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)

In patients with pancreatitis an increase of the total amount of alkaline phosphatase (ALP; EC 3.1.3.1) and the appearance of its macro isoenzyme which parallels the decrease of bone isoenzyme was found. This isoenzymatic profile suggests that the increase of ALP in pancreatitis is due to the concomitant hepatobiliary disorder. Moderate increases of ALP didn't appear to be related to the existence of gallstones.
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PMID:[Isoenzyme profile of alkaline phosphatase in patients with pancreatitis]. 159 67

The diagnostic values of CA 19-9 and CEA were evaluated in 187 cases (including 31 gastric, 41 colorectal, 12 pancreatic, 7 hepatobiliar and 5 hepatocellular carcinomas). These tumor markers were compared to the other laboratory parameters [hemoglobin, erythrocyte sedimentation rate, serum bilirubin, ASAT (aspartate amino transferase), ALAT (alanine amino transferase) GGT (gamma glutamil transpeptidase), ALP (alkaline phosphatase)]. The specificity of CA 19-9 was 89.5%, while the sensitivity of this tumor markers was 91.7% in pancreatic carcinoma, 54.8% in gastric carcinoma and 43.9% in colorectal carcinoma. The sensitivity of CEA only in colorectal patients was higher than that of CA 19-9 (specificity 73.9%, sensitivity 64.5%). Although the CA 19-9 and CEA are not known to give any cross-reaction with each other, simultaneous measurement and evaluation of these two tumor antigens did not result in a better diagnostic sensitivity. After undergoing a gastrointestinal carcinoma operation, CA 19-9 indicated the appearance of tumor recidiva with a 62% sensitivity. Calculated together with CEA the sensitivity elevated to 88.9%. In most of the patient with benign cholostasis, the CA 19-9 and CEA values were out of the normal range (53.3% and 36.4% respectively), so these tumor markers are not suitable to differentiate between benign and malign cholostasis. According to the authors, CA 19-9 is the most useful diagnostic tool to differentiate between pancreatic carcinoma and pancreatitis chronica (both group without cholostasis), as well as for monitoring the patients after surgery of a gastrointestinal cancer.
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PMID:[Diagnostic value of CA 19-9 and CEA in gastrointestinal pathology]. 160 81

Pancreatic juice gamma-glutamyltransferase (GGT, EC 2.3.2.2) has been proposed as a marker of pancreatic disease. We have collected pancreatic juice endoscopically from 24 control patients and 43 patients with a variety of hepatic, pancreatic, and biliary disorders. Pancreatic juice GGT, alanine transaminase (ALT, EC 2.6.1.2), and alkaline phosphatase (ALP, EC 3.1.3.1) were measured and found to be present in all samples. GGT was significantly higher in patients with pancreatic cancer (range 21-1175 IU/liter, P less than 0.005) compared with controls (range 2-52 IU/liter). Of 17 patients with pancreatic juice GGT concentrations greater than 52 IU/liter, eleven had definite pancreatic disease (seven pancreatic cancer, four chronic pancreatitis) and, in the remaining six, pancreatitis was possible although not proven. Pancreatic juice ALT and ALP provided no useful diagnostic criteria. GGT in pancreatic juice seems to be a nonspecific marker of pancreatic disease and merits further study.
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PMID:Pancreatic juice gamma-glutamyltransferase, alanine transaminase, and alkaline phosphatase in pancreatic disease. 610 99

In this study we observed the discriminative ability of five commonly measured laboratory tests to distinguish between gallstone- and non-gallstone-associated pancreatitis. We also assessed the ability of the lipase-amylase ratio to discriminate between alcohol- and non-alcohol-induced pancreatitis. One hundred sixty-two patients with acute pancreatitis were included in the study. Group A consisted of patients presenting to our hospital in 1988 and 1989. Group B consisted of patients presenting in 1992. Models developed using group A patients were validated using group B patients. For gallstone pancreatitis, AST (threshold value 80 IU/liter) alone and a three-factor model, AST, ALP and bilirubin (threshold values of 80 IU/liter, 115 IU/liter, and 15 mumol/liter, respectively) were the best predictors, correctly classifying at least 80% of cases in group A and B. A lipase-amylase ratio of two correctly classified only 48% of cases in group A and 54% in group B. We conclude that biochemical models are useful in predicting the presence of gallstone pancreatitis but not alcoholic pancreatitis.
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PMID:Biochemical models as early predictors of the etiology of acute pancreatitis. 768 46

Medical records and histologic sections of 40 cats with acute pancreatitis were reviewed. Two distinct groups of cats with pancreatitis were established by histologic analysis of tissue. Group 1 (32 cats) had acute pancreatic necrosis (APN). Group 2 (8 cats) had suppurative pancreatitis. Ages of affected cats ranged from 3 weeks to 16 years. The majority consisted of indoor cats of the Domestic Short-Haired breed but Siamese cats were over-represented relative to the general population (P < 0.05). Twenty-two percent of cats were obese and 57% were underweight. Thirty-eight percent of cats had acute disease. In the other cats, two stages in the progression of the disease were evident: (1) anorexia, weight loss, and lethargy, followed by (2) acute deterioration, development of shock, and a moribund state, despite fluid therapy. The most common clinical signs were severe lethargy (100%), reduced appetite (97%), dehydration (92%), and hypothermia (68%). The initial hemogram occasionally showed a neutrophilia (30%) and anemia (26%) but packed cell volume (PCV) decreased markedly to the extent that 55% of cats were anemic terminally. Serum biochemical abnormalities included increased activities of ALT (68%) and ALP (50%), and increased concentrations of bilirubin (64%) and cholesterol (64%). Cats with APN were hyperglycemic (64%), glycosuric (60%) and ketonuric (20%), whereas cats with suppurative pancreatitis tended to be hypoglycemic (75%). Renal failure and electrolyte abnormalities were mild or infrequent except for hypokalemia (56%). This study characterizes a severe necrotizing pancreatitis in the cat similar to that reported in other species, and a histologically distinct suppurative pancreatitis.
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PMID:Acute necrotizing pancreatitis and acute suppurative pancreatitis in the cat. A retrospective study of 40 cases (1976-1989). 1146 88

Overproduction of tumor necrosis factor (TNF-), interleukin-1beta (IL-1beta), and nitric oxide (NO) is believed to be detrimental during the progression of acute pancreatitis, yet little is known about the hepatic production of these mediators and their role in mediating pancreatitis-induced hepatic dysfunction. Rats were randomized to receive a single intraperitoneal injection of the macrophage-pacifying compound, CNI-1493 (1.0 mg/kg), or vehicle 1 hour before the induction of retrograde bile salt pancreatitis. Sham-operated animals served as controls. Animals were killed 18 hours later, with serum and livers harvested to determine the degree of hepatocellular injury and the induction of TNF-, IL-1beta, and inducible nitric oxide synthase (iNOS). In addition, serum TNF- and nitrites (end-product of NO breakdown) were determined in each group to assess the mechanism of action of CNI-1493. TNF-, IL-1beta, and iNOS gene expression (by reverse-transcription polymerase chain reaction) as well as aspartate transaminase (AST), alanine transaminase (ALT), and lactic dehydrogenase (LDH) (but not alkaline phosphatase [ALP]) increased following the development of pancreatitis (all P < .05). Macrophage pacification significantly prevented the induction of TNF- and IL-1beta mRNA (but not iNOS), resulting in lessened serum AST, ALT, and LDH (all P < .05). Serum TNF- protein and nitrites correlated with gene induction in that both were increased following the onset of pancreatitis, and TNF- protein production was significantly attenuated in animals receiving CNI-1493. Hepatocellular, but not bile duct, injury occurs during experimental pancreatitis that is associated with hepatic TNF-, IL-1beta, and iNOS mRNA gene induction, as well as TNF- protein and nitrite production. Preventing the production of TNF- and IL-1beta by macrophage pacification attenuates the hepatocellular damage, suggesting that these mediators play a role in pancreatitis-induced hepatic injury.
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PMID:Macrophage pacification reduces rodent pancreatitis-induced hepatocellular injury through down-regulation of hepatic tumor necrosis factor alpha and interleukin-1beta. 979 13

Practical guidelines for the diagnosis of acute pancreatitis are presented so that a rapid and adequate diagnosis can be made. When acute pancreatitis is suspected in patients with acute onset of abdominal pain and tenderness mainly in the upper abdomen, the diagnosis of acute pancreatitis is made on the basis of elevated levels of pancreatic enzymes in the blood and/or urine. Furthermore, other acute abdominal diseases are ruled out if local findings associated with pancreatitis are confirmed by diagnostic imaging. According to the diagnostic criteria established in Japan, patients who present with two of the following three manifestations are diagnosed as having acute pancreatitis: characteristic upper abdominal pain, elevated levels of pancreatic enzymes, and findings of ultrasonography (US), CT or MRI suggesting acute pancreatitis. Detection of elevated levels of blood pancreatic enzymes is crucial in the diagnosis of acute pancreatitis. Measurement of blood lipase is recommended, because it is reported to be superior to all other pancreatic enzymes in terms of sensitivity and specificity. For measurements of the blood amylase level widely used in Japan, it should be cautioned that, because of its low specificity, abnormal high values are also often obtained in diseases other than pancreatitis. The cut-off level of blood pancreatic enzymes for the diagnosis of acute pancreatitis is not able to be set because of lack of sufficient evidence and consensus to date. CT study is the most appropriate procedure to confirm image findings of acute pancreatitis. Elucidation of the etiology of acute pancreatitis should be continued after a diagnosis of acute pancreatitis. In the process of the etiologic elucidation of acute pancreatitis, judgment whether it is gallstone-induced or not is most urgent and crucial for deciding treatment policy including the assessment of whether endoscopic papillary treatment should be conducted or not. The diagnosis of gallstone-induced acute pancreatitis can be made by combining detection of elevated levels of bilirubin, transamylase (ALT, AST) and ALP detected by hematological examination and the visualization of gallstones by US.
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PMID:New diagnostic criteria of acute pancreatitis. 2001 28

Autoimmune pancreatitis (ALP) represents a distinct form of chronic pancreatitis initially described in Japan but now reported worldwide. AIP often presents with obstructive jaundice/pancreatic mass as well as pancreatic exocrine and endocrine insufficiency. Histologically, it is characterised by a lymphoplasmacytic infiltrate with fibrosis. The disease responds readily to steroids in 70-80% of cases. Given the absence of unified diagnostic criteria, the diagnosis of AIP proves difficult. In particular, distinguishing ALP from pancreatic or biliary cancer remains a challenging task. In order to avoid unnecessary resections for an otherwise benign and easily treatable condition, it is urgent to refine diagnostic criteria and to reach an international consensus.
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PMID:[Autoimmune pancreatitis]. 2093

Background and Aim. There are no accurate methods of differentiating acute biliary pancreatitis. Obstructions of biliary ducts, idiopathic pancreatitis may be related with biliary origin which needs identification for acute treatment. We searched for the predictivity of biochemical markers in early acute biliary pancreatitis. Patients and Methods. Serum levels of AST (Aspartate Transaminase),ALT (Alanine Transaminase), ALP (Alkaline Phosphatase), GGT (Gamma Glutamyl Transferase), total bilirubin, direct bilirubin, LDH (Lactate Dehydrogenase), amylase, lipase, CRP (C-Reactive Protein) and WBC (White Blood Cell) were measured in 157 patients with acute pancreatitis. Biliary and nonbiliary pancreatitis were differentiated by Magnetic Resonance Cholangiopancreatography (MRCP), Endoscopic Retrograde Cholangiopancreatography (ERCP), Intraoperative Cholangiopancreatography (IOC). Cut-off points of admission biochemical markers with sensitivity, specifity, positive predictive value and negative predictive value were determined after identification of significant variables. Receiver Operator Curves were plotted for each biochemical marker. Results. Serum Alkaline Phosphatase, total bilirubin, direct bilirubin, amylase and lipase levels were significantly higher in biliary pancreatitis with a positive predictive value of 80.8%, 83.9%, 81.6%, 78.8%, 79.7%. Conclusion. Increased Alkaline Phosphatase,total bilirubin, direct bilirubin, amylase and lipase levels may be used in prediction of biliary pancreatitis.
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PMID:The predictivity of serum biochemical markers in acute biliary pancreatitis. 2199 1

We report the finding of alkaline phosphatase-immunoglobulin complex (macro-alkaline phosphatase (macro-ALP)) in a patient with persistently increased ALP activity. The identification of macro-ALP is important to rule out pathological causes of increased ALP activity and to avoid unnecessary diagnostic investigation. The patient was subsequently diagnosed with vitamin D deficiency, gallstone pancreatitis, and monoclonal gammopathy of undefined significance (MGUS). Macro-ALP can coexist with disease that can increase serum ALP activity. We report, for the first time, a case of macro-ALP in a patient with a monoclonal protein (M-protein).
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PMID:Persistent Increase in Serum Alkaline Phosphatase in a Patient with Monoclonal Gammopathy of Undefined Significance. 3208 56


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