Inhibition of Cyclooxygenase-2 in Experimental Severe Acute Pancreatitis

Almeida, Jorge; Jukemura, José; Coelho, Ana Maria M.; Patzina, Rosely Antunes; Machado, Marcel Cerqueira César; Cunha, José Eduardo Monteiro da

doi:10.1590/s1807-59322006000400005

Cited by 25 publications

(18 citation statements)

References 44 publications

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“…Protective effect of nonsteroidal anti-inflammatory drugs (NSAIDs) against the death outcome that was observed in our study is in accordance with recent reports on effectiveness of these drugs in prevention of acute pancreatitis after endoscopic retrograde cholangiopancreatography (ERCP) (9)(10)(11). It has been also observed in animal studies of acute pancreatitis that cyclooxygenase (COX) enzyme, especially isoform COX -2 plays a significant role in early phase of inflammation in acute pancreatitis (12,13). Phospholipase A2, the enzyme, which produces substrate for COX, is also elevated in serum of patients with acute pancreatitis, and may contribute to the development of acute and chronic complications of this disease (14,15) through production of prostaglandins.…”

Section: Discussionsupporting

confidence: 92%

Analysis of Treatment-Related Factors Affecting Mortality in Patients with Severe Necrotizing Acute Pancreatitis

Praznik¹,

Spasić²,

Radosavljevic³

et al. 2016

Acta Facultatis Medicae Naissensis

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The aim of the paper was to determine the factors related to the initial therapy that may contribute to death from severe necrotizing acute pancreatitis and to analyze their clinical importance as well as possible additive effects.A retrospective case-control study included all adult patients treated for severe necrotizing acute pancreatitis in the Clinical Center of Kragujevac, Serbia, during the five-year period (2006-2010.). The cases (n = 41) were patients who died, while the controls (n = 69) were participants who survived. In order to estimate the relationship between potential risk factors and observed outcome, crude and adjusted odds ratios (OR) with 95 % confidence intervals (CI) were calculated in logistic regression models.Significant association with observed outcome was shown for the use of gelatin and/or hydroxyethyl starch (adjusted OR 12.555; 95 % CI 1.150-137.005), use of albumin (adjusted OR 27.973; 95 % CI 1.741-449.373), use of octreotide (adjusted OR 16.069; 95 % CI 1.072-240.821) and avoiding of enteral feeding (adjusted OR 3.933; 95 % CI 1.118-13.829), while the use of nonsteroidal anti-inflammatory drugs had protective role (adjusted OR 0.057; 95 % CI 0.004-0.805).The risk of death in patients with predicted severe necrotizing acute pancreatitis could be reduced with avoidance of treatment with colloid solutions, albumin and octreotide, as well as with an early introduction of oral/enteral nutrition and use of nonsteroidal anti-inflammatory drugs. O r i g i n a l a r t i c l e I NT ROD U CT I ONSevere necrotizing acute pancreatitis is a multisystem disorder, characterized by pancreatic and/or peripancreatic tissue necrosis and widespread inflammatory response leading to single or multiple organ dysfunction which does not resolve within the first 48 hours (the so-called persistent organ failure according to revised Atlanta criteria 2012) (1). It occurs in about 15-20 % of all cases of acute pancreatitis (AP) and is considered the most serious disease course due to high complications and death rates despite recent diagnostic and therapeutic advancements; the mortality may be particularly high if necrotic areas become infected, exceeding 50 % when infection and persistent organ failure develop during the first week of the illness (1-4).In the light of these facts, taking also into account variable and unpredictable course of AP, current recommendations emphasize appropriate early management based on careful initial risk assessment in all patients presenting with AP on admission to hospital (1, 4). Dealing with this issue, previous studies have identified numerous factors that are only associated with or may contribute to the development of severe disease and increased mortality rate in patients with AP. Many of them are well-documented, such as older age, obesity, idiopathic AP, important comorbidities, as well as certain clinical, laboratory and radiologic parameters of disease severity on initial evaluation (signs of systemic inflammatory response syndrome, hypotension, altered mental sta...

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Section: Discussionsupporting

confidence: 92%

Analysis of Treatment-Related Factors Affecting Mortality in Patients with Severe Necrotizing Acute Pancreatitis

Praznik¹,

Spasić²,

Radosavljevic³

et al. 2016

Acta Facultatis Medicae Naissensis

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“…Several substances have been tested in various studies in an attempt to block the effects of inflammatory mediators that have an established role in the pathogenesis of AP. 26 The inhibition of TNF-> reduced the local and systemic inflammatory response, which, in turn, reduced systemic inflammation. These findings provide a possible improvement in the treatment of AP.…”

Section: Discussionmentioning

confidence: 99%

Ameliorative Effect of Adalimumab on Experimentally Induced Acute Pancreatitis in Rats

Yılmaz¹,

Tekekoglu²,

Herek³

et al. 2010

Pancreas

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“…Cytokines are released from monocytes and macrophages [22]. In order to prevent the pancreatic damage caused by released free oxygen radicals and cytokines, substances such as pentoxifylline [23], cyclooxygenase inhibitors [24], melatonin [25,26], allopurinol [27] and octreotide [28] were used in experimental studies. In this study, acute necrotizing pancreatitis was induced by retrograde infusion of taurocholic acid into the biliopancreatic duct, as Aho et al [29,30] described previously.…”

Section: Discussionmentioning

confidence: 99%

Melatonin Modulates the Severity of Taurocholate-Induced Acute Pancreatitis in the Rat

Gülben¹,

Özdemir²,

Berberoğlu³

et al. 2009

Dig Dis Sci

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The aim of this study was to investigate the effects of melatonin on serum amylase, tumor necrosis factor-alpha (TNF-alpha) and histological changes in rats with taurocholate-induced acute pancreatitis. Thirty male Wistar rats were randomly divided into three groups; group 1, group 2 and group 3 were enrolled as melatonin, control and sham groups, respectively (n = 10 per group). Acute pancreatitis was induced by 1 ml/kg body weight using 5% taurocholate injection into the biliopancreatic duct in groups 1 and 2 after clamping the hepatic duct. Those in group 1 received 50 mg/kg body weight melatonin by intraperitoneal (i.p.) injection. Group 2 received physiological saline i.p. at the same dose. Group 3 solely underwent laparotomy with cannulation of the biliopancreatic duct. Twenty-four hours after the intervention, the rats were killed, and serum samples were collected to measure amylase and TNF-alpha levels. Simultaneously, pancreatic tissues were removed, stained with hematoxylin-eosin and examined under a light microscope. Serum amylase and TNF-alpha levels were significantly lower in the melatonin group compared to the controls (P < 0.001). The total histological score, including edema, inflammation, perivascular infiltrate, acinar necrosis, fat necrosis and hemorrhage, was also significantly lower in the melatonin group as compared to the control (P < 0.0001). In conclusion, melatonin is potentially capable of reducing pancreatic damage by decreasing serum TNF-alpha levels in taurocholate-induced acute pancreatitis in rats. This result supports the idea that melatonin might be beneficial in ameliorating the severity of acute pancreatitis.

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Inhibition of Cyclooxygenase-2 in Experimental Severe Acute Pancreatitis

Cited by 25 publications

References 44 publications

Analysis of Treatment-Related Factors Affecting Mortality in Patients with Severe Necrotizing Acute Pancreatitis

Analysis of Treatment-Related Factors Affecting Mortality in Patients with Severe Necrotizing Acute Pancreatitis

Ameliorative Effect of Adalimumab on Experimentally Induced Acute Pancreatitis in Rats

Melatonin Modulates the Severity of Taurocholate-Induced Acute Pancreatitis in the Rat

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