Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The elements of the mechanized fluorometric lipase (EC 3.1.1.3) assay of Fleisher and Schwartz [Clin. Chem. 17, 417 (1971)] were made optimum; a manual adaptation was also developed. Hydrolysis of the monodecanoyl fluorescein substrate by hog pancreatic lipase is a zero-order reaction. The hydrolytic activity of normal human serum, serum from hospitalized patients without pancreatitis, and serum from patients with acute pancreatitis showed considerable overlap. Bile salts, considered activators in titrimetric or turbidimetric lipase assays, inhibited hydrolysis of the substrate by human serum. We conclude that monodecanoyl fluorescein is not a specific substrate for the serum lipase measured in acute pancreatitis.
Clin Chem 1975 Sep
PMID:Fluorometric serum lipase assay: evaluation of monodecanoyl fluorescein as substrate. 115 17

We developed an assay for methemalbumin in biological fluids by using diethylaminoethyl-Sephadex ion-exchange chromatography to separate this protein from interfering components, including hemopexin, transferrin, hemoglobin, and haptoglobin/hemoglobin complex. Initial screening of the samples requires measurement of A280/A405 ratios of the peak tubes of the isolated albumin fraction. Values exceeding 30 indicate that methemalbumin is absent, and no further work is required. Values of less than 30 suggest that methemalbumin is present in the original sample, whereupon the presence and amount of methemalbumin can be ascertained by coloremetric assay for iron with use of ferrozine. Results may be expressed either in terms of micrograms of methemalbumin iron per gram of albumin or in milligrams of methemalbumin per liter. The reproducibility of the method is of the order of +/- 7% (SD). Normal persons have essentially no methemalbumin iron in their serum. Three individuals with hemorrhagic pancreatitis showed values of 65, 98, and 198 mug of methemalbumin Fe per gram of albumin.
Clin Chem 1975 Sep
PMID:Clinical determination of methemalbumin. 115 22

The effects of tolbutamide infusion (1 gm. over forty minutes) on plasma pancreatic glucagon-like immunoreactivity (PGLI), serum insulin, and blood glucose were studied in six patients with chronic pancreatitis and six matched controls.asal PGLI levels were significantly higher in the patients, despite higher fasting glucose concentrations. Tolbutamide infusion had no significant effect on mean PGLI levels in controls but was associated with significant elevation in pancreatitis patients, despite higher circulating glucose levels in the latter. The data suggest that chronic calcific pancreatitis patients hypersecrete immunoreactive glucagon, possibly from a nonpancreatic source and that this immunocreactive material may be stimulated by sulfonylureas.
Diabetes 1975 Sep
PMID:Immunoreactive glucagon responses to intravenous tolbutamide in chronic pancreatitis. 115 44

The changes in elastase levels were studied in the plasma before and after bile-induced pancreatitis. Although the anylase and lipase levels increased markedly, there was no significant increase in the plasma elastase levels, as measured by enzymatic assay. On the other hand, the elastase levels of the blood in the femoral and pancreatic veins as measured by radioimmunoassay, increased to about ten times above the control levels. Similarly, in pancreatitis, large amounts of elastase, determined by radioimmunoassay, was found in the ascitic fluid. At that time, no elastase activity could be determined in the ascitic fluid. In this study, it is suggested that circulating inhibitors interfere with the determination of elastase enzymatic activity but do not interfere with the radioimmunoassay of elastase.
Surg Gynecol Obstet 1975 Sep
PMID:Elastase levels during bile-induced pancreatitis in dogs determined by radioimmunoassay. 116 60

The anatomic pattern seen in the three patients with contiguous gastric duplications associated with pancreatic ducts evidently predisposes the patient to pancreatitis. In the previous patient reported upon from this institution, the correlation of severe bleeding episodes with attacks of pancreatitis strongly supports the concept of blood blocking the pancreatic ductal system, thereby producing pancreatitis. Passage of viscous mucoid secretions from the aberrant gastric mucosa into the pancreatic ductal system also might retard the normal flow of pancreatic juice, producing elevation of the serum amylase level and pain. Overdistention of the gastric duplication also might be considered as a source of pain, but such mechanisms can be considered only speculation at present. Diagnosis is usually made after more than one exploratory laparotomy. Hemorrhage may result, should the gastric duplication contain parietal cells, leading to hemoductal pancreatitis, hematemesis or melena and anemia. At least one in five patients with a gastric duplication possesses another intestinal duplication. Developmental defects commonly are associated with gastric cysts. Almost identical anatomy was present in the patients with contiguous duplications. That two such rare pancreatic disorders were documented in the same institution within two years suggests that this pattern of developmental defect is more common that had previously been expected.
Surg Gynecol Obstet 1975 Sep
PMID:Pancreatitis of unusual origin. 116 66

The redistribution of cathepsin B, a lysosomal enzyme, from the lysosomal pellet to the zymogen pellet in the subcellular fractionation, the colocalization of cathepsin B with digestive enzyme, and increased cellular, lysosomal, and mitochondrial fragility within acinar cells have been found during the early stages of caerulein-induced acute pancreatitis in rats. In the present study, the authors investigated the protective effects of prostaglandin E1 and E2, a combined therapy of these prostaglandins, and a new, synthetic, low molecular weight protease inhibitor, ONO3307, on the exocrine pancreas in this noninvasive model of experimental pancreatitis in vivo and in vitro. Prostaglandin E2, but not E1, prevented hyperamylasemia, congestion of amylase and trypsinogen in the acinar cells, redistribution of cathepsin B, and amylase and lactate dehydrogenase discharge from the dispersed acini. It also prevented cathepsin B leakage from the lysosomes and malate dehydrogenase leakage from the mitochondria in an almost dose-dependent manner, particularly at the dose of 100 micrograms/kg/hr continuous infusion. Furthermore, the combined therapy of prostaglandin E2 with ONO3307 strongly inhibited all the parameters tested in this study. This combination therapy seems to be the most effective against secretagogue-induced pancreatic injuries. These results indicate that cellular and subcellular organellar fragility seem to be closely involved in the pathogenesis of acute pancreatitis. Prostaglandin E2 seems to have important cytoprotective effects on the biologic membranes, such as a stabilizer of lysosomal or mitochondrial membranes. In addition, these findings also suggest the crucial roles of some unknown proteases in the etiology of acute pancreatitis, and indicate the clinical effectiveness of prostaglandins and this type of low molecular weight protease inhibitor for acute pancreatitis.
Am J Med Sci 1992 Sep
PMID:Cytoprotective effects of prostaglandins and a new potent protease inhibitor in acute pancreatitis. 128 94

The purpose of this study consisted in following-up the biological and clinical parameters in HIV infected patients treated with tacrine (THA). THA (150-300 mg/d) was administrated to 70 patients (39 IVC I and 31 IVC II and III). Thirty-five were treated after discontinuation of AZT treatment and 35 as a first intention treatment. Thirty (43%) patients showed an increase in the CD4+ cell count by more than 50% relative to pretreatment levels and fifteen (21%) showed an increase of more than 25%. p24 antigenemia (Ag p24) became negative in eight of the twenty-seven patients who were initially positive, and decreased by 25 and 50% in nine and six patients, respectively. Ag p24 was therefore decreased in 80% of the patients. From a clinical point of view, there were two deaths (3%) and five opportunistic infections (7%). The treatment with THA was stopped in five patients because of side effects (nausea, rash). Neither hepatotoxicity, hematotoxicity, nor pancreatitis was observed during the THA treatment. In group II and III only two patients (6%) developed an opportunistic infection.
Int J Clin Pharmacol Ther Toxicol 1992 Sep
PMID:Open trial of tacrine therapy in 70 HIV-infected patients. 135 32

The effects of a long-acting somatostatin analog (SMS 201-995) were studied in an established model of acute necrotizing pancreatitis in rats. SMS 201-995, when given prior to induction of pancreatitis, decreased the mortality rate from 100% to 40% (P = 0.0001). When treatment was given after induction of pancreatitis, the mortality rate was 75% (P = 0.2). Administration of SMS 201-995 did not influence the serum concentrations of amylase markedly, but the lipase levels were significantly lowered (P less than 0.05). The low levels of serum insulin and the glucose level in whole blood were not influenced. The volume of ascitic fluid was reduced (P less than 0.01). Moreover, less peritoneal fat necrosis was seen, suggesting a reduction in toxic factors in the ascitic fluid. Treatment with SMS 201-995 prior to induction of pancreatitis caused a significant increase in the levels of circulating 6-keto-PGF1 alpha, the stable metabolite of prostaglandin I2 (P less than 0.01). The levels of thromboxane B2 and prostaglandin E2 did not change significantly. The present data support the hypothesis that SMS 201-995 is an activator of prostaglandin I2, thereby modifying the course of the disease.
Dig Dis Sci 1992 Sep
PMID:Effects of long-acting somatostatin analog (SMS 201-995) on eicosanoid synthesis and survival in rats with acute necrotizing pancreatitis. 138 Apr 26

The operative management and clinical course of 17 patients treated for severe pancreatico-duodenal injuries from 1983 to 1990 was reviewed. The etiology of these injuries was gunshot wound in 15 patients; stab wound in 1 patient; and a motor vehicle accident in 1 patient. Seven patients presented in shock with a systolic blood pressure of less than 80. At exploration, 57 associated injuries were found in the 17 patients including 16 major vascular injuries. All patients were treated with pyloric exclusion and drainage. Vagotomy was performed in eight patients. None of these 17 patients were felt to have extensive enough damage to require pancreatico-duodenectomy. Two patients died in the immediate postoperative period of severe coagulopathy and two patients died of sepsis. Seven patients had complications related to the pancreatico-duodenal injury. All seven developed pancreatic fistulas; three also had pancreatitis and two developed multiple enterocutaneous fistulas. Systemic complications included pulmonary complications in eight patients and sepsis in five patients, including two patients with abdominal abscesses. Six patients bled in the immediate postoperative period secondary to coagulopathy. Three patients had complications related to pyloric exclusion. One developed afferent loop syndrome necessitating reoperation. The other two had marginal ulcers, which either perforated or bled and required reoperation. Of interest, neither of these two patients had vagotomy initially. The results of this series confirm the effectiveness of pyloric exclusion with vagotomy for severe pancreatico-duodenal injury.
Am Surg 1992 Sep
PMID:Severe pancreatico-duodenal injuries: the effectiveness of pyloric exclusion with vagotomy. 138 82

The importance of platelet activating factor in acute pancreatitis was examined by determining the tissue content of endogenous platelet activating factor and the protective effects of TCV-309, a highly selective platelet activating factor blocker, against caerulein induced pancreatitis in rats. Infusion of caerulein (10 micrograms/kg/h) for five hours resulted in about 70% increase in pancreatic weight, 22% rise in protein content, 50% reduction in tissue blood flow, nine fold increase in tissue level of platelet activating factor and 165% rise in plasma amylase as well as histological evidence of acute pancreatitis. Such infusion of caerulein in chronic pancreatic fistula rats caused a marked increase in protein output from basal secretion of 10 mg/30 minutes to 40 mg/30 minutes in the first hour of infusion followed by a decline in protein output to 15-20 mg/30 minutes in the following hours of the experiment. Exogenous platelet activating factor (50 micrograms/kg) injected ip produced similar alterations in weight, protein content, blood flow, and histology of the pancreas but the increment in serum amylase was significantly smaller and pancreatic secretion was reduced below the basal level. TCV-309 (50 micrograms/kg) given ip before caerulein or platelet activating factor administration significantly reduced the biochemical and morphological alterations caused by caerulein and abolished those induced by exogenous platelet activating factor. These results indicate that platelet activating factor plays an important role in the pathogenesis of acute pancreatitis probably by reducing the blood flow and increasing vascular permeability in the pancreas.
Gut 1992 Sep
PMID:Role of platelet activating factor in pathogenesis of acute pancreatitis in rats. 138 72


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