Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149521 (chronic pancreatitis)
 7,199 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper reviews recent developments of analytical methods for the determination of alpha-amylase, of its isoenzymes, and of lipase. The evaluation of severity and etiology of acute pancreatitis by enzyme assays, e.g., pancreatic elastase 1, phospholipase A2, and routine enzymes are discussed. The limited significance of enzyme determinations as compared to imaging and endoscopic procedures for the diagnosis of chronic pancreatitis is demonstrated. Indirect "tubeless" tests for the evaluation of pancreatic exocrine insufficiency with respect to the secretion of chymotrypsin (chymotrypsin in stool and NBT-PABA test) and cholesterol esterase (pancreolauryl test) are reviewed. Finally, the superiority of morphologic investigations over biochemical tests for the timely detection of pancreatic carcinoma is shown.
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PMID:Advances in the enzyme diagnosis of pancreatic diseases. 225 33

We have measured serum immunoreactive pancreatic elastase 1 concentrations in 90 patients with pancreatic cancer in order to determine its usefulness in the diagnosis of this tumor. Abnormal elastase 1 concentrations were found in only 58 (64.4%) of the 90 patients. Fifty (55.5%) had abnormally high values, and eight (8.9%) had abnormally low values. No significant differences in elastase 1 levels were observed between patients with resectable cancer (n = 15) and those with unresectable cancer (n = 75). Moreover, no significant differences were found between elastase 1 concentrations of patients with pancreatic cancer and those of 71 patients with chronic pancreatitis. We conclude that serum elastase 1 measurement does not represent a significant advance in the diagnosis, whether early or late, of pancreatic cancer.
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PMID:Serum immunoreactive elastase: is it useful for the diagnosis of pancreatic cancer? 273 76

Serum pancreatic elastase 1 content in 45.9% of 203 samples from 32 patients with acute pancreatitis was found to be greatly elevated to greater than 1000 ng/dl, much higher than the control values (90 to 270 ng/dl), whereas serum alpha-amylase activity, in 62.3% of the same samples, was within the control range (100 to 460 IU/L). The increased pancreatic elastase 1 content persisted for several days after serum alpha-amylase activity returned to normal, suggesting that, compared with serum alpha-amylase activity, pancreatic elastase 1 content truly reflects the clinical course of acute pancreatitis. The measurement of pancreatic elastase 1 content appears to be more valuable in the diagnosis and prognosis of acute pancreatitis than that of serum alpha-amylase activity. In 41 patients with chronic pancreatitis, on the other hand, pancreatic elastase 1 content and serum alpha-amylase activity were within the normal range in 38.3% and 56.2% respectively, of 336 samples.
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PMID:Alterations in serum pancreatic elastase 1 content in acute and chronic pancreatitis: comparison with alpha-amylase activity. 387 32

By light and electron microscopic immunocytochemistry the distribution is described of human pancreatic elastase 1 (E1) during ontogenesis, in adults, in cases of acute and chronic pancreatitis, acute pancreatic ischaemia as well as pancreatic tumours. E1-positive cells were first detected in ductal sprouts in the 14th gestational week. Complete acini expressing E1 could be found from the 17th to the 20th week of gestation onwards. Scattered distinct E1-positive epithelia could be found in the ducts of fetal and adult pancreas. By immunoelectron microscopy, E1 was localized in rough endoplasmic reticulum, condensing vacuoles, zymogen granules of acinar epithelia and in acinar lumina. E1 appeared to be distributed homogeneously in zymogen granules. As specific markers of acinar cells, both monoclonal antibodies under study identified heterotopic pancreatic acini in peribiliar glands of the liver and also helped to visualize different damage patterns in pancreatitis. The acinar epithelia surrounding acute lipolytic necroses initially reacted more intensely with the E1-antibodies than undamaged pancreatic tissue. In acute ischaemia, acinar cells which are dissociated from intercalated ducts lost their immunocytochemical reactivity for E1. Pancreatic parenchyma involved in advanced acute pancreatitis as well as in chronic inflammation was detected only weakly by both E1-antibodies. However, atrophic lobules in post-inflammatory scars were stained more intensely by the E1-antibodies than normal parenchyma. Pancreatic tumours (adenomas, adenocarcinomas, solid-cystic tumours and islet cell tumours) were not labelled by these antibodies.
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PMID:Immunocytochemical localization of elastase 1 in human pancreas. 763 50

Many tests are available to assess pancreatic function. The ideal test would be simple and have adequate sensitivity in mild to moderate chronic pancreatitis (MCP) and severe CP (SCP). Fecal pancreatic elastase 1 (FPE1) assay (ScheBo Tech) has been proposed as a reliable test to evaluate pancreatic exocrine function, with sensitivities of up to 100% in diagnosing CP. Cutoff values (microgram/g stool) of < 100 have been suggested as SCP, 100-200 as MCP, and > 200 as normal. The test's ability to detect MCP distinguished by the absence of steatorrhea, and its specificity among various etiologies of malabsorption, has not been fully evaluated. The aim of this study was to evaluate this assay in subjects including patients with SCP with steatorrhea, patients with MCP with no steatorrhea, healthy controls, and diseased controls with nonpancreatic malabsorption. Thirty-six subjects [15 healthy controls, 7 malabsorption controls, and 14 subjects with CP (7 MCP, 7 SCP)] had FPE1 assays. One hundred fifty-four assays for FPE1 were run for analysis. The intraassay and interassay intraclass correlation coefficients were 0.93 and 0.90, respectively. All SCP had values of < 100 micrograms/g but more than half of the MCP subjects had FPE1 levels within the normal range. The subjects with nonpancreatic malabsorption had FPE1 values ranging from 55 to > 500 micrograms/g of stool. Although the assay detected SCP with steatorrhea, it did not consistently separate the MCP patients from normals. The majority of those with nonpancreatic malabsorption had false-positive values. These results may differ from previously described data because of the purposeful inclusion of MCP subjects, documented by the lack of steatorrhea, and the inclusion of disease controls with nonpancreatic malabsorption. Although PE1 concentrates in the stool and is not significantly degraded, subtle changes in this enzyme, as in MCP, do not seem to be detectable by this assay. This group continues to be the most difficult group to diagnose clinically.
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PMID:Fecal pancreatic elastase 1 is inaccurate in the diagnosis of chronic pancreatitis. 888 41

Views on the existence of a negative feedback between pancreatic secretion and intraduodenal of proteases in humans are controversial. The objective of the study was to find out whether enzyme substitution will have an impact on pancreatic enzyme secretion and pain in chronic pancreatitis. The preparation Panzytrate 2500 (2 x 3 capsules/day containing 1250 units of proteases per capsule) was administered for a 4-week period. In 18 patients with chronic pancreatitis (7 with the severe and 11 with the medium severe and mild form of pancreatitis) the faecal and serum pancreatic elastase was assessed one day before and one day after enzyme substitution therapy. A significant reduction of the faecal elastase concentration (p = 0.03) and serum elastase (p = 0.00375) was recorded in patients with mild and medium severe CP. The values of faecal and serum pancreatic elastase 1 were insignificantly reduced also in patients with severe chronic pancreatitis. Pain relief was statistically significant already after two weeks' administration of enzyme substitution therapy (p = 0.0233) and after four weeks' treatment (p = 0.00766). The results support the importance of the negative feedback on regulation of pancreatic secretion and the positive effect of substitution therapy on pain in chronic pancreatitis.
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PMID:[Effect of pancreatic substitutes on fecal and serum elastase and on pain in patients with chronic pancreatitis]. 1122 80

There are still too few conclusive reports about conspicuous vitamin D deficiency in patients with chronic pancreatitis, or any connection of the deficiency to the severity of the disease. Between October 1999 and September 2000, we investigated 42 patients at an average age of 53 years, suffering from chronic pancreatits, as well as 20 healthy male controls at an average age of 49 years. Serum levels of D3 vitamins, 1,25-(OH)2-vitamin D3 and 25-(OH)-vitamin D3, as well as the concentration of fecal elastase 1 were determined in patients and controls. Furthermore, the severity of chronic pancreatitis in patients was determined via endoscopic retrograde cholangiopancreatography (ERCP) into 3 grades, based on the Cambridge classification. Elastase 1 in feces revealed sensitivities of 14%, 87%, and 95% for Cambridge-grades I, II, and III, respectively, and correlated significantly with this classification of severity of chronic pancreatitis (P < 0.01). In patients with Cambridge-grade II and III 1,25-(OH)2-D3 was markedly decreased (26.7 +/- 7.7 pg/ml and 27.6 +/- 9.0 pg/ml) compared to those with Cambridge-grade I (38.0 +/- 10.5 pg/ml; between I and II P = 0.027, between I and III P = 0.033). 25-(OH)-D-3 did not differ significantly within the various Cambridge-grade groups (P = 0.07). Nevertheless, vitamin D3 and fecal elastase 1 in patients correlated significantly (P < 0.01) and, compared to controls, both were extremely low (means in patients: fecal elastase 1 140.7 +/- 75.7 microg/g, 1,25-(OH)2-D3 29.9 +/- 9.5 pg/ml, 25-(OH)-D3 26.7 +/- 9.7 nmol/liter; controls: fecal elastase 1 694.9 +/- 138.6 microg/g, 1,25-(OH)2-D3 67.5 +/- 4.3 pg/ml, 25-(OH)-D3 69.5 +/- 13.5 nmol/liter). The amounts of both D3 vitamins in patients were significantly lower when the content of fecal elastase 1 was under 200 microg/g compared to the others [for 1,25-(OH)2-D3 P < 0.01, for 25-(OH)-D3 P < 0.05]. Therefore, ERCP and fecal elastase 1 verify the severity grade of a chronic pancreatitis, and thus show a vitamin D3 deficiency, depending on the progress of the disease. There seems to be a connection between inflammatory pancreas destruction (Cambridge classification), exocrine insufficiency (fecal elastase 1), and perhaps even the characteristics of sterol-binding of pancreatic elastase 1, which seems to be relevant for vitamin D supply.
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PMID:Vitamin D3 in patients with various grades of chronic pancreatitis, according to morphological and functional criteria of the pancreas. 1275 66

Fecal pancreatic elastase 1 (PE-1) has been advocated as a noninvasive marker of pancreatic function and allows detection of moderate and severe exocrine insufficiency. Few studies have evaluated the utility of measuring PE-1 in duodenal fluid for the diagnosis of pancreatic insufficiency. Our purpose was (1) to determine the feasibility of measuring PE-1 concentrations in duodenal aspirates obtained through our endoscopic pancreatic function test (ePFT) in healthy subjects and patients with chronic pancreatitis (CP) and (2) to determine correlations between duodenal PE-1 concentrations and bicarbonate and lipase concentrations in duodenal fluid. Healthy subjects (HS) and CP patients underwent an ePFT with CCK or secretin. CP was defined as endoscopic retrograde pancreatography (ERP) Cambridge class III-IV, endoscopic ultrasound (EUS) score >5, or presence of pancreatic calcifications on CT scan. Duodenal fluid PE-1, lipase, and bicarbonate concentrations were measured in each study group. Duodenal lipase and bicarbonate concentrations were measured using an autoanalyzer (Roche Diagnostics, Indianapolis, IN). PE-1 was measured using an ELISA (Genova Diagnostics, Asheville, NC). Ten HS and 10 CP patients were studied. In the CCK test the median peak lipase for HS and CP was 1605 and 113 IU/L, respectively (P < 0.008). In the secretin test the median peak bicarbonate for HS and CP was 102 and 40 mEq/L, respectively (p < 0.008). Median PE-1 concentrations for HS and CP were 317 and 63 microg/ml, respectively, after CCK stimulation (p = 0.046) and 87 and 17 microg/ml, respectively, after secretin stimulation (p = 0.033). Statistically significant correlations were found between [PE-1] and peak [lipase] (r = 0.83, P < 0.001), as well as [PE-1] and peak [HCO3(3)-] (r = 0.65, P = 0.037). Conclusions are as follows: (1) PE-1 concentrations can be measured from duodenal fluid obtained by endoscopic aspiration. (2) Duodenal fluid PE-1 concentrations are decreased in CP compared to HS. (3) Duodenal fluid [PE-1] has an excellent correlation with [lipase] and therefore is a marker of acinar cell function. (4) Secretin-stimulated endoscopic function testing with measurement of bicarbonate and PE-1 may provide a simultaneous assessment of both ductal cell and acinar cell function.
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PMID:Analysis of pancreatic elastase-1 concentrations in duodenal aspirates from healthy subjects and patients with chronic pancreatitis. 1548 11