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Approach to the patient with elevated serum amylase or lipase

INTRODUCTION

Serum amylase and lipase are common tests obtained as biochemical markers for acute pancreatitis. However, the interpretation of these tests can be difficult since several non-pancreatic conditions can present with abnormal serum amylase and lipase levels [1,2]. In addition, some patients with pancreatitis have normal serum amylase and lipase levels when a blood sample is examined [3,4]. (See "Clinical manifestations and diagnosis of acute pancreatitis".)

Several factors can influence serum amylase and lipase levels.

  • The levels depend upon the rate of production from different tissues and the rate of clearance. As an example, serum amylase and lipase levels may be elevated in patients with renal failure. (See "Serum enzymes in patients with renal failure".)
  • Organs other than the pancreas can produce these enzymes. Alcoholics, for example, may have an elevated serum amylase of salivary origin. The most commonly used amylase assays cannot differentiate between salivary and pancreatic amylase.
  • Certain serum factors influence amylase and lipase enzyme activity. As an example, patients with pancreatitis due to hypertriglyceridemia may appear to have normal amylase levels, most likely due to a circulating factor that inhibits the enzyme's activity [5].

This topic review will present an approach the patient with an elevated serum amylase or lipase. Elevation of these measures in the context of individual disorders (such as pancreatitis) is discussed separately. (See "Clinical manifestations and diagnosis of acute pancreatitis", section on 'Pancreatic enzymes and products'.)

AMYLASE

Amylase is derived from the Greek word "amylone," which means starch. The main sources of amylase in humans are the pancreas and salivary glands, but it can be found in other tissues in small quantities [6]. The main function of amylase is to cleave starch into smaller polysaccharides at the internal 1 to 4 alpha linkage in the process of digestion.

            

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Literature review current through: Mar 2014. | This topic last updated: Apr 22, 2013.
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References
Top
  1. Chase CW, Barker DE, Russell WL, Burns RP. Serum amylase and lipase in the evaluation of acute abdominal pain. Am Surg 1996; 62:1028.
  2. Gumaste VV, Roditis N, Mehta D, Dave PB. Serum lipase levels in nonpancreatic abdominal pain versus acute pancreatitis. Am J Gastroenterol 1993; 88:2051.
  3. Clavien PA, Robert J, Meyer P, et al. Acute pancreatitis and normoamylasemia. Not an uncommon combination. Ann Surg 1989; 210:614.
  4. Lankisch PG, Burchard-Reckert S, Lehnick D. Underestimation of acute pancreatitis: patients with only a small increase in amylase/lipase levels can also have or develop severe acute pancreatitis. Gut 1999; 44:542.
  5. Fallat RW, Vester JW, Glueck CJ. Suppression of amylase activity by hypertriglyceridemia. JAMA 1973; 225:1331.
  6. Pieper-Bigelow C, Strocchi A, Levitt MD. Where does serum amylase come from and where does it go? Gastroenterol Clin North Am 1990; 19:793.
  7. Berk JE, Kizu H, Wilding P, Searcy RL. Macroamylasemia: a newly recognized cause for elevated serum amylase activity. N Engl J Med 1967; 277:941.
  8. Sachdeva CK, Bank S, Greenberg R, et al. Fluctuations in serum amylase in patients with macroamylasemia. Am J Gastroenterol 1995; 90:800.
  9. Deprettere AJ, Eykens A, Van Hoof V. Disappearance of macroamylasemia in a celiac patient after treatment with a gluten-free diet. J Pediatr Gastroenterol Nutr 2001; 33:346.
  10. Barera G, Bazzigaluppi E, Viscardi M, et al. Macroamylasemia attributable to gluten-related amylase autoantibodies: a case report. Pediatrics 2001; 107:E93.
  11. Rabsztyn A, Green PH, Berti I, et al. Macroamylasemia in patients with celiac disease. Am J Gastroenterol 2001; 96:1096.
  12. Eleccion CB, Hathaway AA. Macroamylasemia in HIV infection. Tex Med 1998; 94:77.
  13. Bonetti G, Serricchio G, Giudici A, et al. Hyperamylasemia due to macroamylasemia in adult gluten enteropathy. Scand J Clin Lab Invest 1997; 57:271.
  14. Yoshida K, Minegishi Y, Okawa H, et al. Epstein-Barr virus-associated malignant lymphoma with macroamylasemia and monoclonal gammopathy in a patient with Wiskott-Aldrich syndrome. Pediatr Hematol Oncol 1997; 14:85.
  15. Cutolo M, Sulli A, Barone A, et al. Macroamylasemia: a possible cause of unexplained hyperamylasemia in rheumatoid arthritis. Br J Rheumatol 1995; 34:290.
  16. Fujimura Y, Nishishita C, Uchida J, Iida M. Macroamylasemia associated with ulcerative colitis. J Mol Med (Berl) 1995; 73:95.
  17. Van Gossum A, Cremer M. Macroamylasemia disappearance after gluten withdrawal. Dig Dis Sci 1989; 34:964.
  18. Carroccio A, Di Prima L, Scalici C, et al. Unexplained elevated serum pancreatic enzymes: a reason to suspect celiac disease. Clin Gastroenterol Hepatol 2006; 4:455.
  19. Ben-Horin S, Farfel Z, Mouallem M. Gastroenteritis-associated hyperamylasemia: prevalence and clinical significance. Arch Intern Med 2002; 162:689.
  20. Coté GA, Gottstein JH, Daud A, et al. The role of etiology in the hyperamylasemia of acute liver failure. Am J Gastroenterol 2009; 104:592.
  21. Clavien PA, Burgan S, Moossa AR. Serum enzymes and other laboratory tests in acute pancreatitis. Br J Surg 1989; 76:1234.
  22. Spechler SJ, Dalton JW, Robbins AH, et al. Prevalence of normal serum amylase levels in patients with acute alcoholic pancreatitis. Dig Dis Sci 1983; 28:865.
  23. Toskes PP. Hyperlipidemic pancreatitis. Gastroenterol Clin North Am 1990; 19:783.
  24. Orebaugh SL. Normal amylase levels in the presentation of acute pancreatitis. Am J Emerg Med 1994; 12:21.
  25. Yadav D, Nair S, Norkus EP, Pitchumoni CS. Nonspecific hyperamylasemia and hyperlipasemia in diabetic ketoacidosis: incidence and correlation with biochemical abnormalities. Am J Gastroenterol 2000; 95:3123.
  26. Argiris A, Mathur-Wagh U, Wilets I, Mildvan D. Abnormalities of serum amylase and lipase in HIV-positive patients. Am J Gastroenterol 1999; 94:1248.
  27. Gullo L. Day-to-day variations of serum pancreatic enzymes in benign pancreatic hyperenzymemia. Clin Gastroenterol Hepatol 2007; 5:70.
  28. Ranson JH, Pasternack BS. Statistical methods for quantifying the severity of clinical acute pancreatitis. J Surg Res 1977; 22:79.
  29. Ranson JH. Etiological and prognostic factors in human acute pancreatitis: a review. Am J Gastroenterol 1982; 77:633.
  30. Shah AM, Eddi R, Kothari ST, et al. Acute pancreatitis with normal serum lipase: a case series. JOP 2010; 11:369.
  31. Steinberg WM, Goldstein SS, Davis ND, et al. Diagnostic assays in acute pancreatitis. A study of sensitivity and specificity. Ann Intern Med 1985; 102:576.
  32. Tietz NW, Huang WY, Rauh DF, Shuey DF. Laboratory tests in the differential diagnosis of hyperamylasemia. Clin Chem 1986; 32:301.
  33. Werner M, Steinberg WM, Pauley C. Strategic use of individual and combined enzyme indicators for acute pancreatitis analyzed by receiver-operator characteristics. Clin Chem 1989; 35:967.
  34. Levitt MD. Clinical use of amylase clearance and isoamylase measurements. Mayo Clin Proc 1979; 54:428.
  35. Johnson SG, Ellis CJ, Levitt MD. Mechanism of increased renal clearnace of amylase/creatinine in acute pancreatitis. N Engl J Med 1976; 295:1214.
  36. Levine RI, Glauser FL, Berk JE. Enhancement of the amylase-creatinine clearance ratio in disorders other than acute pancreatitis. N Engl J Med 1975; 292:329.
  37. Gumaste VV, Dave PB, Weissman D, Messer J. Lipase/amylase ratio. A new index that distinguishes acute episodes of alcoholic from nonalcoholic acute pancreatitis. Gastroenterology 1991; 101:1361.
  38. Tenner SM, Steinberg W. The admission serum lipase:amylase ratio differentiates alcoholic from nonalcoholic acute pancreatitis. Am J Gastroenterol 1992; 87:1755.
  39. King LG, Seelig CB, Ranney JE. The lipase to amylase ratio in acute pancreatitis. Am J Gastroenterol 1995; 90:67.
  40. Sadowski DC, Sutherland LR. The lipase/amylase ratio: sensitive but not specific. Gastroenterology 1992; 103:352.
  41. Balthazar EJ, Robinson DL, Megibow AJ, Ranson JH. Acute pancreatitis: value of CT in establishing prognosis. Radiology 1990; 174:331.
  42. Balthazar EJ. CT diagnosis and staging of acute pancreatitis. Radiol Clin North Am 1989; 27:19.
  43. McMenamin DA, Gates LK Jr. A retrospective analysis of the effect of contrast-enhanced CT on the outcome of acute pancreatitis. Am J Gastroenterol 1996; 91:1384.
  44. Lecesne R, Taourel P, Bret PM, et al. Acute pancreatitis: interobserver agreement and correlation of CT and MR cholangiopancreatography with outcome. Radiology 1999; 211:727.
  45. Morgan DE, Baron TH, Smith JK, et al. Pancreatic fluid collections prior to intervention: evaluation with MR imaging compared with CT and US. Radiology 1997; 203:773.
  46. Taylor AC, Little AF, Hennessy OF, et al. Prospective assessment of magnetic resonance cholangiopancreatography for noninvasive imaging of the biliary tree. Gastrointest Endosc 2002; 55:17.
  47. Arvanitakis M, Delhaye M, De Maertelaere V, et al. Computed tomography and magnetic resonance imaging in the assessment of acute pancreatitis. Gastroenterology 2004; 126:715.