J.R. Coll. Surg. Edinb., 43, October 1998, 306-307

Isoenzyme analysis of hyperamylasaemia associated with ruptured abdominal aortic aneurysms

D. E. BODDIE, G. W. COUPER, H. WATSON* AND G. G. COOPER+
Department of Surgery, University of Aberdeen, and Departments of *Biochemistry and + Vascular Surgery, Aberdeen Royal Infirmary, Foresterhill, Aberdeen, UK

Hyperamylasaemia may occur following abdominal aortic aneurysm rupture and its use as a prognostic indicator has been suggested. However, the isoenzyme responsible for the rise in serum amylase has not been investigated. In this study, isoenzyme analysis was performed on the serum of patients noted to have a raised amylase from their routine biochemistry samples. Individual cases were then reviewed regarding clinical course and outcome. The pancreas has been thought to be the predominant source of the observed hyperamylasaemia. However, in this study a mixed picture of pancreatic and salivary isoenzymes was found. Of the four highest recorded amylase levels two were salivary in origin, one pancreatic and one mixed. The highest recorded amylase level was of salivary origin in a patient that survived without any major complication. The four patients that died all showed evidence of gut infarction/ischaemia. Two had hyperamylasaemia of a mixed pattern, one pancreatic and one of salivary origin.

Keywords: hyperamylasaemia, isoenzymes, ruptured aortic aneurysm.

Hyperamylasaemia was first associated with pancreatitis by Elman et al. in 1929.¹ Since the discovery of pancreatic and salivary iso-enzymes by Berk et al. 1966,² high serum amylase levels that would previously have been attributed to pancreatic disease have been shown to be of non pancreatic origin.^3,4 It is well recognized that patients with ruptured abdominal aortic aneurysms (AAA) may have raised serum amylase levels with the pancreas generally regarded as the source.^4-6 In studies looking at various surgical procedures a significant proportion of hyperamylasaemia is attributable to the s-amylase isoenzyme.^4,7 The aim of our study was to determine the origin of the amylase isoenzyme accounting for the elevated serum amylase activity seen in patients with ruptured AAA.

During the study period serum amylase was routinely measured in patients with ruptured AAA for 48 h post-operatively. Twelve consecutive patients, who had an elevated serum amylase in either sample, were identified and isoenzyme analysis performed. Total serum amylase, p-amylase and s-amylase were measured using the Pancreatic alpha-amylase EPS kit from Boehringer Mannheim. A retrospective review of the case notes was performed studying the clinical details and complications encountered in each case.

Serum total amylase, pancreatic and salivary amylase activities are shown in Table 1 along with the clinical outcome at 30 days. Raised amylase activities of both pancreatic and salivary subtypes were observed. Four control subjects, with normal total amylase, were studied, p-amylase ranging from 21 to 36% of the total amylase and s-amylase 64—79%. Four of the patients died. The principal cause of death was gut infarction in three patients and myocardial infarction in one, although the fourth patient also showed evidence of gut ischaemia. An elevated pancreatic amylase was a feature in the three patients who died of gut infarction, although the pancreatic isoenzyme was the predominant source of the hyperamylasaemia in only one of these patients, the other two showing a mixed rise in both the p-amylase and s-amylase isoenzymes. One patient developed cardiac complications with predominantly p-amylase elevation. One patient had cardiorespiratory complications and displayed the s-amylase subtype predominantly. One other patient suffered respiratory complications alone, and had a predominance of the p-amylase isoenzyme. All of the patients that developed renal complications died.

Table 1 Table of total, pancreatic and salivary amylase results with Outcome at 30 days

Hyperamylasaemia occurring after both major and minor abdominal and extra-abdominal procedures has been widely reported.^4,7,8 Isoenzyme studies of post-operative hyperamylasaemia have shown that both pancreatic and salivary isoenzymes may be responsible for the elevated activities,^3,4,7,9 but this has not previously been studied in patients following AAA rupture. Bagley et al.¹⁰ reported that a significantly raised total serum amylase activity was associated with a worse prognosis in these patients.

In a study of autopsies performed following ruptured AAA, Warshaw and O’Hara highlighted the high frequency of pancreatic abnormalities with 18 of 63 patients exhibiting acute pancreatitis, pancreatic necrosis or pancreatic abscess¹¹ It would seem reasonable, therefore, to expect the hyperamylasaemia which occurs following ruptured AAA to be mainly of pancreatic origin, but this was not our finding with 50% of patients having a salivary subtype.

Previous studies have shown a predominantly pancreatic origin for the hyperamylasaemia occurring in patients with the highest total serum amylase activity.^12,13 In our series, of the four patients with an. amylase level greater than 1000 U/L, two were of s-amylase subtype, one mixed and only one of p-amylase subtype. The highest recorded serum amylase level of 4379 U/L was of s-amylase subtype and occurred in a patient with an uncomplicated post-operative course. Harada et al.³ reported similar findings with 12 out of their 18 patients found to have post-operative hyperamylasaemia demonstrating salivary amylase, the most striking elevations being of the s-amylase subtype.

Morrisey et al.⁴ found in 12 patients that the two highest levels of amylase activity were in the p-amylase subtype following AAA repair and a hepatectomy. However, they stated that excluding these two cases in which they attributed the rise in p-amylase to direct stimulation of the pancreas, the most striking elevations in serum amylase activity from extra-abdominal procedures was due to the s-amylase subtype.

Hyperamylasaemia following AAA rupture has been associated with a poor prognosis.¹⁰ The present study has shown that hyperamylasaemia in patients with ruptured aortic aneurysm may be of salivary or pancreatic origin but no conclusion can be drawn from this study about the relative importance of either isoenzyme as a prognostic indicator.

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Correspondence: Mr G. G. Cooper, Consultant Vascular Surgeon, Ward 36, Aberdeen Royal Infirmary, Foresterhill Aberdeen AB25 2ZD, UK

© 1998 The Royal College of Surgeons of Edinburgh, J.R. Coll. Surg. Edinb., 43, October 1998, 306-307