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Disease relevance of Hyperamylasemia


High impact information on Hyperamylasemia


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


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


  1. Water immersion stress induces heat shock protein 60 expression and protects against pancreatitis in rats. Lee, H.S., Bhagat, L., Frossard, J.L., Hietaranta, A., Singh, V.P., Steer, M.L., Saluja, A.K. Gastroenterology (2000) [Pubmed]
  2. Role of substance P and the neurokinin 1 receptor in acute pancreatitis and pancreatitis-associated lung injury. Bhatia, M., Saluja, A.K., Hofbauer, B., Frossard, J.L., Lee, H.S., Castagliuolo, I., Wang, C.C., Gerard, N., Pothoulakis, C., Steer, M.L. Proc. Natl. Acad. Sci. U.S.A. (1998) [Pubmed]
  3. Experimental gallstone pancreatitis. Pathogenesis and response to different treatment modalities. Broe, P.J., Cameron, J.L. Ann. Surg. (1982) [Pubmed]
  4. Hyperamylasemia, specific pancreatic enzymes, and hypoxanthine during recovery from diabetic ketoacidosis. Møller-Petersen, J., Andersen, P.T., Hjørne, N., Ditzel, J. Clin. Chem. (1985) [Pubmed]
  5. Hyperamylasemia in patients with the acquired immunodeficiency syndrome. Murthy, U.K., DeGregorio, F., Oates, R.P., Blair, D.C. Am. J. Gastroenterol. (1992) [Pubmed]
  6. Effects of short-term pancreatic duct obstruction in rats. Ohshio, G., Saluja, A., Steer, M.L. Gastroenterology (1991) [Pubmed]
  7. Role of oxygen-derived free radicals in diet-induced hemorrhagic pancreatitis in mice. Rutledge, P.L., Saluja, A.K., Powers, R.E., Steer, M.L. Gastroenterology (1987) [Pubmed]
  8. Cimetidine in the treatment of acute alcoholic pancreatitis. A randomized, double-blind study. Meshkinpour, H., Molinari, M.D., Gardner, L., Berk, J.E., Hoehler, F.K. Gastroenterology (1979) [Pubmed]
  9. The role of CFTR and SPINK-1 mutations in pancreatic disorders in HIV-positive patients: a case-control study. Felley, C., Morris, M.A., Wonkam, A., Hirschel, B., Flepp, M., Wolf, K., Furrer, H., Battegay, M., Bernasconi, E., Telenti, A., Frossard, J.L. AIDS (2004) [Pubmed]
  10. The role of acetaldehyde in the pathogenesis of acute alcoholic pancreatitis. Nordback, I.H., MacGowan, S., Potter, J.J., Cameron, J.L. Ann. Surg. (1991) [Pubmed]
  11. Susceptibility of the pancreas to ischemic injury in shock. Warshaw, A.L., O'Hara, P.J. Ann. Surg. (1978) [Pubmed]
  12. Hyperamylasemia following methyl alcohol intoxication. Source and significance. Eckfeldt, J.H., Kershaw, M.J. Arch. Intern. Med. (1986) [Pubmed]
  13. Demonstration of macroamylasemia by polyethylene glycol (PEG) precipitation requires correct PEG concentration. Gillett, M.G., Gunneberg, A., Goldie, D.J. Clin. Chem. (1995) [Pubmed]
  14. Octreotide 24-h prophylaxis in patients at high risk for post-ERCP pancreatitis: results of a multicenter, randomized, controlled trial. Testoni, P.A., Bagnolo, F., Andriulli, A., Bernasconi, G., Crotta, S., Lella, F., Lomazzi, A., Minoli, G., Natale, C., Prada, A., Toti, G.L., Zambelli, A. Aliment. Pharmacol. Ther. (2001) [Pubmed]
  15. Asymptomatic transient hyperamylasemia after a large intravenous dose of steroid hormone. Takagi, H., Yasue, M., Morimoto, T., Kuroyanagi, Y., Imanaga, H. Am. J. Surg. (1977) [Pubmed]
  16. Hyperbilirubinemia without common bile duct abnormalities and hyperamylasemia without pancreatitis in patients with gallbladder disease. Kurzweil, S.M., Shapiro, M.J., Andrus, C.H., Wittgen, C.M., Herrmann, V.M., Kaminski, D.L. Archives of surgery (Chicago, Ill. : 1960) (1994) [Pubmed]
  17. Hyperamylasemia in acute carbon monoxide poisoning. Takahashi, M., Maemura, K., Sawada, Y., Sugimoto, H., Ohashi, N., Yoshioka, T., Sugimoto, T. The Journal of trauma. (1982) [Pubmed]
  18. A new synthetic protease inhibitor, E-3123, reduces organelle fragility of acinar cells in rat caerulein pancreatitis. Hirano, T., Manabe, T., Imanishi, K., Yotsumoto, F., Kyogoku, T., Tobe, T. Nippon geka hokan. Archiv für japanische Chirurgie. (1991) [Pubmed]
  19. Protective effects of combined therapy with a protease inhibitor, ONO 3307, and a xanthine oxidase inhibitor, allopurinol on temporary ischaemic model of pancreatitis in rats. Hirano, T., Manabe, T., Ohshio, G., Nio, Y. Nippon geka hokan. Archiv für japanische Chirurgie. (1992) [Pubmed]
  20. In vitro excess ammonia production in human myeloma cell lines. Otsuki, T., Yamada, O., Sakaguchi, H., Ichiki, T., Kouguchi, K., Wada, H., Hata, H., Yawata, Y., Ueki, A. Leukemia (1998) [Pubmed]
  21. Macroamylasemia in patients with celiac disease. Rabsztyn, A., Green, P.H., Berti, I., Fasano, A., Perman, J.A., Horvath, K. Am. J. Gastroenterol. (2001) [Pubmed]
  22. Indicators of inflammation and cellular damage in chronic asymptomatic or oligosymptomatic alcoholics: correlation with alteration of bilirubin and hepatic and pancreatic enzymes. Borini, P., Guimarães, R.C. Revista do Hospital das Clínicas. (1999) [Pubmed]
  23. Interaction of immobilized anti-salivary amylase antibody with human macroamylases: implications for use in a pancreatic amylase assay to distinguish macroamylasemia from acute pancreatitis. Mifflin, T.E., Forsman, R.W., Bruns, D.E. Clin. Chem. (1989) [Pubmed]
  24. Clinical value of routine isoamylase analysis of hyperamylasemia. Kameya, S., Hayakawa, T., Kameya, A., Watanabe, T. Am. J. Gastroenterol. (1986) [Pubmed]
  25. Cholecystokinin in the early course of acute post-ERCP pancreatitis. Räty, S., Sand, J., Laine, S., Harmoinen, A., Nordback, I. J. Am. Coll. Surg. (1999) [Pubmed]
  26. Infusion of C1-inhibitor plasma concentrate prevents hyperamylasemia induced by endoscopic sphincterotomy. Testoni, P.A., Cicardi, M., Bergamaschini, L., Guzzoni, S., Cugno, M., Buizza, M., Bagnolo, F., Agostoni, A. Gastrointest. Endosc. (1995) [Pubmed]
  27. Hypercalcemia associated with pancreatitis and hyperamylasemia in renal transplant recipients. Data from the Minnesota randomized trial of cyclosporine versus antilymphoblast azathioprine. Frick, T.W., Fryd, D.S., Sutherland, D.E., Goodale, R.L., Simmons, R.L., Najarian, J.S. Am. J. Surg. (1987) [Pubmed]
  28. Disappearance of macroamylasemia in a celiac patient after treatment with a gluten-free diet. Deprettere, A.J., Eykens, A., Van Hoof, V. J. Pediatr. Gastroenterol. Nutr. (2001) [Pubmed]
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