatory Agents, Non-Steroidal / therapeutic use
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Female
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Gene Expression / drug effects
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Humans
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Intestinal Diseases / etiology
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Leukocytes, Mononuclear / drug effects
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Leukocytes, Mononuclear / metabolism
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Male
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Middle Aged
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Pancreatitis, Acute Necrotizing / complications
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Pancreatitis, Acute Necrotizing / drug therapy
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Pancreatitis, Acute Necrotizing / metabolism*
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Pancreatitis, Acute Necrotizing / mortality
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Piroxicam / analogs & derivatives*
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Piroxicam / pharmacology
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Piroxicam / therapeutic use
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Prospective Studies
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Survival Analysis
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Toll-Like Receptor 2 / genetics
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Toll-Like Receptor 2 / metabolism*
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Toll-Like Receptor 4 / genetics
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Toll-Like Receptor 4 / metabolism*
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Treatment Outcome
Substances
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Anti-Inflammatory Agents, Non-Steroidal
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TLR2 protein, human
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TLR4 protein, human
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Toll-Like Receptor 2
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Toll-Like Receptor 4
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Piroxicam
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lornoxicam