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ORIGINAL ARTICLE
Year : 2013  |  Volume : 1  |  Issue : 2  |  Page : 42-45

Prevalence, causes, and outcome of non-diagnostic amylase in acute pancreatitis: A single institution experience


Department of Surgery, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia

Date of Web Publication15-Jan-2014

Correspondence Address:
Munaser S Alamoodi
Department of Surgery, Faculty of Medicine, King Abdulaziz University, Jeddah 21589
Saudi Arabia
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2320-3846.125035

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  Abstract 

Objectives: To determine the prevalence, common causes, and outcome of non diagnostic amylase in acute pancreatitis. Materials and Methods: The data of 81 patients was looked at retrospectively. This was extracted from the patient's records with the diagnosis of acute pancreatitis from June 2010 to June 2012. These patients were admitted to King Abdulaziz University Hospital. The data included demographics, amylase level, causes and outcome. Two groups were devised group 1, non diagnostic amylase, and group 2, diagnostic amylase. Results: Out of 81 patients, 33(41%) were males, and 48(59%) were females. Age ranging from 24-75 years with a mean age of 49. Only 10(12%) of the patients were found to have amylase that is not raised up to the diagnostic level. Gallstones were the commonest cause in both groups, while hyperlipidemia was higher in group 1(20%), than group 2(8.5%). Idiopathic in 40% and 14% in group 1 and 2 respectively. Post ERCP acute pancreatitis was only seen in group 2(8.5%). The outcome was indicated by; pseudocyst which was not present in both groups, necrosis which was only present in group 2 in 4%, Intensive care unit (ICU) admission was seen in 20% of group 1 patients due to delay in diagnosis, and in 4% of group 2 due to necrosis, and mortality was absent in both groups. Conclusion: Prevalence of acute pancreatitis in non diagnostic amylase is found to be 10%. The most common cause after gallstones is idiopathic together with hyperlipidemia. The outcome is usually favorable provided the diagnosis is not delayed.

Keywords: Acute pancreatitis, amylase, computed tomography scan


How to cite this article:
Alamoodi MS, Aldaqal SM. Prevalence, causes, and outcome of non-diagnostic amylase in acute pancreatitis: A single institution experience. Saudi Surg J 2013;1:42-5

How to cite this URL:
Alamoodi MS, Aldaqal SM. Prevalence, causes, and outcome of non-diagnostic amylase in acute pancreatitis: A single institution experience. Saudi Surg J [serial online] 2013 [cited 2020 Jul 11];1:42-5. Available from: http://www.saudisurgj.org/text.asp?2013/1/2/42/125035


  Introduction Top


Acute pancreatitis (AP) is the inflammation of the pancreas due to auto digestion. In the majority of patients, it is mild. In 10-20% the various pathways that contribute to increased intrapancreatic and extra pancreatic inflammation may result into pancreatic necrosis as well as multi-organ failure [1],[2],[3] The diagnosis is often reached clinically, by raised amylase or lipase and in a small number by computed tomography (CT). Specifically those patients with characteristic abdominal pain in whom the rise in enzymes is not sufficient enough to reach a diagnosis require a high degree of clinical suspicion. In general, both amylase and lipase are elevated during the course of AP. The degree of rise of these enzymes does not correlate with the severity of the disease. It is usually not necessary to measure both, but lipase is preferable as it is more sensitive and specific.

Early mortality in AP is the result of systemic inflammatory response with multiple organ failure. Although late mortality is the result of infection of pancreatic necrosis and peripancreatic fluid collections, which result in sepsis and is seen in more than 50% of deaths.


  Materials and Methods Top


The data of 81 patients was looked at retrospectively. This was obtained from the patient's records with the diagnosis of AP from June 2010 to June 2012. These patients were admitted to King Abdulaziz University Hospital. The data included demographics, pain site, amylase level, causes and outcome. Two groups were devised namely non-diagnostic amylase (group 1), amylase level taken to be <480 IU/L and diagnostic amylase (group 2), amylase level taken to be >480 IU/L on admission. Group 1 patients were all diagnosed by CT.


  Results Top


A total number of patients was 81, with age ranging from 24 to 75 years with a mean age of 49. The number of males was 33 (41%), whereas the females were 48 (59%). All presented with epigastric pain. Only 10 (12%) of the patients were found to have amylase that is not raised up to the diagnostic level [Table 1]. This level was taken to be a threefold rise above the upper normal limit which in our hospital is 160 IU/L. The remaining patients, 71 (88%) made up group 2. Gallstones were the commonest cause in both groups, while hyperlipidemia was higher in group 1 (20%), than 2 (8.5%). The Cause was unknown in 40% and 14% in group 1 and 2 respectively. Post endoscopic retrograde cholangiopancreatography AP was only seen in group 2 (8.5%) [Table 2]. The outcome indicators [Table 3] namely; (a) Pseudocyst, was not present in both groups, (b) necrosis which was only present in group 2 in 4%, (c) intensive care unit (ICU) admission seen in 20% of group 1 patients due to delay in diagnosis and in 4% of group 2 due to necrosis and (d) mortality was absent in both groups. CT scan done on group 1 showed Grade B in 40%, Grade C in 20%, and Grade D in 40% according to the Balthazar grading system [Table 4].
Table 1: Summarizing the data collection


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Table 2: Causes (total number of patients=81)


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Table 3: Outcome (total number of patients=81)


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Table 4: CT findings graded using the Balthazar grading system


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  Discussion Top


AP in the majority of cases is mild and its diagnosis relays on clinical as well as laboratory findings of high amylase 3-6 times increase from the upper normal range of 160 IU/L. Serum amylase level increases rapidly over 3-6 h, with a half-life of 10-12 h; it remains elevated for 3-5 days [4] . AP can also be diagnosed by an increase in lipase which is thought to be more sensitive and its half-life is longer (7-14 days) [5] . In about 19% of patients these values are normal or non-diagnostic that is the rise in amylase is less than 3 fold [4] . This study's figure was 12% which is slightly lower but reinforces the emphasis of the importance of such occurrence. The diagnosis of AP is made when two of the following three features are present: Characteristic abdominal pain, a 3 fold rise in amylase and/or lipase, and characteristic CT findings [4] . This study concentrated mainly on those patients who had epigastric pain with a rise in amylase that is sub diagnostic. Since other conditions such as perforated peptic ulcer disease, acute cholecystitis, bowel obstruction amongst other conditi ons can lead to raised amylase the diagnosis of AP might be over looked. It is these patients that end up visiting the ER department a number of times before a definitive diagnosis is made. Hence the need for an early diagnosis. AP is not invariably associated with elevated serum amylase. Multiple factors may contribute to the absence of hyperamylasemia on admission, including a return to normal enzyme levels before hospitalization or the inability of inflamed pancreases to produce amylase . A study done by Clavien et al. attributed the lack of rise to one of three reasons namely; the prevalence of alcoholic etiology, previous attacks on alcoholic pancreas, and longer duration of symptoms before admission. They also observed that these patients tend to follow a milder course [4] . This study found the contrary, the patients with non-diagnostic amylase run the risk of delayed in diagnosis which might lead to an increase in morbidity. This was seen in 2 (20%), of our patients who ended up in ICU, while the admission to ICU for the high amylase group was due to necrosis. This indicates that ICU admission can be avoided in the non-diagnostic amylase group with early diagnosis. Pujar et al. in their study have suggested that a non-diagnostic rise in amylase is often commonly seen in cases of AP due to hyperlipidemia [6] . This study found that hyperlipidemia was the cause in 20% of the non-diagnostic amylase group and not the highest cause. Hyperlipidemia as a cause of AP should be suspected in patients with non-diagnostic amylase. This needs to be dealt with to ensure patient recovery. Most patients with AP experience abdominal pain that is located generally in the epigastrium and radiates to the back in approximately half of the cases. The onset may be sudden and the pain often persists for more than 24 h without relief. Physical examination often reveals severe upper abdominal tenderness with guarding [7] . Jones et al. recommended that patients with non-diagnostic hyperamylasemia must be investigated and managed as per AP [8] . Many patients with AP do not require CT during their initial admission. The CT is often done on the 2 nd or 3 rd day after the initial attack to detect any complications and also aid in prognosis [9],[10],[11] . CT done before the 2 nd day usually does not show any changes [12] . Reasons for doing a CT usually are to distinguish interstitial from necrotizing pancreatitis where there is clinical evidence of increased severity after admission. Contrast enhanced CT is the best imaging technique to exclude conditions that masquerade as AP, to diagnose the severity of AP and to identify complications of pancreatitis [12] . This study found that CT is a vital tool in diagnosing patients with non-diagnostic amylase levels. Findings on CT that confirm the diagnosis of AP include enlargement of the pancreas with diffuse edema, heterogenecity of pancreatic parenchyma, peripancreatic stranding and peripancreatic fluid collections, with the use of iv contrast, a diagnosis of pancreatic necrosis can be established. As was seen in this study, the extent of the rise in amylase has no relation to the severity of the disease, some patients with amylase of 212 IU/L were found to have severe disease hence the emphasis on performing CT on these patients early on for diagnosis and later for prognosis. In a patient with abdominal pain characteristic of AP and serum enzyme levels that are lower than ×3 the upper limit of normal, a CT must be performed to confirm a diagnosis of AP [13] . Studies have found that CT sensitivity index (Balthazar Index) is superior to Ranson's criteria and APACHE 2 scoring system in predicting AP outcome [14] . CT Sensitivity Index is an early prognostic tool for AP [15] . By doing an early CT in these patients in whom the amylase was not diagnostic a diagnosis was reached as well as ruling out other causes that might lead to a rise in amylase and the patients were managed expectantly. Some studies have suggested that magnetic resonance imaging and magnetic resonance cholangiopancreatography are superior to CT in the diagnosis of AP since they can delineate pancreatic duct anatomy [16],[17],[18] . This needs further evaluation and could be the gold standard in the future.


  Conclusion Top


Prevalence of non-diagnostic amylase in AP is found to be 10%. The most common cause after gallstones is idiopathic together with hyperlipidemia. The outcome is usually favorable provided the diagnosis is not delayed. Patients with such presentations and appropriate clinical setting should have early CT to confirm the diagnosis of AP and avoid unnecessary morbidity.

 
  References Top

1.Papachristou GI, Sass DA, Avula H, Lamb J, Lokshin A, Barmada MM, et al. Is the monocyte chemotactic protein-1 -2518 G allele a risk factor for severe acute pancreatitis? Clin Gastroenterol Hepatol 2005;3:475-81.  Back to cited text no. 1
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2.Bhatia M, Ramnath RD, Chevali L, Guglielmotti A. Treatment with bindarit, a blocker of MCP-1 synthesis, protects mice against acute pancreatitis. Am J Physiol Gastrointest Liver Physiol 2005;288:G1259-65.  Back to cited text no. 2
    
3.Rahman SH, Ibrahim K, Larvin M, Kingsnorth A, McMahon MJ. Association of antioxidant enzyme gene polymorphisms and glutathione status with severe acute pancreatitis. Gastroenterology 2004;126:1312-22.  Back to cited text no. 3
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4.Clavien PA, Robert J, Meyer P, Borst F, Hauser H, Herrmann F, et al. Acute pancreatitis and normoamylasemia. Not an uncommon combination. Ann Surg 1989;210:614-20.  Back to cited text no. 4
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5.Cartier T, Sogni P, Perruche F, Meyniard O, Claessens YE, Dhainaut JF, et al. Normal lipase serum level in acute pancreatitis: A case report. Emerg Med J 2006;23:701-2.  Back to cited text no. 5
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6.Pujar AK, Kumar V R A, M S, S V K. An interesting case of hypertriglyceridaemic pancreatitis. J Clin Diagn Res 2013;7:1169-71.  Back to cited text no. 6
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7.Kwon RS, Banks PA. How should acute pancreatitis be diagnosed in clinical practice? In: Dom´ýnguez-Mu˜noz JE, editor. Clinical Pancreatology for Practicing Gastroenterologists and Surgeons. Vol. 4. Malden, MA: Blackwell; 2005. p. 34-9.  Back to cited text no. 7
    
8.Jones HG, Jardine N, Williamson J, Puntis MC, Morris-Stiff GJ. Patients with non-diagnostic hyperamylasaemia must be investigated and managed as per acute pancreatitis. JRSM Short Rep 2012;3:7.  Back to cited text no. 8
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9.Balthazar EJ, Freeny PC, vanSonnenberg E. Imaging and intervention in acute pancreatitis. Radiology 1994;193:297-306.  Back to cited text no. 9
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10.Balthazar EJ, Fisher LA. Hemorrhagic complications of pancreatitis: Radiologic evaluation with emphasis on CT imaging. Pancreatology 2001;1:306-13.  Back to cited text no. 10
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11.Mortele KJ, Wiesner W, Intriere L, Shankar S, Zou KH, Kalantari BN, et al. A modified CT severity index for evaluating acute pancreatitis: Improved correlation with patient outcome. AJR Am J Roentgenol 2004;183:1261-5.  Back to cited text no. 11
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12.Balthazar EJ. Acute pancreatitis: Assessment of severity with clinical and CT evaluation. Radiology 2002;223:603-13.  Back to cited text no. 12
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13.Banks PA, Freeman ML, Practice Parameters Committee of the American College of Gastroenterology. Practice guidelines in acute pancreatitis. Am J Gastroenterol 2006;101:2379-400.  Back to cited text no. 13
    
14.Leung TK, Lee CM, Lin SY, Chen HC, Wang HJ, Shen LK, et al. Balthazar computed tomography severity index is superior to Ranson criteria and APACHE II scoring system in predicting acute pancreatitis outcome. World J Gastroenterol 2005;11:6049-52.  Back to cited text no. 14
    
15.Vriens PW, van de Linde P, Slotema ET, Warmerdam PE, Breslau PJ. Computed tomography severity index is an early prognostic tool for acute pancreatitis. J Am Coll Surg 2005;201:497-502.  Back to cited text no. 15
    
16.Hirota M, Kimura Y, Ishiko T, Beppu T, Yamashita Y, Ogawa M. Visualization of the heterogeneous internal structure of so-called "pancreatic necrosis" by magnetic resonance imaging in acute necrotizing pancreatitis. Pancreas 2002;25:63-7.  Back to cited text no. 16
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17.Miller FH, Keppke AL, Dalal K, Ly JN, Kamler VA, Sica GT. MRI of pancreatitis and its complications: Part 1, acute pancreatitis. AJR Am J Roentgenol 2004;183:1637-44.  Back to cited text no. 17
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18.Arvanitakis M, Delhaye M, De Maertelaere V, Bali M, Winant C, Coppens E, et al. Computed tomography and magnetic resonance imaging in the assessment of acute pancreatitis. Gastroenterology 2004;126:715-23.  Back to cited text no. 18
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  [Table 1], [Table 2], [Table 3], [Table 4]



 

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