Severe Form Of Acute Pancreatitis Research Articles

Serum profiles of E-selectin, interleukin-10, and interleukin-6 and oxidative stress parameters in patients with acute pancreatitis and nonpancreatic acute abdominal pain.

Excessive inflammatory response is one of the major causes of early mortality in acute pancreatitis (AP). To evaluate the serum profiles of E-selectin, interleukin (IL)-6, and IL-10 along with their correlation to the markers of oxidative stress and neutrophil activation in patients with AP and patients with nonpancreatic acute abdominal pain (NPAAP). This prospective clinical study included 56 patients with AP (28 with mild AP and 28 with severe AP) as well as 15 patients with NPAAP. Serum concentrations of E-selectin, IL-10, and IL-6 and plasma concentrations of polymorphonuclear leukocyte elastase (determined on days 1-3, 5, and 10 after admission) were the highest in severe AP during the first 3 days and then declined. At day 10, the E-selectin level in severe AP was still higher than that in mild AP, and the IL-10 concentration increased again. There was no elevation in the E-selectin concentration in NPAAP patients, and IL-10 levels remained unchanged in mild AP. Oxidative stress, measured by serum malondialdehyde and 4-hydroxyalkenals levels, was the most pronounced in severe AP. The serum E-selectin concentration is markedly elevated in severe AP and is less in mild AP but not in NPAAP. It may result from stimulation with different inflammatory mediators or indicate vascular endothelium injury mediated by oxidative stress, especially in the severe form of AP.

Serum Profiles of Interleukin-18 in Different Severity Forms of Human Acute Pancreatitis

Background: Interleukin 18 (IL-18) is a new mediator and modulator of the immune response; its role in acute pancreatitis (AP), however, has not yet been fully explained. The aim of our study was to evaluate the profile IL-18 serum concentrations in the course of acute pancreatitis. Methods: The prospective study involves 30 patients with AP ( n = 15 with mild AP and n = 15 with severe AP) as well as 10 healthy subjects. AP severity was defined according to Ranson's and Balthazar's criteria, supplemented by serum CRP concentration measurements. In the course of hospitalization, 2 patients with severe AP died. Serum IL-18 and plasma polymorphonuclear leukocyte elastase (PMN-E) concentrations were measured at admission (day 1) and on days 2, 3, 5 and 10. Results: In both the mild and the severe forms of AP, serum IL-18 concentration was significantly higher than in the healthy controls. In severe AP, serum IL-18 reached the highest levels in all observed periods compared to that in patients with mild AP. Significant correlations, calculated for day 1, were found between serum IL-18 and plasma PMN-E (Rs = 0.514, P < 0.001) and between IL-18 and CRP (Rs = 0.463, P < 0.001) levels. Conclusions: Serum profile IL-18 during AP indicates that this cytokine was released early after AP onset and may play the key role in inflammatory and immune response. Positive correlation between serum IL-18 and commonly known early prognostic markers of AP severity suggest that serum IL-18 concentrations may represent another early marker indicating severe course of AP.

The role of antibiotic treatment in severe form of acute pancreatitis: A randomized prospective study

The role of antibiotic treatment in severe form of acute pancreatitis: A randomized prospective study

The role of antibiotic treatment in severe form of acute pancreatitis: A randomized prospective study

The role of antibiotic treatment in severe form of acute pancreatitis: A randomized prospective study

Management of fluid collections and necrosis in acute pancreatitis.

According to the Atlanta classification, the most widely accepted clinically based classification system for acute pancreatitis, four pathologic entities of fluid collections and necrosis are recognized. Acute fluid collections occur early as an exudative reaction to the pancreatic inflammation, have no fibrous wall, and resolve spontaneously. Pancreatic necrosis, the most severe form of acute pancreatitis, is diagnosed on dynamic contrast-enhanced computerized tomography and requires early aggressive cardiorespiratory resuscitation, nutritional support, and appropriate systemic antibiotics to prevent superinfection. Development of infection (infected necrosis) is the indication for operative debridement, preferably as late in the course of the disease as possible. Acute pseudocysts are collections of pancreatic, enzyme-rich fluid caused by pancreatic ductal disruption that occur 3 to 6 weeks after onset of acute pancreatitis and have a well-defined, nonepithelial fibrous wall. If communication with the ductal system is present, internal enteric drainage (either operative or endoscopic) is more effective; if communication is not present, the pseudocysts are amenable to percutaneous drainage. A pancreatic abscess is an infected, circumscribed peripancreatic collection, associated with minimal or no parenchymal necrosis, that occurs late (4 to 6 weeks) after onset of severe pancreatitis and may represent an infected pseudocyst; percutaneous drainage is the treatment of choice.

Inhibition of bradykinin B2 receptor preserves microcirculation in experimental pancreatitis in rats.

The effect of B2 receptor bradykinin antagonist icatibant on postcapillary leukostasis, microcirculatory stasis, and tissue necrosis was studied in acute pancreatitis. In rats, pancreatitis was induced by intraductal injection of sodium taurocholate (ST), intravenous caerulein and intraductal infusion of glucodeoxycholic acid (GDOC), or intravenous caerulein infusion alone. Intravital pancreatic microcirculation was observed. Icatibant or vehicle was given 30 min before induction of pancreatitis. In ST pancreatitis, the number of perfused capillaries increased in icatibant-pretreated rats (77% vs. 0% for controls, P < 0.001). Capillary flow was preserved in icatibant-treated rats; total stasis was observed in controls. Mean venular leukocyte adherence decreased in icatibant-treated rats (26% vs. 74% for controls, P < 0.001), and median histopathologic score was reduced (icatibant vs. controls, 5.0 vs. 12 points, respectively; P < 0.01). Kinase II inhibitor captopril or exogenous bradykinin in addition to an otherwise effective dosage of icatibant resulted in microcirculatory stasis, extensive venular leukocyte adherence, and severe histological damage. With a 100 times greater icatibant dosage, this adverse effect was compensated. The beneficial effects of icatibant were also observed in intermediate pancreatitis (caerulein + GDOC). In ST and intermediate pancreatitis, icatibant preserved microcirculation, reduced venular leukocyte adherence, and prevented pancreatic tissue damage. B2 receptor bradykinin-mediated postcapillary leukostasis plays an important role in the pathogenesis of severe forms of acute pancreatitis.

CAPAP in acute pancreatitis: just another marker or real progress?

See article on page97 There are no pathognomonic symptoms in acute pancreatitis. In reaching a diagnosis the patient’s history, physical findings, and serum amylase or lipase concentrations have to be...

Neopterin in acute pancreatitis.

Activation of the cellular immune system may play a role in the pathogenesis of acute pancreatitis (AP); it has recently been proposed that excessive leukocyte stimulation may lead to the most severe forms of AP. The aim of this study was to investigate serum neopterin, a useful in vivo marker of macrophage activation, in mild and severe AP and its relationship with other markers of leukocyte activation, such as interleukin-6 (IL-6) and tumor necrosis factor (TNF). Serum levels of neopterin (mmol/ml), IL-6 (pg/ml), and TNF (pg/ml) were measured on the 1st and 7th day of hospitalization in 17 patients with severe AP and 24 with mild AP. Severe AP was defined in accordance with the Atlanta criteria: all patients have necrosis at contrast-enhanced computerized tomography scan. Day 1: Neopterin and IL-6 levels were significantly higher in severe than in mild AP and normal controls; mild AP values were also significantly higher than in normal controls. The best neopterin cutoff level we obtained (30 mmol/ml) reached a specificity of 76% and a sensitivity of 46% in distinguishing severe from mild AP. Day 7: Neopterin was significantly higher in severe AP than in mild AP and in normal controls; no difference was seen between mild AP values and normal controls; neopterin serum levels were significantly higher on day 7 than on day 1 in severe AP but not in mild AP; in both groups of patients IL-6 was significantly higher on day 1 than on day 7. Using a neopterin cutoff level of 40 mmol/ml, we found specificity and sensitivity value of 92% in differentiating severe from mild AP. With regard to TNF values, no difference was seen on day 1 and 7 in the two groups of patients in comparison with normal controls. Neopterin serum values did not correlate with IL-6 and TNF on either day. These results confirm the activation of the cellular immune system in AP. Initially enhanced NEOP and IL-6 serum levels reflect the severity of the disease; neopterin may be considered a reliable prognostic indicator also at a distance from AP onset because its levels increase during the 1st week of AP in patients with severe forms only.