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

In 1972 and 1973 the authors studied the problems of involvement of the pancreas in mumps. As the laboratory criterion they used the determination of serum alpha-amylase activities by Babson's method, which proved to be satisfactory and valuable. The incidence of pancreatitis in mumps has risen in recent years, as seen from the greater frequency of clinical signs of pancreatitis and pathologically elevated serum alpha-amylase activities. In our series of 190 patients, clinical signs of pancreatitis were present in 42% of all the patients with mumps. In some of these patients, the signs of pancreatitis did not appear until a few days after the onset of the disease. It is therefore desirable to put all patients with mumps on a suitable diet, to follow them up for a long period, including the convalescent phase, and to check their alpha-amylas activities from time to time.
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PMID:Diagnosis and follow-up of parotitic pancreatitis by means of the determination of serum alpha-amylase activity. 30 4

An experimental xenogeneic immune pancreatitis was induced in AB-mice by repeated intraperitoneal injections of rabbit immune sera directed against purified pancreatic enzymes (alpha-amylase, lipase, trypsin) for 3 hours up to 8 days. Histologically, the immune pancreatitis is characterized by three different findings: 1. Multiple acinar cell necroses on the 2nd, 3rd and 5th day of immune serum application. 2. A dedifferentiating acinar cell atrophy with development of pseudocanalicular acini on the 5th and 9th day. 3. An increasing interstitial histiolymphoplasmocytic pancreatitis on the 5th and 9th experimental day. Ultrastructurally, the acinar cell necroses proved as the final stage of a step-by-step developing acute lethal cell damage. The dedifferentiating acinar cell atrophy corresponds to a chronic sublethal cell injury with alteration of different cytoplasmic components. The interstitial pancreatitis in immune serum treatment is characterized by differently activated histiocytes and lymphocytes as well as by mature plasma cells. Because of immune histological findings (peri- and intraacinar deposition of rabbit globulin, specific fixation of guinea-pig complement, and appearance of mouse globulin in the mouse exocrine pancreas) and control experiments with rabbit and mouse normal serum as well as with physiological saline, the pathogenesis of the induced xenogeneic immune pancreatitis is regarded as a twophase process: 1. The acinar cell necroses are mainly due to a cytotoxic immune reaction (possibly in combination with an immune complex reaction) caused by specific anti-pancreatic enzyme antibodies of the applied immune sera. The dedifferentiating acinar cell atrophy may be the result of a specific action of the anti-enzyme antibodies against the corresponding pancreatic enzymes in the apical secretion granules of the pancreatic acinar cells. 2. The interstitial histiolymphoplasmocytic pancreatitis is mainly the morphologic substrate of an extravascularly (intraperitoneally) induced serum sickness reaction (immune complex reaction) due to the foreign proteins applied with the xenogeneic immune sera.
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PMID:Experimental immune pancreatitis in the mouse by rabbit immune sera directed against purified enzymes of the exocrine pancreas. 30 66

Incidence and extent of increased alpha-amylase concentration were examined in serum and urine following routine surgical intervention in the epigastrium. Only patients with non-specific clinical symptoms (n=49) and a control group who had undergone surgery for inguinal hernia (n=10) were included in the study. Patients previously subjected to gastric surgery (selective gastric vagotomy = 10, gastric resection according to Billroth I = 10) were significantly more often found to have results within a range usually considered pathological. Patients who had undergone surgery of the bile duct were markedly less affected. The diagnosis, based on the benefit of the hindsight, of a postoperative pancreatitis in cases where specific complaints and increased maylase concentration coincide does therefore not appear justified--particularly following gastric surgery. This becomes significant if a choice between various conservative treatments or relaparotomy is being considered.
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PMID:[Postoperative pancreatitis]. 81 25

A simple modification of an alpha-amylase (E.C. 3.2.1.1.) procedure, using blue starch substrate, permits quantitative results after three minutes of incubation. The procedure, performed on blank, control, and unknown speciemns, takes advantage of the heat stability of the enzyme and provides immediate and reliable data for acutely ill patients. The performance characteristics of the test on serum and urine are described. The method is distinctly advantageous in prividing rapid results for serum amylase, urine amylase, and amylase clearance in patients with suspected pancreatitis.
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PMID:A rapid, manual test for amylase at 52C. 97 Apr 6

The activity of the alpha-amylase was estimated in the parotid resting saliva of 17 subjects without evidence of pancreatic disease, 17 patients with chronic relapsing pancreatitis in the intervals between acute attacks, and also in 4 patients with acute pancreatitis and 3 patients with an acute attack of chronic relapsing pancreatitis. In the patients with chronic relapsing pancreatitis between attacks the concentration, output and specific activity of the salivary amylase were significantly lowered. The patients with acute pancreatitis exhibited salivary amylase concentrations in the uppper normal to grossly supranormal range, whereas those of the patients with acute attacks of chronic relapsing pancreatitis were distinctly reduced. Unlike the amylase output, the amylase concentration was independent of the rate of salivary flow. Simultaneous infusion of secretin and pancreozymin produced a significant increase in the parotid salivary amylase levels in both the patients without pancreatic disease and in those with chronic relapsing pancreatitis between acute attacks.
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PMID:Amylase activity of parotid saliva in acute and chronic pancreatitis. 98 61

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

In the serum and saliva of 45 patients with eating disorders and in 30 normal controls, alpha-amylase activity and isoamylase levels were measured. Of the 45 patients evaluated, 12 had restrictive anorexia nervosa, 13 were bulimic anorectics and 20 had bulimia nervosa. In all these groups, the mean alpha-amylase values in serum and saliva were higher than that of the control group. The proportion of pancreatic (P)- and salivary (S)-alpha-amylase isoenzymes in serum were within the normal range for the patient group with restrictive anorexia nervosa, whereas the bulimic anorexia nervosa and bulimia nervosa patients showed significantly greater increases in S- than P-isoamylase activity. The correlation of the salivary alpha-Amylase isoenzym pattern in serum and saliva pointed to the salivary glands as origin of the elevated salivary isoamylase levels in serum. Hyperamylasemia was found in 10 (25%) of the 45 patients with eating disorders. Three of these patients showed besides an increased S-alpha-amylase activity also pathologically elevated P-alpha-amylase and lipase activity in serum; however there were no abdominal symptoms, laboratory data or ultrasonic signs of pancreatitis. In all patients with eating disorders, the mean concentration and secretion of alpha-amylase in saliva were increased. Swelling of the salivary glands was present in 14 patients. In these cases the percentage of salivary-isoamylase activity in total serum alpha-amylase activity was increased significantly, whereas the alpha-amylase secretion in the resting saliva was decreased.
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PMID:[Alpha-amylase isoenzymes in serum and saliva of patients with anorexia and bulimia nervosa]. 195 41

Serum and urine total alpha-amylase isoenzymes values were estimated in two groups of patients, who underwent either elective cholecystectomy and operative cholangiogram (group A-59 patients) or cholecystectomy without operative cholangiogram (group B - 68 patients). Serum and urine total alpha-amylase and pancreatic isoamylase (p-type) values were statistically significantly increased within the first 24 postoperative hours as compared to the preoperative levels only in group A (p less than 0.05). No clinical signs of pancreatitis were observed. Serum lipase alterations did not reach any statistically significant difference in either group. It is concluded that transient hyperamylasaemia after preoperative cholangiogram may be due to a reversible chemical pancreatitis caused by the infused opacifying agent into the common bile duct.
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PMID:Serum and urine alpha--amylase isoenzymes levels after operative cholangiogram. A prospective clinical and biochemical study. 209 Jan 89

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

Oxygen-derived free radicals mediate an important step in the initiation of experimental acute pancreatitis in the ex vivo perfused canine pancreas model. In other organ systems, circulating leukocytes may serve as one source of oxygen-derived free radical production. The current experiments were designed to evaluate the role of circulating leukocytes in the generation of injury in this model. Four experimental groups of animals were studied: group I consisted of controls (n = 6); group II had white blood cell (WBC) depletion (n = 4) in which the recirculating whole blood perfusate was depleted of 98% of its circulating leukocytes; group III had oleic acid infusion (FFA) alone (n = 9), which induced pancreatitis; group IV had WBC depletion and FFA (n = 6), in which oleic acid was infused after depletion of the circulating leukocytes in the perfusate. During the 4-hour perfusion period, the pancreatic preparations were monitored hourly for the development of edema, weight gain, and release of alpha-amylase into the perfusate. Animals in groups I and group II manifested no gross edema, gained minimal weight, and did not manifest hyperamylasemia. Leukocyte depletion alone had no effect. In group IV animals marked edema, significant weight gain, and hyperamylasemia developed to the same extent as in group III animals. These results demonstrate that circulating leukocytes are not essential to the development of pancreatitis in this model and suggest that another source of oxygen-derived free radicals mediates this injury.
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PMID:The role of leukocytes in the production of oxygen-derived free radicals in acute experimental pancreatitis. 382 56


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