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Query: UMLS:C0001339 (acute pancreatitis)
 10,593 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To clarify the relationship between the diminution of the serum protease inhibitor capacity and the severity of pancreatitis, the binding capacity of serum protease inhibitors for exogenous elastase 1 (E1) was investigated by gel filtration, the elastase activity of the alpha 2-macroglobulin (alpha 2-M)-elastase complex was measured, and the relationship between these findings and the severity of pancreatitis was studied in 13 patients with pancreatic disease and 6 healthy subjects. When 125I-labeled E1 was added to the sera of healthy subjects, it bound to alpha 2-M and alpha 1-protease inhibitor (alpha 1-PI) with a mean ratio of 72:28. In mild acute pancreatitis (n = 5), the binding capacity of alpha 2-M was less than that in healthy subjects. In severe pancreatitis (n = 4), most of the exogenous E1 bound to alpha 1-PI (alpha 2-M vs. alpha 1-PI, 13:87). This diminution in the binding capacity of alpha 2-M correlated well with the severity of acute pancreatitis. In the sera of patients (n = 4) with pancreatic cancer containing much immunoreactive E1, the proportion of exogenous E1 bound by alpha 2-M and alpha 1-PI (25:75) was similar to that seen in severe acute pancreatitis. A significant inverse relationship between the binding capacity of alpha 2-M and the activity of the endogenous elastase bound to alpha 2-M was seen in various pancreatic diseases.(ABSTRACT TRUNCATED AT 250 WORDS)
Pancreas 1992
PMID:Serum protease inhibitor capacity for elastase and the severity of pancreatitis. 128 Mar 65

During studying the literature a big confusion around the item abscess can be recognized. Especially in the English publications it is used for sterile tissue necrosis, infected necrosis, infected pseudocyst or suppuration. Pancreas phlegmon means there a sterile mass of pancreas and peripancreatic oedema. With us an abscess still is a located plus collection surrounded by a more or less tight capsule and a phlegmon is a diffuse purulent infection in the tissue. This definition is important because the frequency and prognosis of a true abscess is far below an infected necrosis (with us 4 abscess in 48 necrotising pancreatitis but 54% infected necrosis). Abscess formation needs two to four weeks whereas pseudocyst develops rather fast in one to two weeks. Although spontaneous resorption of pseudocyst is possible, we recognized ten and operated on all of them either by internal drainage or by resection of the tail of the pancreas. Mortality of one series of 124 patients with acute pancreatitis was at 30 days 4% and 27%, respectively, when necrosis was present and overall mortality having treated all patients to final discharge was 5% and 44%, respectively. Mortality rate was constant in the last years but Ranson score was continuously increasing.
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PMID:[Abscesses and pseudocysts as a sequela of acute pancreatitis]. 152 48

An intraluminal duodenal diverticulum (IDD) and a partial pancreas divisum were diagnosed in a 22-year-old man who exhibited recurrent attacks of acute pancreatitis. Resection of the diverticulum resulted in a complete disappearance of symptoms. The possible etiological relationship between IDD and recurrent acute pancreatitis is discussed.
Pancreas 1992
PMID:Recurrent acute pancreatitis and intraluminal duodenal diverticulum. 155 76

In a small percentage of patients with acute pancreatitis, recurrent attacks of pain and hyperamylasaemia occur when feeding is commenced. Recurrences of this type may occur because the pancreas is still swollen and inflamed, and indicate the need for a longer period of "pancreatic rest" before food is introduced. Alternatively, they may reflect the presence of "mechanical" factors leading to the recurrent pancreatitis, such as a gallstone in the common bile duct, a pseudocyst of the pancreas, or pancreatic duct obstruction. Successful resolution of the pancreatitis may require treatment of underlying causative factors. A stone in the pancreatic duct (probably a gallstone) was found to be the cause of recurrent acute pancreatitis in an elderly patient with severe cardiovascular disease, who was unfit for surgery. Pancreatitis settled after percutaneous drainage of the pancreatic duct, the technique described.
Pancreas 1992
PMID:Treatment of acute pancreatitis caused by calculous obstruction of the pancreatic duct by ultrasound-guided percutaneous drainage. 155 36

Radiologic findings in 7 adult patients with bile duct cysts were reviewed. Endoscopic retrograde cholangiopancreatography (ERCP) was performed in 6 patients, percutaneous transhepatic cholangiography (PTC) in 4, CT and ultrasonography (US) in 4, and angiography in 6. ERCP and PTC were the only methods which exactly showed the extent of the cysts and the anomalous pancreatico-biliary junction present in 5 patients. ERCP and PTC were mandatory for surgical planning and treatment. Pancreas divisum was revealed in 3 patients, all of whom had suffered from acute pancreatitis. Intracystic adenocarcinoma was depicted at cholangiography in 2 patients. US and CT were valuable in showing cystic masses between the pancreatic head and the hilum of the liver, but in no patient was the diagnosis made by any of these methods. Angiography was performed for preoperative vascular mapping.
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PMID:Radiologic approach to bile duct cysts in adults. 159 Nov 26

This study was undertaken to determine the involvement of endogenous cholecystokinin (CCK) in the regeneration of pancreatic tissue after cerulein-induced acute pancreatitis treated by the CCK receptor antagonist L364,718. Acute pancreatitis was induced in rats by s.c. injections of cerulein in gelatin (12 micrograms/kg) three times a day for 2 days with controls receiving saline in gelatin. Rats were then divided into four treatment groups: saline-dimethyl sulfoxide (DMSO) (SD), saline-L364,718 (SA), cerulein-pancreatitis-DMSO (CD), and cerulein-pancreatitis-L364,718 (CA). In the first experiment, rats were treated for 3 or 10 days with DMSO or L364,718 (0.1 mg/kg, twice a day). In the second experiment, rats were treated for 13 days with DMSO or L364,718 (1.0 mg/kg, twice a day). After the rats were killed, pancreata were weighed and evaluated for their total protein, amylase, chymotrypsin, RNA, and DNA. We found that destruction of the pancreatic tissue occurred after cerulein-induced pancreatitis and that regeneration of the tissue was in progress but incomplete after 10 days; the low dose of L364,718 did not prevent regeneration. After 13 days, regeneration was still incomplete but the 1-mg dose of L364,718 strongly inhibited spontaneous regeneration. These data suggest that endogenous CCK is an important and potent trophic factor in the regeneration process of pancreatic tissue following an episode of acute pancreatitis.
Pancreas 1992
PMID:Involvement of endogenous cholecystokinin in pancreatic regeneration after cerulein-induced acute pancreatitis. 159 50

Kinetics and distribution of i.v. human pancreatic phospholipase A2 (h-PLA2) were determined in intact and nephrectomized rats, and tissue localization of rat pancreatic PLA2 (r-PLA2) was studied by immunohistochemistry in experimental acute pancreatitis. The concentration of h-PLA2 and the catalytic activity of phospholipase A2 in plasma decreased exponentially in intact and nephrectomized animals after the injection. The initial 15-min half-life was considerably longer in nephrectomized animals, and higher h-PLA2 concentrations and PLA2 catalytic activities were found in plasma. h-PLA2 was localized in endocytotic vesicles and apical cytoplasmic vacuoles in proximal tubule cells of the kidney. The intensity of the immunoreaction decreased considerably between 15 and 50 min in these cells. No signs of tubular damage were seen by light microscopy. Neither immunoreactive h-PLA2 nor PLA2 catalytic activity was found in urine. r-PLA2 was observed in proximal tubule cells 15 min after an injection of sodium taurocholate (necrotizing pancreatitis group) or saline (edematous pancreatitis group) into the pancreatic duct. Signs of tubular damage were present in necrotizing pancreatitis, but tubular morphology was normal in the animals with edematous pancreatitis. We conclude that the proximal tubule cells of the kidney participate in the metabolism of circulating pancreatic PLA2, and considerably higher PLA2 levels persist in plasma in nephrectomized animals. Endogenous pancreatic PLA2 is detected in kidneys in acute pancreatitis.
Pancreas 1992
PMID:Pancreatic phospholipase A2 in proximal tubules of rat kidney in experimental acute pancreatitis and after intravenous injection of the enzyme. 159 53

The present studies were done to evaluate the therapeutic potential of several antioxidants and free radical scavengers in three different models of acute pancreatitis. (a) Edematous pancreatitis with acinar cells necrosis was induced by seven hourly intraperitoneal injections of 50 micrograms of caerulein per kg in mice. (b) Hemorrhagic pancreatitis was induced by feeding a choline-deficient, ethionine-supplemented (CDE) diet in mice. (c) Hemorrhagic pancreatitis was induced by retrograde infusion of 0.6 ml of 5% sodium taurocholate into the pancreatic duct in rats. The following antioxidants and free radical scavengers were given at various doses intravenously, subcutaneously, or intraperitoneally before the onset of pancreatitis: Ebselen [2-phenyl-1,2-benzisoselenazol-3(2H)-one], superoxide dismutase, catalase, deferoxamine (Desferal), dimethyl sulfoxide, or allopurinol. The severity of pancreatitis was assessed at various times after its onset by determination of serum amylase and pancreatic weight (edema), by grading of histological alterations, and by determination of survival (survival determined in models of hemorrhagic pancreatitis). In general, free radical scavengers and antioxidants ameliorated edema and inflammation to a greater degree than necrosis and the increase in serum amylase. Superoxide dismutase (as did Ebselen in previous studies) exerted beneficial effects on survival in diet-induced pancreatitis in the absence of marked effects on pancreatic necrosis, suggesting that these beneficial effects are due to amelioration of extrapancreatic complications that often contribute to mortality in acute pancreatitis. None of the antioxidants had major beneficial effects in taurocholate-induced hemorrhagic pancreatitis. Thus, formation of free radicals may be important for progression and outcome in diet-induced and, to a lesser degree, in caerulein-induced pancreatitis but not at all in taurocholate-induced pancreatitis. Different models of pancreatitis may, therefore, involve different degrees and mechanisms of free radical formation. Despite the amelioration of edema and the beneficial effects on mortality seen for some antioxidants in some of the models, antioxidants and free radical scavengers appear to have only a limited potential for treatment of acute pancreatitis.
Pancreas 1992
PMID:Effects of antioxidants and free radical scavengers in three different models of acute pancreatitis. 164 91

The single most important risk factor for chronic and acute pancreatitis is the abuse of ethanol, which, theoretically, could affect the pancreas by interacting either with some of its cell receptors or with any of its intracellular signal transduction mechanisms. Therefore, we determined in isolated pancreatic acini from 3 month ethanol-fed rats and controls the dose-response effects of secretagogues on enzyme secretion, both in the presence and absence of ethanol in the incubation medium. In ethanol-fed rats, pancreatic amylase activity was decreased by 40%, compared to controls (with identical carbohydrates intakes), whereas lipase and trypsinogen activities were unaffected. With no ethanol in the incubation medium, basal enzyme releases and enzyme dose-response curves to CCK-8, VIP, secretin, bombesin, and bethanechol were essentially unchanged in ethanol-fed rats compared to controls. In contrast, with 0.1 M ethanol present in the medium, enzyme responses to VIP, secretin, and CCK-8 were inhibited and that to CCK-8 also shifted to the right in ethanol-fed rats compared to controls. Hence, if rechallenged to ethanol, acini from ethanol-fed rats show inhibited secretions, in response to two secretagogues acting through the release of cyclic AMP, and an inhibited and right-shifted secretory response to CCK.
Pancreas 1990
PMID:Differing effects of ethanol on in vitro stimulated pancreatic enzyme secretion in ethanol-fed and control rats. 168 87

Pancreas-specific protein (PASP) was compared with serum amylase in 95 episodes of acute pancreatitis with the diagnoses supported by elevated amylase levels. The etiology was typical for Scandinavian countries, with alcohol as the predominant factor, followed by cholelithiasis. PASP values were clearly raised in all patients, except in three cases found to have high salivary-type amylase levels, and one patient with recurrent alcohol pancreatitis. The rise of PASP levels were in general more pronounced than the corresponding amylase elevations, especially in severe pancreatitis. The elevations were generally parallel for the two analytes, but in 41% of the cases PASP levels remained elevated 2-11 days longer than the corresponding amylase levels. PASP was, however, eliminated from the circulation at a rate comparable to that of amylase. The serum range of PASP for 259 healthy subjects was 15-111 micrograms/L with 95% of the values within 16-98 micrograms/L. The upper reference level was set at 100 micrograms/L. PASP levels were also determined for 291 patients with disorders other than acute pancreatitis. Serum levels in patients with renal insufficiency (n = 12), primary biliary cirrhosis (n = 9), and diabetes mellitus (n = 17) were equal to those in healthy subjects. Eight patients of 173 with acute abdominal disorders and no evidence of pancreatitis had elevated PASP levels as well as 4 patients with prostatic carcinoma (n = 28) and 2 patients with benign prostatic hyperplasia (n = 16). PASP values were low in chronic painful pancreatitis (n = 15) and pancreatic cancer (n = 11).
Pancreas 1990
PMID:A novel assay for pancreatic cellular damage: IV. Serum concentrations of pancreas-specific protein (PASP) in acute pancreatitis and other abdominal diseases. 168 89


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