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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The diagram of the mortality of acute pancreatitis is characterized by two distinct peaks, in a similar manner to other generalized acute inflammatory responses. In the first phase, which is characterized by "hyper-inflammatory" mechanisms, death occurs due to overwhelming SIRS and subsequent multi-organ failure. The second peak of death is usually detected much later, at least two weeks after the onset of acute pancreatitis. Infection in necrotising pancreatitis is frequently observed in this so-called "compensatory antiinflammatory" phase. Since there has been no effective therapy evolved to prevent the activation of inflammatory and proteolytic cascades, the treatment of acute pancreatitis is merely symptomatic. Adequate fluid resuscitation and analgesia are the mainstays of treatment. In case of development of multi-organ failure, extensive medical and ventilatory supportive therapy is usually necessary. However, recent studies suggested certain methods might decrease the incidence of infection in pancreatic necrosis, which is usually due to bacterial translocation from the gut. Numerous attempts have been published in the literature to decrease the frequency of septic complications. Furthermore, the outcome of studies favouring antibiotic prophylaxis in acute pancreatitis were debatable. The development of multi-resistant strains of Gram-positive bacteria and Candida, due to long-term antibiotic use, is a strong argument against the indication of prophylactic antibiotic use. Recently, various clinical studies aimed to decrease bacterial translocation, including probiotic use and enteral feeding as part of the treatment. This paper provides a systematic review on data available in the evidence based literature on the use of antibiotics and the role of alternative and supportive therapy in the treatment of severe acute pancreatitis.
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PMID:Preventive strategies for septic complications of acute pancreatitis. 1796 33

Septic shock is the 13th leading cause of death in the United States. The rate of severe sepsis nearly doubled and mortality increased more than 60% during the 10-year period ending in 2003. Systemic inflammatory response syndrome has noninfectious and infectious causes. Noninfectious ones include burns, trauma, severe pancreatitis, and therapy with monoclonal antibodies or immunomodulatory drugs such as interleukin 2. Progression from sepsis syndrome to septic shock is caused by a series of immune responses. As an infectious injury progresses, host activation of the coagulation, immunological, and stress response systems ensues, resulting in tissue hypoperfusion and organ failure. Early studies with small numbers of patients suggest that treatment with low-dose corticosteroids has marked beneficial effects on shock reversal, the immune system, and the hemodynamic profile. Low-dose corticosteroids should only be administered to a subset of patients with septic shock who are unresponsive to fluid replacement and vasopressor therapy.
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PMID:Low-dose corticosteroids to treat septic shock: a critical literature review. 2213 28

The incidence of acute pancreatitis per 100,000 of population ranges from 5 to 80. Patients suffering from hemorrhagic-necrotizing pancreatitis die in 10-24% of cases. 80% of all cases of acute pancreatitis are etiologically linked to gallstone disease immoderate alcohol consumption. As of today no specific causal treatment for acute pancreatitis exists. Elevated C-reactive protein levels above 130,mg/L can also predict a severe course of acute pancreatitis. The essential medical treatment for acute pancreatitis is the correction of hypovolemia. Prophylactic antibiotics should be restricted to patients with necrotizing pancreatitis, infected necrosis or other infectious complications. However, as premature intracellular protease activation is known to be the primary event in acute pancreatitis. Severe acute pancreatitis is characterized by an early inflammatory immune response syndrome (SIRS) and a subsequent compensatory anti-inflammatory response syndrome (CARS) contributing to severity as much as protease activation does. CARS suppresses the immune system and facilitates nosocomial infections including infected pancreatic necrosis, one of the most feared complications of the disease. A number of attempts have been made to suppress the early systemic inflammatory response but even if these mechanisms have been found to be beneficial in animal models they failed in daily clinical practice.
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PMID:Differential roles of inflammatory cells in pancreatitis. 2232 Sep 16

Systemic inflammatory response syndrome (SIRS) is triggered by various factors such as surgical operation, trauma, burn injury, ischemia, pancreatitis and bacterial translocation. Sepsis is a SIRS associated with bacterial infection. SIRS and sepsis tend to trigger excessive production of inflammatory cytokines and other inflammatory molecules and induce multiple organ failure, such as acute lung injury, acute kidney injury and inflammatory cardiac injury. Epithelial and endothelial cells in some major organs express inflammatory receptors on the plasma membrane and work as alert cells for inflammation, and regulation of these alert cells could have a relieving effect on the inflammatory response. In inflammatory conditions, initial cardiac dysfunction is mediated by decreased preload and adequate infusion therapy is required. Tachyarrhythmia is a complication of inflammatory conditions and early control of the inflammatory reaction would prevent the structural remodeling that is resistant to therapies. Furthermore, there seems to be crosstalk between major organs with a central focus on the kidneys in inflammatory conditions. As an alert cell strategy, volatile anesthetics, sevoflurane and isoflurane, seem to have anti-inflammatory effects, and both experimental and clinical studies have shown the beneficial effects of these drugs in various settings of inflammatory conditions. On the other hand, in terms of intravenous anesthetics, propofol and ketamine, their current status is still controversial as there is a lack of confirmatory evidence on whether they have an organ-protective effect in inflammatory conditions. The local anesthetic lidocaine suppressed inflammatory responses upon both systemic and local administration. For the control of inflammatory conditions, anesthetic agents may be a target of drug development in accordance with other treatments and drugs.
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PMID:Alert cell strategy: mechanisms of inflammatory response and organ protection. 2522 71

A shortcut review was carried out to establish whether the presence of systemic inflammatory response criteria in emergency department patients with pancreatitis is predictive of the risk of death. Eight papers presented the best evidence to answer the clinical question. The review concludes that the presence of SIRS in emergency department patients with pancreatitis is associated with a higher risk of mortality.
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PMID:BET 1: SIRS criteria as a way of predicting mortality in acute pancreatitis. 2882 92

Almost every kind of inflammation in the human body is accompanied by rising C-reactive protein (CRP) concentrations. This can include bacterial and viral infection, chronic inflammation and so-called sterile inflammation triggered by (internal) acute tissue injury. CRP is part of the ancient humoral immune response and secreted into the circulation by the liver upon respective stimuli. Its main immunological functions are the opsonization of biological particles (bacteria and dead or dying cells) for their clearance by macrophages and the activation of the classical complement pathway. This not only helps to eliminate pathogens and dead cells, which is very useful in any case, but unfortunately also to remove only slightly damaged or inactive human cells that may potentially regenerate with more CRP-free time. CRP action severely aggravates the extent of tissue damage during the acute phase response after an acute injury and therefore negatively affects clinical outcome. CRP is therefore a promising therapeutic target to rescue energy-deprived tissue either caused by ischemic injury (e.g., myocardial infarction and stroke) or by an overcompensating immune reaction occurring in acute inflammation (e.g., pancreatitis) or systemic inflammatory response syndrome (SIRS; e.g., after transplantation or surgery). Selective CRP apheresis can remove circulating CRP safely and efficiently. We explain the pathophysiological reasoning behind therapeutic CRP apheresis and summarize the broad span of indications in which its application could be beneficial with a focus on ischemic stroke as well as the results of this therapeutic approach after myocardial infarction.
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PMID:Selective Apheresis of C-Reactive Protein for Treatment of Indications with Elevated CRP Concentrations. 3293 87


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