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)

Serum elastase 1 has been evaluated in 115 patients with pancreatic and nonpancreatic gastrointestinal diseases and in 36 healthy controls. Increased serum elastase 1 values were found in all 27 patients with acute pancreatitis. If the diagnostic cutoff was established as the 2-fold increase above the upper normal range, sensitivity of elastase 1 (100%) was superior to pancreatic lipase (90%), immunoreactive trypsin (87%) and pancreatic amylase (78%). Specificity was 96% for elastase 1 at this cutoff. No distinction was possible between edematous and necrotizing acute pancreatitis on the basis of peak serum elastase 1 concentrations. Among 32 patients with chronic pancreatitis increased serum elastase 1 values were found in 22% and decreased values in 16% of patients, showing a striking parallelism to serum values of pancreatic lipase and immunoreactive trypsin. Specificity, established in controls and 49 patients with different gastrointestinal diseases, was 77% for elastase 1, 76% for immunoreactive trypsin, 83% for pancreatic lipase and 91% for pancreatic amylase. In addition, we investigated 21 patients with severe chronic renal diseases. In patients with renal insufficiency elastase was increased in 33%, comparable to the frequency of increased amylase and pancreatic amylase serum levels, whereas immunoreactive trypsin was increased in 95%. Immunoreactive trypsin showed a significant correlation to creatinin serum concentration, whereas the other enzymes did not.
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PMID:Serum elastase 1 in inflammatory pancreatic and gastrointestinal diseases and in renal insufficiency. A comparison with other serum pancreatic enzymes. 244 75

We compared serum concentrations of cathodic trypsin-like immunoreactivity, pancreatic lipase, and pancreatic isoamylase as diagnostic tests of chronic pancreatitis (and of pancreatic steatorrhea in the 41 patients with steatorrhea) in 105 patients (57 men, 48 women) consecutively investigated because of clinical suspicion of chronic pancreatitis. Chronic pancreatitis (36 patients), pancreatic steatorrhea (24 patients), and other diseases were diagnosed without knowledge of the serum levels of the three enzymes. When evaluated by means of receiver operating characteristic curves, no differences were found in diagnostic performance of the enzymes with regard to chronic pancreatitis or pancreatic steatorrhea. The sensitivity and specificity for recognition of chronic pancreatitis ranged from 0.306 to 0.444 and from 0.942 to 0.986 when the discrimination values were chosen to give highest efficiencies. The similar ranges for pancreatic steatorrhea were 0.500-0.708 and 0.882-0.941. In conclusion, none of the three enzymes had any advantage over the others as diagnostic tests of chronic pancreatitis or of pancreatic steatorrhea. Only positive test results have clinical importance because of the low sensitivities of the three enzymes.
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PMID:Serum cathodic trypsin-like immunoreactivity, pancreatic lipase, and pancreatic isoamylase as diagnostic tests of chronic pancreatitis or pancreatic steatorrhea. 329 Oct 84

Serum elastase 1 was determined in the serum of 38 patients with acute pancreatitis, using specific radioimmunoassay technique. Serving as controls were 36 healthy people, 33 patients with chronic pancreatitis, 49 patients with various GI-tract diseases, and 6 patients with pancreatic carcinoma. Sensitivity of elastase 1 for the diagnosis "acute pancreatitis" was 97% after admission to the hospital and 100% within 48 h after onset of acute pancreatitis. The determination of elastase 1 is clearly superior to that of trypsin, pancreatic lipase, or pancreatic amylase, if diagnosis has to be made more than 48 h after the onset of the disease. The specificity is restricted, because there are some cases with chronic pancreatitis and GI-diseases with raised values. There is no possibility to estimate the severity of acute pancreatitis by measuring serum elastase 1.
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PMID:Diagnostic and prognostic value of serum elastase 1 in acute pancreatitis. 364 49

The determination of basal pancreatic serum enzymes is of little value in the diagnosis of chronic pancreatitis. The organ specificity of a recently introduced immunochemical method of determining pancreatic lipase is guaranteed. The diagnostic value of the basal and stimulated serum-lipase determination by the immunochemical assay in chronic pancreatitis was investigated on 84 patients and controls. In 46 patients with chronic pancreatitis the serum increase of pancreatic lipase after secretin stimulation (1 U/kg) was significantly (P less than 0.01) higher than the pancreatic lipase increase in patients with non-pancreatic intestinal disorders and in healthy controls. Patients with chronic pancreatitis deserve to be classified in subgroups, according to the degree of the exocrine pancreatic insufficiency established by means of the secretin-ceruletide test. Of the patients with chronic pancreatitis and a slight to moderate exocrine pancreatic insufficiency 87% show an abnormal serum pancreatic-lipase increase and differ significantly (P less than 0.01) from patients with severe exocrine insufficiency who exhibit an increase of the pancreatic serum lipase only in exceptional cases. Specificity is limited, since an abnormal serum lipase increase after stimulation is found in 20% of controls.
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PMID:[Clinical relevance of immunochemical determination of pancreatic lipase in chronic pancreatitis]. 388 51

Pancreatic steatorrhea and pancreatic diabetes are the dominant symptoms of patients in the decompensated stage of chronic pancreatitis (CP). In this stage, the nutritional state is greatly disturbed and hypoglycemia and labile infection are involved. Pancreatic enzyme replacement therapy is the principal treatment method for pancreatic steatorrhea. Before initiating this therapy, dietary fat intake must be determined and pancreatic lipase and bicarbonate secretion function must be evaluated. Upper small intestinal pH is regulated by gastric acid secretion, and abnormal gastric emptying changes lipolysis. In addition, precipitation of bile acids in the upper small intestine and ileal brakes due to undigested fats and carbohydrates must be considered. Porcine pancreatin, bacterial lipase, and acid-resistant fungal lipase are used as enzymes for replacement therapy. Conventional, entero-coating, and enteric-coated microsphere preparations of porcine pancreatin are available for treatment and are formulated to protect against gastric acids, to dissolve enzymes at optimum pH, and to be emptied simultaneously with food from the stomach. Gastric acid secretion suppressants, such as H2 blockers or a proton pump inhibitor, can also be used concomitantly with pancreatin preparations. In consideration of both strengths and weaknesses of these preparations, types and dosages of enzyme replacement therapy should be carefully prescribed, and fecal fats should be examined repeatedly by a simple and rapid method during treatment. Attention should also be paid to changes in body weight and nutritional indices (e.g., nutritional parameters, fat-soluble vitamins). The relationship between carbohydrate maldigestion/malabsorption in CP patients and treatment of pancreatic diabetes are topics for future research.
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PMID:Pancreatic dysfunction and treatment options. 954 75

We simultaneously assessed gastric emptying and gallbladder contraction after oral administration of a liquid meal by noninvasive ultrasonography in 17 patients with chronic pancreatitis (CP) and in 17 healthy controls. Gastrointestinal (GI) transit was also assessed by a noninvasive radioopaque marker method. Exocrine pancreatic function was evaluated by analyzing pure pancreatic juice and by analyzing the autonomic nervous system by cardiovascular reflex tests. Patients with CP showed impaired gallbladder contraction at 15 min and hastened gastric emptying. The cause of the former is unclear, whereas the latter was closely related with decreased pancreatic lipase output, but not with autonomic dysfunction. GI transit time did not differ between controls and patients with CP. In conclusion, we succeeded in clearly demonstrating impaired gallbladder contraction and hastened gastric emptying in patients with CP by a single noninvasive test, ultrasonography. We also revealed for the first time that hastened gastric emptying is associated with insufficient pancreatic lipase output.
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PMID:Gastrobiliary dysmotility in patients with chronic pancreatitis as assessed by a single noninvasive test. 954 95

Male WBN/Kob rats derived from the Wistar strain spontaneously develop chronic pancreatitis as late as 3 months old. To assess the degree of disease severity, we compared the lipolytic enzyme levels in pancreas of 2-, 4-, and 6-month-old WBN/Kob rats fed isocaloric no fat (NF) and high fat (HF, 57% of total calories) diets and its pathology. Diet treatment did not significantly affect lipase and group Ib phospholipase A(2) (PLA(2)) levels in the pancreas at all ages. Development of chronic pancreatitis at the age of 4 and 6 months was consistent with the tendency of decreasing group Ib PLA(2) specific content determined by enzyme immunoassay and lipase activity, and the decreased number of group Ib PLA(2)-positive acinar cells. Pancreatic lipase and group Ib PLA(2) levels of 4-month-old WBN/Kob rats were significantly lower than those of control Wistar rats at age 4 months irrespective of diet. This allowed us to adopt 4-month-old WBN/Kob rats as a model of pancreatic insufficiency, which could be a useful tool to examine the role of gastrointestinal enzymes in lipid digestion. Ca(2+)-independent PLA(2) activity of brush border membrane-associated phospholipase B/lipase (PLB/LIP) in ileal mucosa increased significantly in 4-month-old WBN/Kob rats while its content and transcript levels remained constant, suggesting its activation at the enzyme level. In WBN/Kob rats fed the HF diet at age 4 months, PLA(2) activity catalyzed by PLB/LIP in the proximal ileal mucosa was four times the total PLA(2) activity in the intestinal lumen. These results indicate that PLB/LIP compensates for the depletion of pancreatic lipolytic enzymes in WBN/Kob rats with pancreas insufficiency.
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PMID:Increased intestinal phospholipase A(2) activity catalyzed by phospholipase B/lipase in WBN/Kob rats with pancreatic insufficiency. 1101 77

Malabsorption due to severe pancreatic exocrine insufficiency is one of the most important late features of chronic pancreatitis. Generally, steatorrhea is more severe and occurs several years prior to malabsorption of other nutrients because synthesis and secretion of lipase are impaired more rapidly, its intraluminal survival is shorter, and the lack of pancreatic lipase activity is not compensated for by nonpancreatic mechanisms. Patients suffer not only from nutritional deficiencies but also from increased nutrient delivery to distal intestinal sites, causing symptoms by profound alteration of upper gastrointestinal secretory and motor functions. Adequate nutrient absorption requires delivery of sufficient enzymatic activity into the duodenal lumen simultaneously with meal nutrients. The following recommendations are based on modern therapeutic concepts: 25,000 to 40,000 units of lipase per meal using pH-sensitive pancreatin microspheres, with dosage increases, compliance checks, and differential diagnosis in case of treatment failure. Still, in most patients, lipid digestion cannot be completely normalized by current standard therapy, and future developments are needed to optimize treatment.
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PMID:Pancreatic enzyme replacement therapy. 1127 76

During chronic pancreatitis exocrine pancreatic insufficiency develops leading to a loss of pancreatic enzymes in the duodenum, especially pancreatic lipase. As a result, lipid maldigestion occurs (on a clinical standpoint it is more serious than proteic maldigestion) responsible for greasy diarrhoea with steatorrhoea and abdominal discomfort. Stearorrhoea is diagnosed thanks to a direct measurement of the total lipid content in the stool rather than indirect test. The pancreatic origin of the steatorrhoea is demonstrated in view of the clinical history of the disease, the normal duodenal biopsy specimen or by imaging or biological testing. Steatorrhoea is treated by pancreatic extract given as a form of enteric coated microcapsules (which are protected from proteolitic and acidic digestion) together with some dietary advises.
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PMID:[Maldigestion during chronic pancreatitis]. 1145 12

Thirty years ago, it was reported that a linear relationship does not exist between the amounts of human pancreatic lipase secreted in chronic pancreatitis and the degree of steatorrhea, which was considered to appear only after more than 90% of the pancreatic secretory capacity had been lost. From these observations, it was generally thought that the lipolytic potential of the pancreas is much higher than required. In recent years, however, it has been noted that: 1) the level of inhibition of digestive lipases and gastrointestinal lipolysis by the lipase inhibitor orlistat were almost linearly correlated with the amount of excreted fat; 2) in minipigs with experimentally-induced pancreatic exocrine insufficiency, the amounts of enteric-coated pancreatic extracts needed for restoring fat digestion to normal levels were estimated to be much higher than those usually administered; 3) human pancreatic lipase specific activity on meal triglycerides is 3 orders of magnitude lower than the very high specific activity usually measured under experimental in vitro conditions which are far from physiological conditions; 4) in patients with reduced human pancreatic lipase secretion, gastric lipase plays a significant role in fat digestion. This last observation might explain the absence of a linear relationship between human pancreatic lipase secretion in chronic pancreatitis and steatorrhea. From the low specific activity displayed by human pancreatic lipase on meal triglycerides, one can better understand why more lipase than expected is needed, why fat digestion lasts for more than a few minutes and, finally, why there is not such an excess secretory capacity for lipase as had been previously thought.
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PMID:Does the pancreas really produce much more lipase than required for fat digestion? 1588 71


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