Phase Of Pancreatitis Research Articles

Atomic force microscopy of erythrocytes of patients with different severity of pancreatitis

Aim of the study was to prove the possibility of using red blood cell probe microscopy as a predictor of the development of pancreonecrosis.Material and methods. Atomic force microscopy was performed in 143 people (82 were male and 61 were female). The study was performed on an Integra Aura probe microscope (ZAO NT-MDT, Russia). Each erythrocyte was scanned for cell membrane and cell as a whole. A total of 940 red blood cells were examined. According to the severity of acute pancreatitis, patients are distributed in three groups. As a control group, 37 people without somatic pathology were examined. Diagnosis and treatment of patients was carried out in the public health institution “Design Bureau” Russian Railways-Medicine “Krasnoyarsk” from 2015–2019.Results. The study showed that the shape of erythrocyte does not depend on the severity of pancreatitis and does not change, however, structural changes of the membrane occur in the form of the formation of multiple erosions on its surface. The membrane is deformed, and its adhesion increases. These changes reduce the transport capacity of the blood, which, in our opinion, leads to an increase in the general intoxication of the body and to a deterioration in the condition of the patient.Conclusions. Apparently, pancreatic enzymes entering the free bloodstream in the first phase of pancreatitis cause not only oxidative stress, but also the reorganization and destruction of the erythrocyte membrane. The increase in membrane rigidity and deformation of the erythrocyte surface cytoskeleton against the background of increased adhesion seems to disrupt the gas transmission function of erythrocyte and microrheological properties of blood, which in turn disrupts the exchange of amino acids, lipids and detoxification capabilities of blood. The appearance of erythrocytes in the free bloodstream with the presence of erosion on the surface of the erythrocyte membrane can serve as a prediction of a non-favorable course of acute pancreatitis and a predictor of a possible transition of edema pancreatitis to pancreonecrosis.

Technical aspects of minimally invasive percutaneous approach for local complications of acute pancreatitis

Aim. To improve the results of treatment for patients with acute pancreatitis by optimizing the technique of performing percutaneous methods of drainage and sequestrectomy.Material and methods. We have considered experience of treating pancreatic necrosis in 257 patients, confirmed by computed tomography, intraoperatively, and postmortem examinations. Moderate severity pancreatitis was detected in 159 (61.9%) patients, severe – in 98 (38.1%) cases.Results. Small focal pancreatic necrosis was detected in 99 (62.3%) patients with moderate pancreatitis, large focal pancreatitis – in 60 (37.7%). Small-focal pancreatic necrosis was in 23 (23.5%) patients, large-focal – in 43 (43.9%), subtotal – in 29 (29.6%), total – in 3 (3.1%) among patients with severe acute pancreatitis. Percutaneous approach was used in combination with transluminal and open surgery in 59 (23%) patients. Infected necrosis was detected in 6 (3.8%) patients with acute moderate pancreatitis and in 44 (44.9%) patients with severe pancreatitis, sepsis – in 12 (12.2%) patients. 27 (10.5%) patient have died from septic shock in the first phase of pancreatitis, included 14 (5.4%) cases after surgery. Overall 41 (16%) patients with pancreatic necrosis have died.Conclusion. Compliance of stages in surgical treatment technology allows optimally combine it with transluminal sequestrectomy, reduces surgical trauma, eliminates additional risks of open approach associated with complications and deaths.

Loss of Tlr3 and its downstream signaling accelerates acinar cell damage in the acute phase of pancreatitis

Loss of Tlr3 and its downstream signaling accelerates acinar cell damage in the acute phase of pancreatitis

Role of heparin on serum VEGF levels and local VEGF contents in reducing the severity of experimental severe acute pancreatitis in rats

Objective.The aims of this study were to examine the effects of prophylactic heparin treatment during taurocholate-induced pancreatitis in rats and its impact on serum VEGF levels and local VEGF contents within the pancreas. Methods.Severe acute pancreatitis (SAP) was induced by injecting 4% sodium taurocholate into the pancreatic duct. Heparin at a dose of 150 IU/kg s.c. was administered 30 min before the operation. The rats were sacrificed 1 h, 3 h, 6 h and 12 h (n = 5 per time point) after the onset of pancreatitis. The severity of pancreatitis, serum VEGF levels and local VEGF contents were evaluated with and without heparin pretreatment. Results.The serum VEGF levels increased at an early phase of pancreatitis, and the highest level was found at 12 h after inducing pancreatitis. The gray value of the local VEGF showed a remarkable increase from the onset of the pancreatitis. However, the gray value of VEGF did not show an increase over time but maintained a high level during the entire process. Prophylactic heparin treatment significantly improved the morphologic changes, myeloperoxidase (MPO), TNF-α and malondialdehyde (MDA) activities. Meanwhile, it decreased the serum VEGF levels and the contents of VEGF within the pancreatic tissue. Conclusions.The present study suggests that prophylactic heparin ameliorates the severity of taurocholate-induced pancreatitis via its anti-inflammatory properties. These protective effects may be partly due to decreasing serum VEGF levels and VEGF contents within the pancreas.

Congenital Bochdalek hernia presenting with acute pancreatitis in an adult

Posterolateral diaphragmatic hernias (Bochdalek) are a common congenital anomaly usually presenting in the neonatal period or infancy. Although well documented, their presentation in adulthood is uncommon. 1-3 We describe the case of an adult Bochdalek hernia presenting with acute pancreatitis and intermittent gastric volvulus.

Role of cholecystokinin-A (CCK-A) receptor in pancreatic regeneration after pancreatic duct occlusion: a study in rats lacking CCK-A receptor gene expression.

We examined the role of the cholecystokinin-A (CCK-A) receptor in acute inflammatory and regenerative stages of experimental pancreatitis using a rat model lacking the CCK-A receptor [Otsuka Long-Evans Tokushima Fatty (OLETF) rats]. OLETF and control [Long-Evans Tokushima Otsuka (LETO)] rats were prepared with an internal bile fistula and with obstruction of pancreatic flow and were sacrificed 1-14 days later. Histological examination was performed, and changes in pancreatic wet weight, protein concentration, CCK-A and -B receptor mRNA levels, tyrosine kinase activities, and plasma amylase and CCK levels were determined. The plasma amylase level showed a transient increase on day 1, the CCK level remained at high levels throughout, and tyrosine kinase activity was increased significantly on day 3 but declined thereafter. These parameters were comparable for both strains during the acute inflammatory stage. However, no regenerative findings were observed by histological examination and the protein concentration in the pancreas was significantly lower in OLETF rats on days 7-14, during which time regeneration was completed in LETO rats. These observations indicate that the absence of the CCK-A receptor did not modify the acute phase of pancreatitis but significantly retarded regeneration of the pancreatic tissue.

Analysis of Potential Risk Factors Associated with the Development of Pancreatitis in Phase I Patients with AIDS or AIDS-Related Complex Receiving Didanosine

Phase I dose-escalating trials of didanosine revealed dose-limiting toxicities, including pancreatitis, and established a total daily dose of 12.5 mg/kg/day as the maximum tolerated dose. Clinical and pharmacokinetic data of 61 patients from two trials were analyzed to further evaluate the risk of pancreatitis: 1 (6.3%) of 16 patients who received < 500 mg/day didanosine, 2 (13.3%) of 15 who received 500-750 mg/day, and 15 (50%) of 30 who received > 750 mg/day developed pancreatitis (P < .001). A relationship between risk of pancreatitis and steady-state plasma concentrations of didanosine and age was also observed, suggesting that knowledge of didanosine pharmacokinetics provided additional information regarding risk of toxicity. Further confirmation of these findings will be necessary to determine if the risk factors for pancreatitis remain the same at lower doses currently used.

Monitoring serum tryptic activity and effect of trypsin inhibitor on rat acute pancreatitis.

The effect of a novel synthetic trypsin inhibitor, 4-(2-succinimidoethylthio)-phenyl 4-guanidinobenzoate methanesulfonate (E3123), on severe acute pancreatitis was studied in trypsin-taurocholate-induced acute experimental pancreatitis in rats. Rats were divided into four groups according to difference of subdivided doses of E3123 with fixing the total dose at 3 mg/kg body weight. Group A: 1.5 mg/kg of E3123 subcutaneously (SC) each at 1 h before and after induction of pancreatitis. Group B: 1 mg/kg SC each at 1 h before, 1 and 3 h after induction. Group C: 1.5 mg/kg SC each at 1 and 3 h after induction. Group D: 1.5 mg/kg SC each at 3 and 5 h after induction of pancreatitis. The survival rate at 24 h was significantly improved in group B (77% in group B, vs. 36% in paired control; p < 0.01) and in group C (70 vs. 38%; p < 0.05), but not in group A or D. Residual tryptic activity of serum alpha 2-macroglobulin trypsin complex (alpha 2M-TRY) was reduced after the injection of E3123 though immunoreactive trypsin remained unchanged in the early phase of pancreatitis. The reduction of alpha 2M-TRY reflected the inhibitory capacity of E3123 in plasma. E3123 showed favorable effects on the initial stage of severe acute pancreatitis and the effects were probably based on the inhibition of alpha 2M-TRY activity in serum.

Simultaneous determinations of pancreatic phospholipase A2 and prophospholipase A2 in various pancreatic diseases.

Pancreatic phospholipase A2 (PLA2) is secreted into the pancreatic juice by pancreatic acinar cells as a proenzyme (proPLA2), which is activated by trypsin. Radioimmunoassays with monoclonal antibodies to PLA2 and proPLA2 were used to examine the serum PLA2 and proPLA2 levels simultaneously in patients with various pancreatic diseases. In healthy subjects, proPLA2 proved to be the major form of the enzyme. The serum PLA2 level were found to be significantly increased in patients with acute pancreatitis, the active phase of chronic relapsing pancreatitis, and the early stage of pancreatic cancer. In the terminal stage of pancreatic cancer the serum PLA2 level became low. In patients with chronic pancreatitis, significant correlations were observed between the levels of factors evaluated by the secretin test and the serum total PLA2 and proPLA2 level, but not the PLA2 level. The serum PLA2 and proPLA2 concentrations, and the proportion of proPLA2 in the total, were within normal ranges in patients with liver cirrhosis, hepatocellular carcinoma, and chronic renal failure. These results suggest that simultaneous measurements of serum PLA2 and proPLA2 are clinically useful for diagnosis and monitoring of the active phase of pancreatitis.

Lactoferrin in Acute Necrotizing Pancreatitis

Lactoferrin, as measured in the pancreatic juice, has been thought to be of diagnostic value in chronic pancreatitis, but due to the hazards in cannulation of the pancreatic duct in the acute phase of pancreatitis the behavior of lactoferrin has remained obscure. In this study, lactoferrin levels were studied in pancreas tissue specimens obtained in ablative surgery for acute necrotizing pancreatitis (ANP) and in serum samples. A higher pancreatic lactoferrin content was found in ANP than in normal pancreas. Lactoferrin seemed not to leak from a necrotic pancreas in any considerable amounts into the circulation, as no differences were found in serum lactoferrin concentrations between ANP and controls. It remains an open question whether the lactoferrin increase is only an unspecific reaction in inflammation or is something specific for pancreatitis.

RECURRING PANCREATITIS AND ASSOCIATED STENOSIS OF THE COMMON BILE DUCT

THE DIAGNOSIS of various phases of pancreatitis and their proper management have been long-recognized problems.1Little has been added to the description of the clinical features of the acute disease since that of Fitz in 1889.2These features are sufficiently characteristic in the acute and severe episodes of pancreatitis to generally permit reliable diagnosis. The less severe forms of the disease were, and are, frequently not recognized. Only since confirmatory laboratory tests have been readily available3has the frequency of pancreatitis become generally recognized. The severe forms of the disease as originally described by Fitz, and generally considered typical, are the fulminating episodes of pancreatitis. Less severe inflammatory reaction within the pancreas produces upper abdominal pain, various gastrointestinal symptoms, and no reliably detectable changes in the blood constituents or gastrointestinal secretions. The anatomical location of the gland, laboratory tests of function that indicate only extensive changes, and