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

Acute pancreatitis (AP) is believed to result from intraparenchymal activation of trypsin and other digestive enzymes within the pancreas followed by autodigestion of the gland. Gabexate mesilate (FOY), a synthetic guanidino acid ester exhibiting potent and versatile inhibitory actions on a number of proteinases (e.g., trypsin, kallikrein, C1-r, C1 esterase, plasmin, thrombin, phospholipase A2), was examined for its ability to protect the rat pancreas against development of AP induced by pharmacological doses of ceruletide (CRT). Rats were i.v. infused for 6 h with either CRT (5 micrograms/kg/h) or CRT + FOY (50 mg/kg/h). In FOY-treated rats the serum amylase and trypsinogen concentrations were reduced by 60 and 80%, respectively, compared to rats infused with CRT alone. Histologically, the extent of acinar cell vacuolization in the pancreas was significantly reduced and interstitial edema, although not assessed by quantitative morphometric techniques, appeared to be qualitatively lessened in the FOY-treated rats. The ability of FOY to inhibit significantly AP produced by supramaximal doses of CRT, coupled with its inhibitory properties on components of the coagulation and complement cascades, stress the importance of continued research on this compound as a potential therapeutic agent for treatment of AP and its systemic sequelae.
Pancreas 1987
PMID:Gabexate mesilate (FOY) protects against ceruletide-induced acute pancreatitis in the rat. 244 41

The plasma levels of certain digestive enzymes and protease inhibitors were determined in 40 patients with severe acute pancreatitis diagnosed as gallstone-induced (GP), alcoholic (AP), or idiopathic (IP). On admission, plasma levels of amylase and immunoreactive cationic trypsin(ogen) (IRCT) and elastase 2 (IRE 2) were found to be 50 +/- 10 ng/ml, 340 +/- 64 ng/ml, and 190 +/- 15 ng/ml, respectively, in all groups of patients. These enzymes levels remained high for the first 2 days following hospitalization and then decreased, although amylase and IRCT levels remained elevated above normal values throughout the study period (2 weeks). In general amylase and IRCT were lower in patients with concomitant ascites, pancreatic pseudocysts, or abscesses, and higher in patients who died, as compared to the pancreatitis group as a whole. In these patients, levels of immunoreactive alpha 1-protease inhibitor (alpha 1-PI) and alpha 2-macroglobulin (alpha 2-M) remained relatively constant at the lower end of the normal range throughout the study period. Inhibitor levels in plasma were unaffected by the etiology of pancreatitis or the occurrence of complications. A similar trend was seen with plasma levels of lysosomal hydrolases. The results indicate that in this group of patients, plasma levels of pancreatic digestive enzymes were reflective of the clinical features and severity of the disease, as well as the time following the acute attack that brought the patient to the hospital.
Pancreas 1987
PMID:Digestive enzymes and protease inhibitors in plasma from patients with acute pancreatitis. 244 42

Lipase, in contrast to amylase, is completely reabsorbed by the proximal tubules after glomerular filtration. Therefore, no lipase is detectable in the unconcentrated urine according to the current opinion. The handling of lipase (detected with an enzyme-immunoassay) by the kidney was investigated in comparison with creatinine, amylase, and beta-2-microglobulin by clearance studies in acute pancreatitis (n = 10), burn injury (n = 4), glomerular proteinuria (n = 8), and controls without evidence of pancreatic or renal diseases (n = 5). In initial stages of acute pancreatitis a measurable clearance of lipase (mean: 49.6 microliters/min, range: 0.5-234) was found in association with corresponding increased clearances of beta-2-microglobulin (mean: 10.5 ml/min, range: 0.02-58.9) and of amylase (mean: 8.9 ml/min, range: 2.4-22.6) in nine of ten patients. This finding is consistent with a defect of tubular function. However, regression analysis failed to show a significant correlation between lipase and beta-2-microglobulin clearance. Repeated measurements during the course of pancreatitis in seven patients showed reversibility of tubular dysfunction. In patients with burn injury a similar elevation of clearances of beta-2-microglobulin and of amylase was found, but tubular dysfunction in this condition was not associated with lipasuria. In glomerular proteinuria a lipase clearance was found in two of five cases with moderate, and in the other three cases with severe impairment of creatinine clearance. beta-2-microglobulin clearance was normal in the former and only slightly elevated in the latter group. In conclusion lipase is measurable in the urine of most patients with acute pancreatitis as a result of a reversible tubular dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)
Pancreas 1987
PMID:Lipasuria in acute pancreatitis: result of tubular dysfunction? 244 47

The variations of serum levels of amylase, pancreatic isoamylase, lipase, trypsinogen, and elastase 1 were evaluated in 21 patients with acute pancreatitis. The patients were studied for a mean period of 7 consecutive days (range 5-12 days) after admission to the hospital. On the day of onset of acute pancreatitis, all enzyme levels were abnormally high; pancreatic isoamylase showed the greatest increase compared with its upper normal limit, whereas the increase increment for elastase 1 was the lowest. Subsequently, all enzyme levels except elastase 1 decreased in a parallel fashion. On the eighth day of the study only elastase 1 levels were above normal values in all patients examined, while abnormally high values of lipase were found in 85% of the patients, trypsinogen in 58% of the patients, pancreatic isoamylase in 43%, and total amylase in 23%. These results indicate that, for the early diagnosis of acute pancreatitis, the determination of any of these enzymes is equally efficient, but that elastase 1 is the most sensitive marker of acute pancreatic damage in later stages of the disease.
Pancreas 1987
PMID:Serum pancreatic enzyme behavior during the course of acute pancreatitis. 244 67

By use of an enzyme-linked immunosorbent assay we established serum reference values of carboxylic ester hydrolase, a pancreatic secretory lipolytic enzyme, and explored to see if a raised serum level is indicative of acute pancreatitis. Postoperative elevation of carboxylic ester hydrolase was observed in seven out of ten patients who underwent pancreatic surgery. Serum levels of carboxylic ester hydrolase and amylase were determined in 129 patients admitted due to abdominal emergency conditions. Amylase was elevated in 27 patients, and in 20 of these raised carboxylic ester hydrolase levels affirmed the diagnosis acute pancreatitis. In five out of the seven patients with elevated amylase alone no etiologic factor of acute pancreatitis was found. Another 11 patients had raised carboxylic ester hydrolase levels without concomitant elevation of amylase. In all these patients, a likely cause of pancreatic inflammation was identifiable. Hence, a raised carboxylic ester hydrolase level, even in presence of normal amylase, could be indicative of acute pancreatic inflammation.
Pancreas 1987
PMID:Carboxylic ester hydrolase: a serum marker of acute pancreatitis. 244 73

Fifty-one patients, 35 men and 16 women, with acute pancreatitis were studied prospectively with early computed tomography (CT). Etiological factors for acute pancreatitis were alcohol abuse (n = 28), gallstones (n = 14), pancreas cancer (n = 3) and miscellaneous (n = 6). Admission serum amylase levels ranged between 68-5,856 U/L with a mean of 1,090 +/- 1,369 U/L. The mean serum amylase level was significantly different between patients with alcoholic pancreatitis (439 +/- 302 U/L) and gallstone pancreatitis (2,480 +/- 1,575) (p less than 0.001). The initial pancreatic CT findings and corresponding mean serum amylase levels were in CT grade A (pancreas normal) 1,499 +/- 1,569 U/L (n = 11), in CT grade B (pancreatic enlargement with inflammation confined to pancreas) 1,144 +/- 1,542 U/L (n = 18), in CT grade C (inflammatory extension into one peripancreatic space) 722 +/- 962 U/L (n = 13) and in CT grade D (inflammatory extension into two or more peripancreatic spaces) 590 +/- 369 U/L (n = 9). However, on separating the etiology subgroups, there was no increase or decrease in the serum amylase level with increasing pancreatic inflammatory involvement. Pancreatic complications (pseudocyst, abscess, necrosis) requiring surgical intervention developed only in patients with CT grades C and D. We conclude that within the etiologic subgroups there is no correlation between the initial serum amylase level and the extent of pancreatic involvement visualized by CT. These findings provide a pathological basis for the clinical observation that the initial serum amylase level cannot predict the outcome in acute pancreatitis.
Pancreas 1988
PMID:Correlation of serum amylase levels with pancreatic pathology and pancreatitis etiology. 245 72

This study was undertaken to investigate serially the development, progression, and healing of acute pancreatitis which was induced in rats by the closed duodenal loop technique. Edematous changes appeared within 2 to 4 h. Pancreatic blood flow increased at 1 h and tended to decrease after 3 h. After injection of fesin into the loop, fesin appeared in the periacinar space and acinar cells after 4 h. Electron microscopy showed that partial destruction of the plasma membrane occurred and serum amylase increased considerably at the same time, suggesting that the initial inflammatory changes caused the release of pancreatic enzymes at approximately 4 h. After elimination of the causal factors, edematous pancreatitis healed completely but hemorrhagic acute pancreatitis was not completely healed 6 months later.
Pancreas 1988
PMID:Serial histologic study of the development, progression, and healing of acute pancreatitis in the rat. 245 73

We examined the protective effects of the trypsin inhibitor, urinastatin, extracted from human urine in experimental acute pancreatitis in conscious rats. Acute pancreatitis was induced by four subcutaneous injections of 20 micrograms/kg body weight of cerulein at hourly intervals. Urinastatin at a dose of 50,000 U/kg body weight/6.5 h was given by continuous i.v. infusion beginning 0.5 h before the first cerulein injection and continuing until 3 h after the last one, for a total of 6.5 h. Urinastatin significantly reduced serum levels of amylase, lipase, and anionic trypsin(ogen) but did not affect pancreatic wet weight or protein or enzyme content. Urinastatin also significantly reduced the degree of acinar cell vacuolization, interstitial edema, and cellular infiltration. These results suggest that urinastatin does not block the induction of acute pancreatitis by cerulein but does substantially reduce its severity.
Pancreas 1988
PMID:The protective effect of the trypsin inhibitor urinastatin on cerulein-induced acute pancreatitis in rats. 245 95

A 66-year-old patient had been admitted four times for recurrent episodes of acute pancreatitis. At each time, elevated serum calcium levels, between 13.5-14.5 mg/dl, were found. Surgical drainage of necrotic pancreatic tissue had to be done on one occasion. Extensive investigations failed to disclose any conventional hypercalcemic disease. At his latest admission, the serum calcium level was 13.4 mg/dl, and the serum amylase level was 440 IU/L (N, less than 85). This time, the serum 25-OH vitamin D levels were investigated using radioimmunology and proved to be raised to 330 micrograms/L (normal, 16-74 micrograms/L). Specific questioning of the patient revealed that he had been taking regularly excessive quantities of vitamin supplements as a self medication. After stopping vitamin intake, his serum amylase levels returned to normal, and he had no more episodes of pancreatitis. This case illustrates vitamin D intoxication as a cause of recurrent pancreatitis. Measuring serum 25-OH vitamin D levels is advocated in pancreatitis associated with hypercalcemia of unclear origin.
Pancreas 1989
PMID:Recurrent pancreatitis secondary to hypercalcemia following vitamin D poisoning. 247 70

The effects of cholecystokinin receptor antagonist CR 1392 was studied in a model of mild acute pancreatitis induced in rats by four subcutaneous injections of the secretagogue caerulein. A single subcutaneous injection of 50 mg/kg body weight of CR 1392 caused a dramatic reduction in serum amylase concentration and pancreatic wet weight as well as histologic improvement of the caerulein-induced acute pancreatitis when given 30 min before the first caerulein injection. CR 1392 was also effective in reducing the elevated serum amylase activity, pancreatic weight, and histologic alterations even when administered after the pancreatitis had been induced. These present observations suggest that CR 1392 remains active for more than 3 h and blocks the action of caerulein on the pancreas.
Pancreas 1989
PMID:Effect of a new cholecystokinin receptor antagonist CR 1392 on caerulein-induced acute pancreatitis in rats. 247 65


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