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Rapid Responses: Rapid Responses published:
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Hyperamaylasaemia
- Chidambaran Ganapathy ganapathy (15 October 2005)
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Hyperamylasemia
- Dr.Yousef Shahin (16 October 2005)
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Hyperamylasaemia
- Tira Galm, RG1 5AN (19 October 2005)
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Amylase isoenzyme determination and diagnosis of pancreatic diseases
- Prasanta Padhan (21 October 2005)
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Laboratory test side effects
- Mohammad A. Al-Jubouri (21 October 2005)
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Back to basics
- Youval Mlynek, 432 44 Varberg, Sweden (25 October 2005)
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Hyperamylasaemia
- Jonathan WJ Bloor, Hotston M (26 October 2005)
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HIV as a cause of hyperamylasaemia
- Katherine M Coyne, Nneka C Nwokolo (30 October 2005)
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Eating disorders: another usual suspect for hyperamylasaemia
- Stephan M Zipfel, Janice D Russell (24 November 2005)
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Chidambaran Ganapathy ganapathy, Hon.Med.Officer,VHS,Chennai,India Chennai,India-600113
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Sir, Thank you for presenting this very interesting case & also giving the information on Artefactual Hyperamylasaemia.I feel that ultrasonogram of the abdomen was done late in this case & it should have been ordered by the surgical registrar & that could have made the decision on the management of case at still earlier stage. Thank you, Dr.Chidambaran Competing interests: None declared |
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Dr.Yousef Shahin, House Officer High Wycombe Hospital,HP11 1QN
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Thank you for an interesting case,I enjoyed reading this article and was surprised the diagnosis was not acute pancreatitis. I think if it was me I would have thought the same as there were no clinical signs of an ovarian tumor and the most common cause of high amylase for me as a clinician would be acute pancreatitis.The ultrasound should have been done earlier to confirm the diagnosis.I always wanted to ask a question, do we have to measure urinary amylase in pancreatitis? Thank you. Dr.Yousef Shahin Competing interests: None declared |
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Tira Galm, ENT SHO Royal Berkshire and Battle Hospital, RG1 5AN
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EDITOR-Srivastava R et al recently published an article in the lesson of the week ‘hyperamylasaemia: not the usual suspects’1. They discussed the causes of high amylase including pancreatitis. The diagnosis of acute pancreatitis according to the United Kingdom guidelines is made by a serum amylase activity four times above the normal level with the appropriate clinical setting (upper abdominal/epigastric pain/diffuse abdominal pain).2 However, in the article published the diagnosis of acute pancreatitis is said to be likely if amylase is above ten times the upper limit of normal (0-100U/I) with acute abdominal pain, and a ‘modest’ rise was said to be caused by other presentations of an acute abdomen such as small bowel obstruction, perforated hollow viscus, peritonitis etc. Are they suggesting that a diagnosis of acute pancreatitis with the clinical setting be made if there is an amylase rise of >1000? , and if below this other causes should be sought. This could be misleading to those less familiar with the diagnosis of acute pancreatitis in relation to the amylase levels. Given that pancreatitis is a common surgical emergency it is important that guidelines are adhered to in order reduce mortality and morbidity associated with acute pancreatitis. 1. Sirvastave R, Fraser C, Gentlemen D, Jamieson A, Murphy M. Hyperamylasaemia: not the usual suspect. BMJ 2005;331: 890-91 2. British Society of Gastroenterology. United kingdom guidelines for the management of acute pancreatitis. Gut 1998;42(supplement 2): S1-13 Competing interests: None declared |
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Prasanta Padhan, MD,SR IN INTERNAL MEDICINE JIPMER,PONDICHERRY,INDIA.605006.
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Dear Editor, Serum amylase shows the greatest increase among the various pancreatic enzymes that increase at the onset of acute pancreatitis. But, the diagnostic value of the total serum amylase activity has been questioned due to its lack of specificity. To differentiate hyperamylasemia due to pancreatic disease from that due to other causes, the activity of pancreatic amylase should be determined by using a monoclonal antibody that specifically binds to pancreatic or salivary amylase, or by electrophoresis. The most useful and accurate method for distinguishing pancreatic from salivary-type hyperamylasemia is isoamylase analysis by electrophoresis. In patients with acute pancreatitis, increase of Amylase-1 and -2 is accompanied by the appearance of Amylase-4, a minor component of the pancreatic-type isoamylases, and by disappearance of the salivary-type isoenzymes, thereby leaving a pattern of the pancreatic isoenzymes alone. This pancreatitis pattern persists for about 10 days after the onset of illness. Therefore, if such a pattern is found in a patient with clinical findings suggesting acute pancreatitis despite a normal serum amylase level, the patient can be diagnosed as having acute pancreatitis or a recent attack of the disease. Further, the existence of an inherited trait of the pancreatitis pattern in some healthy individuals must be kept in mind. Patients with recurrent chronic pancreatitis also show pancreatic-type hyperamylasemia, whereas the pancreatic amylase activity decreases when pancreatic exocrine insufficiency progresses. Hyperamylasemia due to elevated salivary amylase activity is also common in patients with diabetic ketosis or malignancies such as lung cancer (adenocarcinoma). Hyperamylasemia is also found following various types of operation. In most cases, it is salivary-type hyperamylasemia. Competing interests: None declared |
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Mohammad A. Al-Jubouri, Consultant Chemical pathologist St. Helenes & Knowsley Hospitals NHS Trust L35 5DR
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An interesting case of malignant ovarian neoplasm uncovered by unexpected hyperamylasaemia. I am concerned that serum amylase was requested without clinical grounds. This has led to the erroneous labelling of the patient as having acute pancreatitis that could have resulted in inappropriate interventions that could have harmed the patient. I acknowledge that no harm was brought upon this particular case but the potential was there. Clinicians are well aware of the dangers of prescribing drugs erroneously but it is also important for them to recognise that inappropriate requesting of laboratory tests could result in false positive results leading to wrong diagnosis and harmful intervention. Mohammad Al-Jubouri Competing interests: None declared |
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Youval Mlynek, distriktsläkare (GP) Vårdcentralen Västra Vallgatan 14, 432 44 Varberg, Sweden
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Assement of a women patient with abdominal problem should include gynecological manual palpation. Competing interests: None declared |
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Jonathan WJ Bloor, Clinical Research Fellow Department of Surgery, Bristol Royal Infirmary, Bristol, BS2 8HW, Hotston M
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Editor- This ‘Lesson of the Week’ article1 was an important reminder about interpreting a serum amylase rise correctly. As pointed out there are many causes of increased amylase activity. Any test result should not be interpreted alone but in context with the findings from the history, examination and other investigations. This article should also be a reminder of the importance of ensuring amylase levels have been checked in patients with abdominal pain This helps prevent those patients who do have pancreatitis from having their diagnosis delayed and helps ensure they receive appropriate treatment early. 1. Srivastava R, Fraser C, Gentleman D, Jamieson LA, Murphy MJ. Hyperamylasaemia: not the usual suspects. BMJ 2005;331:890-1 Competing interests: None declared |
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Katherine M Coyne, Specialist Registrar in HIV/GUM Victoria Clinic for HIV and Sexual Health, SW1P 2PF, Nneka C Nwokolo
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EDITOR - In their article "Hyperamylasaemia: not the usual suspects" Rajeev Srivastava et al (15 October 2005) did not mention an important group of people at risk of both hyper- and macro- amylasaemia. HIV positive individuals are at increased risk of hyperamylasaemia due to increased pancreatic and salivary gland production of amylase. Increased pancreatic amylase production may occur as a consequence of pancreatitis. This may be a side-effect of certain antiretroviral medications (didanosine, stavudine), or of drugs used to treat complications of HIV disease (e.g. pentamidine and co-trimoxazole used in the prophylaxis and treatment of pneumocystis jiroveci (formerly carinii) pneumonia). Viral infections such as cytomegalovirus pancreatitis; pancreatic involvement by tumours (e.g. Kaposi’s sarcoma and lymphoma) and other opportunistic infections (e.g. cryptococcosis) may also result in raised serum amylase levels. Such processes may not always be symptomatic. Elevations in salivary amylase may result from infection or inflammation of the salivary glands as a consequence of viral parotitis or DILS (Diffuse Infiltrative Lymphocytosis Syndrome, a syndrome characterized by CD8 cell infiltration of the parotid and other salivary glands). Salivary glands in HIV positive individuals may also be affected by neoplastic processes. Macroamylase, as mentioned by the authors, is a large molecule which is formed when amylase binds with plasma proteins; hence conditions such as HIV which cause increased immunoglobulin levels may be associated with macroamylasaemia. Macroamylasaemia is a benign, asymptomatic condition for which no treatment is warranted. As the authors rightly state, this condition can be distinguished from hyperamylasaemia by measuring the amount of amylase in urine. This will be normal in macroamylasaemia in the absence of concurrent pancreatic pathology. Measurement of serum lipase may also be helpful in the assessment of hyperamylasaemia since pancreatic inflammation will cause a rise in levels of both these enzymes. Competing interests: None declared |
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Stephan M Zipfel, Professor of Medicine University Medical Hospital Tuebingen, Janice D Russell
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In the paper by Sirastrava et al. (Oct 15 2005) entitled “Hyperamylasemia not the usual suspects” no mention was made of the commonest cause of this laboratory finding in young people - namely eating disorders. An increase in serum amylase levels is found in about 50% of anorexia nervosa patients treated in a hospital setting. In most cases it is due to vomiting and is not the result of pancreatitis (Mitchell et al. 1983). Correspondingly, this increase is caused by the iso-amylase of the parotid gland (Humphries et al. 1987, Zipfel et al. 2005). A distinct enlargement of the parotid gland is often observed, especially in bulimia nervosa and in emaciated patients with purging anorexia nervosa. Acute pancreatitis can be assumed if the increase in the serum amylase level is more than 3- fold above normal and is associated with abdominal pain. If in doubt, it may be helpful to measure lipase levels. Pancreatitis as a complication of eating disorders is rare; it can, however, develop as a result of refeeding or binge-eating. Eating disorders are a major public health problem with anorexia nervosa in up to 0.5% of late adolescent females (Lucas et al. 1991), bulimia nervosa in 1% of young women and 0.1% of young men, binge eating disorder in possibly 1% (Hoek et al. 2003) and eating disorders not otherwise specified (EDNOS) more prevalent than any if these. The long term mortality rate of anorexia nervosa is high (Zipfel et al. 2000), and the course in most eating disorders is prolonged - more so with decreasing access to definitive treatment for many sufferers (Russell 2004) so this cause for hyperamylasemia should not have been overlooked. Lucas AR, Beard CM, O’Fallon WM, Kurland LT. 50-year trends in the incidence of anorexia nervosa in Rochester Minn.: a population-based study. Am J Psychiatry, 1991;148: 917-922. Hoek HW, van Hoecken D, Katzman MA. Epidemiology and cultural aspects of eating disorders : a review. In: Eating Disorders. Eds: Mario Maj, Katherine Halmi, Juan José López-Ibor, Norman Sartorius, WPA Series Evidence and Experience in Psychiatry John Wiley and Sons Ltd. Chichester, England 2003. p95. Russell J. Management of anorexia nervosa revisited. BMJ. 2004 Feb 28;328:479-80. Zipfel S, Löwe B, Reas DL, Deter H-C, Herzog W. Long-term prognosis in anorexia nervosa: Lessons from a 21-year follow-up study. LANCET 2000; 355: 721-722. Zipfel S, Löwe B, Herzog W. Medical complications in eating disorders. In: The essential Handbook of Eating Disorders. Eds. Treasure J, Schmidt U, van Furth E. John Wiley and Sons Ltd. Chichester, England 2005; 51-74. Competing interests: None declared |
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