Disease relevance of Hyperamylasemia

• RESULTS: The results confirm that prior induction of Hsp60 expression by water-immersion stress significantly ameliorates the severity of cerulein-induced pancreatitis as judged by the markedly reduced degree of hyperamylasemia, pancreatic edema, and acinar cell necrosis [1].
• During pancreatitis, the magnitude of hyperamylasemia, hyperlipasemia, neutrophil sequestration in the pancreas, and pancreatic acinar cell necrosis were significantly reduced in NK1R-/- mice when compared with wild-type NK1R+/+ animals [2].
• Steroid-treated (n=6) and Trasylol-treated (n=6) POSS glands became edematous, and mean weight gain and hyperamylasemia were similar to those seen in untreated POSS glands [3].
• The contribution of the exocrine pancreas to hyperamylasemia in diabetic ketoacidosis was investigated by measuring total amylase, salivary and pancreatic isoamylases, cathodic trypsin-like immunoreactivity, and pancreatic lipase in 12 consecutive patients recovering from diabetic ketoacidosis [4].
• However, by stepwise deletion multiple regression analysis, only non-Caucasian race, pentamidine use, and Mycobacterium avium-intracellulare infection were significant, independent predictors of hyperamylasemia (R2 = 0.65) [5].

High impact information on Hyperamylasemia

• The hyperamylasemia and pancreatic edema (but not the cathepsin B redistribution) that follow rat pancreatic duct obstruction were increased by infusion of a submaximally stimulating dose of the cholecystokinin analogue cerulein [6].
• Neither allopurinol nor dimethylsulfoxide reduced mortality or degree of hyperamylasemia [7].
• By contrast, serum amylase in the cimetidine group peaked at 24 hr after the start of treatment and remained abnormal slightly longer; the duration of hyperamylasemia in the group was 69 +/- 10 hr [8].
• However, among patients with hyperamylasemia, those with CFTR or SPINK-1 mutations had 648 +/- 216 U/l amylase levels compared with 232 +/- 28 U/l for those without (P = 0.025) [9].
• Acetaldehyde at 250 mg/hr induced minimal edema and weight gain (16 +/- 4 g; p less than 0.05), but not significant hyperamylasemia [10].

Chemical compound and disease context of Hyperamylasemia

• Among 13 selected patients examined prospectively after being in shock, pancreatic injury was indicated by hyperamylasemia, hyperlipasemia, elevated amylase/creatinine clearance ratio, and elevated circulating isoamylases specifically of pancreatic origin [11].
• Hyperamylasemia following methyl alcohol intoxication. Source and significance [12].
• Demonstration of macroamylasemia by polyethylene glycol (PEG) precipitation requires correct PEG concentration [13].
• We found no differences in concentrations of hypoxanthine in serum of patients with or without hyperamylasemia or in patients with or without increases in the specific pancreatic enzymes [4].
• Twenty-four hours after the procedure, severe hyperamylasemia (more than five times the upper normal limit) without pancreatic-like pain was recorded in three octreotide-treated patients (5.2%) and six controls (10.7%), the difference being not significant [14].

Anatomical context of Hyperamylasemia

• The source of hyperamylasemia is the pancreas mediated by large intravenous doses of steroid hormone [15].
• Twenty-five percent of the patients with acute calculous cholecystitis had a serum bilirubin level between 34 and 86 mumol/L (2.0 and 5.0 mg/dL) with no common bile duct abnormality and 4% had hyperamylasemia without pancreatitis [16].
• There was a statistically significant difference in amylase levels between the arterial and the external jugular venous blood, indicating the salivary gland as the organ mainly responsible for hyperamylasemia in carbon monoxide poisoning [17].
• This protease inhibitor prevented hyperamylasemia, pancreatic edema, congestion of amylase, and both amylase and lactic dehydrogenase (LDH) discharge from dispersed acini, as well as cathepsin B leakage from lysosomes and malate dehydrogenase (MDH) leakage from mitochondria in a dose-dependent manner, particularly in doses of 2 and 5 mg/kg.hr [18].
• After PBDO with ischemia, we observed hyperamylasemia, pancreatic edema, congestion of amylase and lysosomal enzyme cathepsin B as well as impaired output of amylase and cathepsin B into the pancreatic juice and a redistribution of lysosomal enzyme from the lysosomal fraction to the zymogen fraction [19].

Gene context of Hyperamylasemia

• Recently, a few more clinical features associated with myeloma, such as salivary type hyperamylasemia and elevated serum C-reactive protein (CRP) concentration, have been reported [20].
• CONCLUSIONS: A significant percentage of the newly diagnosed patients with CD have macroamylasemia [21].
• Macroamylasemia in patients with celiac disease [21].
• Hyperamylasemia was found in 20% of the cases and significantly correlated with levels of bilirubin, alkaline phosphatase and gamma-glutamyltransferase [22].
• Further, the immobilized antibody can be used to distinguish most patients with macroamylasemia from those with acute pancreatitis, because sera from the latter contain an increased proportion (greater than 80%) of pancreatic amylase [23].

Analytical, diagnostic and therapeutic context of Hyperamylasemia

• To study incidence and cause of hyperamylasemia in various diseases, serum amylase was determined in 1371 consecutive patients and subsequent isoamylase analysis was carried out in 91 hyperamylasemic sera [24].
• RESULTS: Plasma CCK levels increased five-fold early in the course in post-ERCP pancreatitis patients, but not in post-ERCP hyperamylasemia patients or in uncomplicated ERCP patients, where CCK levels temporarily decreased after ERCP [25].
• Infusion of C1-inhibitor plasma concentrate prevents hyperamylasemia induced by endoscopic sphincterotomy [26].
• Hypercalcemia associated with pancreatitis and hyperamylasemia in renal transplant recipients. Data from the Minnesota randomized trial of cyclosporine versus antilymphoblast azathioprine [27].
• Disappearance of macroamylasemia in a celiac patient after treatment with a gluten-free diet [28].

References