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)

Six alpha-amylase (EC 3.2.1.1) isoenzymes have been resolved electrophoretically on cellulose acetate membranes in a discontinuous buffer system. The fastest migrating isoenzymes are of salivary origin (S1, S2, S3), the slower ones of pancreatic origin (P1, P2, P3). We determined the amylase isoenzyme distribution in the sera of 240 subjects. A specific pancreatic isoenzyme (P3) was observed in all clinically diagnosed cases of acute or chronic pancreatitis as well as in 15 of 40 renal-transplant patients. Moreover, P3 isoenzyme activity declined during apparent recovery from pancreatitis. The P2 isoenzyme appeared in 95% of all specimens, P1 in only 2%. The pancreatic isoenzymes were preferentially excreted in the urine of both renal-transplant patients and normal individuals. The major salivary isoenzyme, S1, was observed in 95% of all serum and urine samples; however, the S2 and S3 appeared less consistently. Our method is simple and rapid, and quite applicable for use in clinical evaluation of patients with pancreatitis or with certain nonpancreatic dysfunctions.
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PMID:Electrophoretic amylase fractionation as an aid in diagnosis of pancreatic disease. 110 10

Single random samples of urine were collected from 50 control subjects; 27 patients with chronic pancreatitis; 19 with acute pancreatitis; 6 with acute on chronic pancreatitis; five in the recovery phase of acute attack; four patients with pseudocysts. Salivary (S) and pancreatic (P) amylase values were measured by cellulose acetate electrophoresis. The P amylase values always exceeded those of S amylase in the control specimens. In acute pancreatitis, both the lower and upper levels of total and P amylase were considerably higher than in the controls, and these high values tended to return to normal during the recovery phase of acute pancreatitis. The S amylase values were often very low or undetectable during the acute phase. Values for P amylase exceeded control values in patients with pseudocysts even in the presence of chronic pancreatitis. In chronic calcific pancreatitis, S amylase was higher than P amylase. We conclude that P amylase is always greater than S amylase in normal urine specimens, and a change in this pattern may be helpful in diagnosing various forms of pancreatitis.
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PMID:P amylase is always greater than S in spot urine of normal subjects. Diagnostic implications. 138 8

To evaluate the effects of acute pancreatitis on the energy metabolism of the liver and on the fragility of hepatic cells and subcellular organelles, we studies (1) the arterial blood ketone body ratio (BKBR) (aceto acetate/beta-hydroxy butyrate), which is in equilibrium with the free NAD+/NADH ratio in liver mitochondria; (2) the hepatic energy charge (EC) = (ATP + 1/2 ADP)/(ATP + ADP + AMP); (3) the cathepsin B leakage from hepatic lysosomes and the malate dehydrogenase leakage from hepatic mitochondria in vitro; and (4) the protective effects of prostaglandin E2 (PGE2) and a new synthetic protease inhibitor ONO 3307 on hepatic injury in acute pancreatitis induced in rats by a supramaximal dose of caerulein. Decreased BKBR and hepatic EC as well as increased hepatic lysosomal and mitochondrial fragility were observed in rats with this type of acute pancreatitis, and both PGE2 and ONO 3307 had a significant protective effect against hepatic injury in these rats, especially ONO 3307. These results suggest that impaired hepatic energy metabolism is closely related to increased hepatic lysosomal and mitochondrial fragility and that some proteases, which are derived from pancreatitis and are susceptible to inhibition by ONO 3307, seem to play an important pathological role in this liver injury induced by pancreatitis. Therefore, it is important to take care of the liver in patients with acute pancreatitis.
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PMID:Impaired hepatic energy metabolism in rat acute pancreatitis: protective effects of prostaglandin E2 and synthetic protease inhibitor ONO 3307. 152 49

A 27-year experience in the surgical management of 160 patients with pancreatic pseudocysts was reviewed. Sixty-eight patients treated from 1964 to 1981 (Group I) were compared to 92 patients managed from 1982 to 1990 (Group II). During the recent period, computed tomography (CT) scanning, endoscopic retrograde cholangiopancreatography (ERCP), selective visceral angiography, and percutaneous catheter drainage (PCD) techniques were available. The mean age of patients was similar in both groups (45 vs 44 years). Most pseudocysts in both periods represented complications of chronic pancreatitis due to alcohol abuse (82% vs 87%). Pancreatitis-associated complications occurring before management (fistula, obstruction, hemorrhage) were more frequent in Group II (19% vs 40%, P less than .05). There was a significant increase in the number of patients managed with external drainage in Group II (10% vs 52%) attributable to the use of PCD as definitive therapy in 46 per cent of patients in the recent period. Use of internal drainage procedures (cystgastrostomy, cystduodenostomy, cystjejunostomy) decreased in Group II (38% vs 16%, P less than .05). The use of lateral pancreaticojejunostomy (LPJ) combined either with caudal resection or cyst drainage has remained constant in both periods (32% vs 24%, NS). Patient morbidity was similar (26% vs 28%, NS) and mortality improved in Group II (9% vs 1%, P less than .05). Internal or external drainage for pseudocyst is often not definitive because of the underlying ductal disease. The authors' current approach is to manage large symptomatic cysts either with internal drainage or PCD; they employ octreotide acetate in the management of persistent pancreatic fistula following external drainage.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changing concepts in the surgical management of pancreatic pseudocysts. 155 35

Acetaldehyde (AA), the first product of ethanol metabolism, has been suggested as an important mediator in alcoholic pancreatitis, but experimental evidence has not been convincing. Prior work using the isolated perfused canine pancreas preparation has suggested that toxic oxygen metabolites generated by xanthine oxidase (XO) may mediate the early injury in pancreatitis. Xanthine oxidase is capable of oxidizing AA, and during this oxidation free radicals are released. The hypothesis that acute alcoholic pancreatitis may be initiated by AA in the presence of active XO (converted from xanthine dehydrogenase [XD]) was tested in the authors' experimental preparation by converting XD to XO by a period of ischemia, and infusing AA. Control preparations remained normal throughout the 4-hour perfusion (weight gain, 7 +/- 4 g; amylase activity, 1162 +/- 202 U/dL). One hour of ischemia or infusion of AA at 25 mg/hr or at 50 mg/hr without ischemia did not induce changes in the preparation. Acetaldehyde at 250 mg/hr induced minimal edema and weight gain (16 +/- 4 g; p less than 0.05), but not significant hyperamylasemia. Changes also were not observed when 1-hour ischemia was followed by a bolus of ethanol (1.5 g) or sodium acetate (3.0 g), or by infusion of 25 mg/hr of AA. One hour of ischemia followed by infusion of AA at 50 mg/hr or at 250 mg/hr induced edema, hemorrhage, weight gain (22 +/- 7 g [p less than 0.05] and 26 +/- 17 g [p less than 0.05]) and hyperamylasemia (2249 +/- 1034 U/dL [p less than 0.05] and 2602 +/- 1412 U/dL [p less than 0.05]). Moreover infusion of AA at 250 mg/hr after 2 hours of ischemia potentiated the weight gain (62 +/- 20 g versus 30 +/- 14 g [p less than 0.05]), but not the hyperamylasemia (3404 +/- 589 U/dL versus 2862 +/- 1525 U/dL) as compared with 2 hours of ischemia alone. Pancreatitis induced by 1 hour of ischemia followed by AA at 50 mg/hr could be inhibited by pretreatment with the free radical scavengers superoxide dismutase and catalase and ameliorated with the XO inhibitor allopurinol. The authors conclude that AA, in the presence of active XO, can initiate acute pancreatitis in the isolated canine pancreas preparation and may be important in the initiation of acute alcoholic pancreatitis in man. Toxic oxygen metabolites appear to play an important intermediary role.
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PMID:The role of acetaldehyde in the pathogenesis of acute alcoholic pancreatitis. 172 Jun 11

Pancreatic pseudocysts represent a complication of severe pancreatic inflammatory disease. Although operative drainage is the cornerstone of therapy for pseudocysts, we have undertaken percutaneous catheter drainage in a selected group of 28 patients over a six-year period (1982-88). This represents 42 per cent of pseudocyst patients managed by the senior author and 1.7 per cent of admissions for pancreatitis at the Medical University Hospitals during that period of time. There were 26 men and two women with an age range of 26-66 years (mean = 42.1). Twenty-six patients had alcohol abuse as the cause of pancreatitis; two were due to surgical trauma. Nondilated pancreatic ducts were demonstrated in 25 patients. Six had pancreatic ascites associated with pseudocysts. Four had previous operative drainage (2 internal and 2 external drainage procedures). Five patients received octreotide acetate, a synthetic peptide which mimics the action of somatostatin, in an attempt to aid closure of external fistulas. The mean length of catheter drainage was 48 days (range 7-210 days). Eight (29%) patients developed procedure-related complications (1 pneumothorax, 1 sheared guidewire, six drain tract infections). There was no mortality. Successful resolution of pseudocysts was achieved in 26 patients (93%). Two patients subsequently had elective caudal pancreaticojejunostomy (CPJ), and one lateral pancreaticojejunostomy (LPJ) to drain obstructed pancreatic ducts. One patient has required repeat external drainage. Percutaneous external drainage is successful in pseudocyst eradication. When underlying pancreatic pathology remains uncorrected, elective surgical decompression of obstructed, dilated ducts may be necessary.
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PMID:Percutaneous catheter drainage of pancreatic pseudocysts. 179 94

We determined the prevalance and significance of hyperamylasemia in 180 patients with idiopathic inflammatory bowel disease (IBD) (83 with ulcerative colitis, and 97 with Crohn's disease). Serum total amylase and pancreatic and salivary isoamylase activity were measured in all patients. In all patients with hyperamylasemia, we measured isoamylase activity by cellulose acetate electrophoresis and lipase activity, assayed for the presence of macroamylase, and carried out pancreatic ultrasound examination and barium studies of the upper gastrointestinal tract. Eight of 97 patients with Crohn's disease (8%) had hyperamylasemia; 4 of them had an elevated pancreatic isoamylase and 2 a raised lipase activity. All patients with hyperamylasemia had normal ultrasonographic scans of the pancreas and no evidence of duodenal involvement on barium meal. None had macroamylasemia. We found no relationship of hyperamylasemia to disease site, activity, and duration or therapy and no patient developed clinical evidence of pancreatitis. We conclude that a small but important number of patients with Crohn's disease have hyperamylasemia not associated with overt pancreatitis. In the absence of appropriate indications, it requires no investigation.
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PMID:Hyperamylasemia in inflammatory bowel disease. 246 72

We noted a frequent increase in the serum enzymes amylase, lipase, and alkaline phosphatase in patients with Wilson's disease who are receiving zinc acetate therapy (25 or 50 mg elemental zinc three times daily). Typically, values are normal before the initiation of zinc therapy, increase to slightly above normal after a few weeks of therapy, and stabilize at the high normal range after approximately a year of treatment. Very large dosages of zinc (800 mg/day) produce even further elevation of serum lipase and amylase without the symptoms of pancreatitis. Pancreatic pathologic studies of a zinc-treated rat model receiving dosages equivalent to up to 25 times the effective dosage in a human being, which is based on milligrams of zinc per kilogram of body weight, reveal that no lesions are induced by zinc treatment in the pancreas. We interpret these findings to indicate that extended maintenance therapy with zinc does not pose a risk of pancreatic damage in patients with Wilson's disease.
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PMID:Treatment of Wilson's disease with zinc. V. Changes in serum levels of lipase, amylase, and alkaline phosphatase in patients with Wilson's disease. 247 44

alpha-Amylase isozymes were separated by electrophoresis in cellulose acetate to detect the isoforms of the chromogenic substrate manufactured by Lachema, Czechoslovakia. In a group of 20 normal subjects aged 25 to 45, alpha-amylase pancreatic isozyme activity prevailed. Patients with acute myocardial infarction developed, during 36 hours after the onset of the anginal attack, a reduction in the ratio of pancreatic amylase/salivary amylase activities in both increased and normal total alpha-amylase activities. The suggested modified technique of electrophoretic separation of alpha-amylase isozymes may become an effective method for differential diagnosis. Use of this method will help locate the source of hyperamylasemia in various diseases and will thus specify the diagnosis, ruling out the useless therapy for pancreatitis.
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PMID:[Separation of alpha-amylase isoenzymes using cellulose acetate electrophoresis]. 248 11

Groups of mice were given 0 mg, 4 mg, or 2 mg of methylprednisolone acetate (MPA) 7 days prior to, the day of, and 7 days after subcutaneous inoculation with 0 or 2 x 10(5) tachyzoites of Neospora caninum. Clinical signs of disease were seen only in mice given both MPA and N. caninum tachyzoites. Mice given 4 mg MPA and N. caninum tachyzoites developed severe disseminated neosporosis and most died or were killed when comatose 11-13 days postinoculation (PI). Acute pneumonia, polymyositis, encephalitis, hepatitis, and pancreatitis were the main lesions in these mice. Mice given 2 mg MPA and N. caninum developed mild pneumonia and many mice began showing neurological signs 14 days PI. Neurological signs consisted mainly of pronounced head-tilting and associated impairment of movement. Grossly visible 1-2-mm single or multiple, white areas of discoloration were seen in the brains of many of these mice. Encephalitis, ganglioradiculoneuritis, pneumonia, and polymyositis were the main changes seen in these mice. Tissue cysts of N. caninum were only seen in mice given 2 mg MPA and were first seen 21 days PI. Tissue cysts were 16-34 by 13-29 microns and had a 1.5-3.0-microns-thick cyst wall. Tissue cysts were seen only in the brain. Mice given 4 mg MPA and tachyzoites and host cells that had been frozen for 1 wk did not develop clinical signs of infection, indicating that freezing kills tachyzoites and that viruses or other agents were not involved in the genesis of disease seen in mice given MPA and viable tachyzoites.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neospora caninum (Protozoa: apicomplexa) infections in mice. 279 80


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