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

The role of early CT scanning in acute gallstone pancreatitis remains ill defined. The purpose of our study was to: 1) determine whether our previously identified admission prognostic factors for gallstone pancreatitis [white blood cell (WBC) count > or = 14.5 x 10(9)/L, blood urea nitrogen (BUN) > or = 12 mmol/L, Acute and Chronic Health Evaluation II score > or = 5, glucose > or = 150 mg/dL, and heart rate > or = 100 beats/min)] correlate with the severity of pancreatic inflammation on CT scan, and 2) to determine the utility of early CT scanning in the management of gallstone pancreatitis. Admission clinical and laboratory variables were collected prospectively. Early CT scan findings were graded using the Balthazar scoring system and subgrouped into mild-moderate (Balthazar grades A-C) or severe (grades D and E) by a radiologist blinded to the patients' clinical status. Ninety-seven patients underwent surgery during their initial hospitalization without preoperative CT scanning. Four had operative complications (4%). Forty-two patients underwent early CT scan (grade A, 19%; B, 5%; C, 21%; D, 10%; and E, 45%), but only four (all grade E) had surgery delayed because of necrotizing pancreatitis, abscess, or pseudocyst. All four had persistent abdominal pain. There was one (2.5%) operative complication in the CT group and no deaths. Admission WBC count > or = 14.5 x 10(9)/L and BUN > or = 12 mmol/L correlated with severe pancreatitis (grades D and E) on CT (P < .05). We conclude that in patients with gallstone pancreatitis, 1) admission WBC count > or = 14.5 x 10(9)/L and BUN > or = 12 mmol/L correlate with the severity of pancreatic inflammation on CT scan, and 2) CT scan findings rarely influence management decisions and CT is therefore unnecessary, except in the minority of patients with objective indications of severe or unresolving pancreatitis.
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PMID:Early computed tomography is rarely necessary in gallstone pancreatitis. 932 70

A severe acute pancreatitis was produced by intraperitoneal injection of lipopolysaccharide (LPS) in rats with preexisting hemorrhagic and necrotizing pancreatitis induced by retrograde injection of a 5% taurocholate plus 1% trypsin solution into the pancreatic duct. Mortality and time-course changes in pancreatic, hepatic, renal and pulmonary functions, and organ myeloperoxidase (MPO) levels were examined in this model. LPS at an intraperitoneal dose of 30 mg/kg, which scarcely caused death and had no marked effect on serum parameters and organ MPO levels in rats without pancreatitis, increased the mortality in rats with taurocholate plus trypsin-induced pancreatitis. Pancreatic weight and ascitic volume increased in rats with taurocholate plus trypsin-induced pancreatitis regardless of the presence or absence of LPS. Serum amylase and lipase levels were also significantly increased in rats with induced pancreatitis, but was higher in the group given LPS. Serum glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), blood urea nitrogen (BUN) and creatinine levels were significantly elevated in LPS-treated rats with induced pancreatitis, whereas levels in rats with induced pancreatitis not given LPS were only slightly elevated. Renal weight was also significantly increased in rats with induced pancreatitis despite the presence or absence of LPS. In LPS-treated rats with induced pancreatitis, the arterial oxygen pressure, pulmonary weight and pulmonary MPO level were significantly elevated. However, the MPO level in the kidney in these rats was not different from that in control rats, indicating that the renal dysfunction was not produced by the infiltration of neutrophils into the kidney. Increase in the pancreatic MPO level was observed in rats with induced pancreatitis, but combination treatment with LPS did not raise it. Protective effects of prophylactic treatment of 2-(3-methylsulfonylamino-2-oxo-6-phenyl-1,2-dihydro-1-pyridyl)-N-( 3,3,3-trifluoro-1-isopropyl-2-oxopropyl)acetamide (compound 1), a neutrophil elastase inhibitor, and trifluoroacetyl-L-lysyl-L-alaninanilide hydrochloride (compound 2), a pancreatic elastase inhibitor, on mortality were also examined in this model. Results were compared with that of the combined treatment of compound 1 and compound 2. In LPS-treated rats with taurocholate plus trypsin-induced pancreatitis, the combined treatment of compound 1 (2 mg/kg/h) and compound 2 (30 mg/kg/h) significantly reduced mortality, whereas single treatment of compound 1 or compound 2 did not show the beneficial effect. These results suggest that marked hepatic and renal dysfunction accompanies pancreatitis in this pancreatitis model rats, which may be good models for acute pancreatitis in humans. It is also suggested that neutrophil and pancreatic elastases may be synergistically involved in the pathogenesis of acute pancreatitis in this model.
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PMID:Protective effect of the combined treatment of pancreatic and neutrophil elastase inhibitors on acute pancreatitis elicited by lipopolysaccharide in rats given intraductal injection of taurocholate plus trypsin. 965 Aug 10

Protective effect of trifluoroacetyl-L-lysyl-L-alaninanilide hydrochloride (compound 1), a pancreatic elastase inhibitor, on three types of acute pancreatitis models was examined in rats. Mild, moderate and severe acute pancreatitis were induced by cerulein, the closed duodenal loop method and retrograde injection of a taurocholate plus trypsin solution into the pancreatic duct, respectively. Intravenous infusion of compound 1 at a dose of 30 mg/kg/hr resulted in lower increases in serum amylase, lipase, blood urea nitrogen (BUN) and creatinine levels in rats with mild cerulein-induced edematous pancreatitis. Compound 1 had no beneficial effect on pancreatitis in rats with moderate pancreatitis. In rats with severe pancreatitis, prophylactic treatment of compound 1 (30 mg/kg/hr) reduced both elevated serum BUN level and ascitic volume, and it histologically inhibited the extent of pancreatic edema and hemorrhage. These results suggest that pancreatic elastase is partially responsible for pancreatic edema and hemorrhage exhibited by rats with severe acute pancreatitis.
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PMID:Protective effect of a pancreatic elastase inhibitor against a variety of acute pancreatitis in rats. 971 66

We retrospectively reviewed the charts of 54 human immunodeficiency virus (HIV) infected patients or acquired immunodeficiency syndrome (AIDS), who were hospitalized at the Bronx-Lebanon Hospital Center with acute pancreatitis between January 1993 and December 1995. Nineteen were female and 35 were male patients. Thirty-five (65%) of 54 patients were younger than 40 years (average age, 42 years). Forty-eight (89%) of the patients had a CD4 count of <200 units/ml of blood. Seventeen (32%) patients died either of complications of acute pancreatitis or of underlying disease. The conventional prognostic criteria used to assess the severity of pancreatitis, including Ranson's and Imrie's criteria and the APACHE II system, were applied. We determined that these criteria were not appropriate to our HIV/AIDS patients. Only serum calcium levels at 48 h after admission and serum creatinine and blood urea nitrogen (BUN) at admission and at 48 h after admission had significant p values (<0.05). We believe that the predictors commonly used to identify the severity of pancreatitis were not useful in these patients because of their low CD4 counts and preexisting liver and renal disease.
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PMID:Predictors of the severity of acute pancreatitis in patients with HIV infection or AIDS. 1043 59

Severe acute pancreatitis is a two-phase systemic disease. The first phase is a clinical response resulting from systemic effects of proinflammatory mediators called SIRS (systemic inflammatory response syndrome), that may lead to multiple organ failure and death. The second phase, if the process is not reversed by natural defences or treatment, may be accompanied by local complications such as infected pancreatic necrosis. The severity of the disease must be established early to identify patients requiring intensive monitoring and support. The clinico-biochemical score (Ranson score) is about 80% accurate at 48 hours but is not accurate before this time; the APACHE II system has the sensitivity to predict severe pancreatitis in 61% of patients on admission. Although not perfect, the prognostic systems of severity remain better than clinical judgement. SIRS followed by local complications is accompanied by increased energy requirements and, with the absence of oral intake, a persistently negative nitrogen balance and mineral and micronutrient deficiencies. Thus, early nutritional support is indicated. Formerly, total parenteral nutrition was the standard practice for providing exogenous nutrients avoiding pancreatic stimulation. The use of early enteral feeding has recently been evaluated. Gastric atony and obstruction of the duodenum by pancreatic oedema or necrosis have been overcome by delivering enteral nutrition to the jejunum, distal to the ligament of Treitz; in this position, regular diets do not stimulate pancreatic secretions. The efficacy, tolerance, clinical outcome and cost of enteral nutrition suggest that this feeding route should be preferred in patients with severe acute pancreatitis.
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PMID:[Nutrition in acute pancreatitis]. 1058 62

Polyglucose dialysis solution (PG-DS) decreases serum amylase activity owing to interference in the analytical method. The interference can make it difficult to diagnose pancreatitis. Our aim was to check whether, during PG-DS administration, serum lipase activity changes simultaneously with serum amylase activity, and, if so, what the reason is for the detected change. Studies were started in 14 continuous ambulatory peritoneal dialysis (CAPD) patients in whom 7.5% PG-DS was applied for the overnight exchange. In addition to standard clinical and laboratory data, serum activity of lipase and of total amylase were evaluated at 1.6 +/- 0.8 months before PG-DS introduction (period I, n = 14), after 1.2 +/- 0.6 months of PG-DS administration (period II, n = 14), after 4.4 +/- 0.8 months of PG-DS administration (period III, n = 11), after 8.8 +/- 2.2 months of PG-DS administration (period IV, n = 9), and at 2.0 +/- 0.6 months after PG-DS discontinuation (period V, n = 11). The PG-DS was also added to serum from CAPD patients with known activity of amylase and of lipase. Immediately and 3 hours after PG-DS addition, a significant decrease in total amylase activity was seen; lipase activity was unchanged. In consecutive study periods, the results (median and range) were: for lipase activity--50 U/L (12-131 U/L), 59 U/L (25-160 U/L; p < 0.05 vs period I), 73 U/L (26-158 U/L; p < 0.05 vs period I), 66 U/L (30-203 U/L; p < 0.05 vs period I), and 44 U/L (15-112 U/L); for amylase activity--81 U/L (43-249 U/L), 14 U/L (5-82 U/L; p < 0.05 vs period I and period V), 15 U/L (5-192 U/L; p < 0.05 vs period I), 15 U/L (10-93 U/L; p < 0.05 vs period I and period V), and 118 U/L (4-221 U/L). An increase in serum lipase activity over the normal range (27-65 U/L) was not accompanied by clinical symptoms of pancreatic dysfunction, but rises were simultaneously shown in blood urea nitrogen, in serum level of creatinine and of total calcium, and in calcium phosphorus product. Our results confirm PG-DS influence on amylase determinations, exclude PG-DS interference in lipase measurements, and indicate that long-term PG-DS administration influences pancreatic exocrine function at a subclinical level.
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PMID:Polyglucose dialysis solution influences serum activity of amylase and of lipase differently. 1104 74

The metabolism of acute pancreatitis is characterized by hypermetabolism and catabolism. Evidence for glucose intolerance occurs in anywhere from 40 to 90% of cases and urine urea nitrogen may increase up to 40 g/day. The most important aspect when considering nutritional therapy is determining the severity of the pancreatitis. The APACHE-II-scoring-system and the time honored Ranson criteria are useful for differentiating severe from mild pancreatitis. Despite some limitations in sensitivity and specificity, studies have suggested that patients with 2 or less Ranson criteria and an APACHE-II-score of 9 or less have mild pancreatitis, while patients with 3 or more Ranson criteria and an APACHE-II-score of 10 or more have severe pancreatitis. Evidence of organ failure on clinical presentation and pancreatic necrosis on dynamic CT scan are also important factors in determining severity of pancreatitis and are probably the two major indicators of patient outcome. Only 3 prospective randomized controlled trials have compared enteral to parenteral nutrition for pancreatitis. All studies described successful use of enteral feeding without exacerbating the disease process although a mild stimulation of exocrine pancreatic secretion could not be prevented, even when the tube was placed below the ligament of Treitz. Kalfarentzos [11] and McClave [14] could show that hyperglycemia was worse in the parenteral feeding patients compared to the enteral feeding group and Windsor [24] concluded with respect to the results of his study, that enteral feeding modulates the inflammatory response in acute pancreatitis. Conclusions regarding the use of enteral or parenteral nutrition in acute pancreatitis are difficult to form, as there is a need of more prospective studies. As ileus may be a problem in patients with greater severity of pancreatitis, limiting the application of early enteral feeding, the route of nutritional support should be determined by the clinical course and the severity of the disease.
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PMID:[Enteral nutrition in acute pancreatitis]. 1122 88

Type B lactic acidosis is a rare and often fatal complication seen in patients receiving the nucleotide analogues zidovudine, stavudine, didanosine, and lamivudine. We describe a case of a 51-year-old human immunodeficiency virus (HIV)-positive woman receiving three nucleotide analogues. She presented with nausea, vomiting, abdominal pain, and hepatic steatosis. Signs of mitochondrial toxicity were demonstrated by diffuse myopathy and pancreatitis. Serum riboflavin levels documented a deficiency that was treated with 50 mg of riboflavin daily. Immediately after treatment, serum blood urea nitrogen level, lactic acid levels, and arterial blood pH all returned to normal values. Her signs of mitochondrial toxicity also improved after treatment with riboflavin. Successful reversal of the patient's type B lactic acidosis after riboflavin therapy suggested that riboflavin deficiency plays a direct role in the development of nucleotide analogue-induced lactic acidosis. It is impossible to predict which patients are predisposed to the development of this syndrome. For this reason, it may be important to screen and treat riboflavin deficiency in patients on nucleoside analogues.
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PMID:Emerging role of riboflavin in the treatment of nucleoside analogue-induced type B lactic acidosis. 1178 75

There are a few prospective studies assessing the severity of acute pancreatitis with exclusive criteria for biliary etiology. In a cohort prospective study, Ranson (biliary etiology), Glasgow-modified, APACHE-II, and APACHE-O prognostic criteria were assessed in 65 patients with acute biliary pancreatitis (ABP). Local complications such as necrosis with fluid peripancreatic collection (3 patients), fluid collection with pancreas enlargement (3 patients), pancreatic fistula (1 patients), and pancreatic pseudocyst (1 patients); and organic failure such as renal (5 patients), hemodynamic (3 patients), and respiratory (3 patients) were found. The prognostic criteria performance, according to parameter number or positive variables evidenced that relative risk (RR) varied from 4.7 to 11.2, sensibility from 33.3% to 83.3%, specificity from 79.2% to 98.1%, positive predictive value from 45.0% to 83.3%, negative predictive value from 86.4% to 95.5%, and accuracy from 78.5% to 89.6%. In isolation, most important parameters correlated to severity included white blood cell count >18,000/mm3, lactate dehydrogenase (LDH) >400 UI/l, 10% drop of the hematocrit, serum calcium <8 mg/dl, increase of urea nitrogen >2 mg/dl, aspartate aminotransferase (AST) >200 mg/dl, LDH >600 UI/l, white blood cell count >15,000/mm3, urea >45 mg/dl, arterial pH < or = 7.33 or > or = 7.49, creatinin < or = 0.6 or > or = 1.4, hematocrit < or = 30 or > or = 45.9, white blood cell count < or = 3,000/mm3 or > or = 14,900/mm3. Ranson, Glasgow-modified, APACHE-II, and APACHE-O acute biliary pancreatitis severity criteria all present good sensibility and excellent specificity.
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PMID:Evaluation of Ranson, Glasgow, APACHE-II, and APACHE-O criteria to predict severity in acute biliary pancreatitis. 1199 72

Pancreatitis presents clinically as acute and chronic form. A common characteristic of these two forms is enzymatic autodigestion of pancreas in the course of the disease. It results from premature activation of pancreatic digestive enzymes and disturbance of subtle balance between proteolytic enzymes and their inhibitors. The way to understand the character of mechanisms leading to development of pancreatitis has been simplified by discovery of genetic factors, which are able to initiate pathological changes at tissue level. Mutations in the PRSS1 gene (first of all R122H and N29I mutations), which encodes for cationic trypsin, cause trypsin to be protected from autodegradation. These mutations also cause precursor of trypsin - trypsinogen, to be activated easier. On the other hand mutations in the SPINK1 gene have been identified. SPINK1 gene encodes for the most important protease inhibitor of the pancreatic fluid. The most frequent mutation, namely N34S, decrease SPINK1 protein in its activity. The link between the genotype and phenotype is not clear in every case. It is probable that pancreatitis will be recognized as poligenic with many genes engaged in the disease development. Pancreatic cancer is a frequent consequence of pancreatitis. It is a very invasive cancer with high mortality. In the course of pancreatic inflammation intensive cell proliferation takes place for regeneration of pancreas damage. It is the chance for amplification of pathological changes in DNA, which have arisen as a ROS's (Reactive Oxygen Species) and RNOS's (Reactive Nitrogen Oxide Species) action effect. ROS and RNOS are generated in the course of pancreas inflammation.
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PMID:[Hereditary aspects of pancreatitis]. 1313 Jan 70


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