Long-Term Outcome of Acute Pancreatitis: A Prospective Study with 118 Patients

Abstract

118 patients who had recovered from acute pancreatitis underwent endoscopic retrograde pancreatography (ERCP) during a long-term follow-up (mean 4.4 years, range 1 -17) to investigate the frequency and features of residual ductal lesions. Oedematous and necrohaemorrhagic pancreatitis occurred in 35 and in 83 patients, respectively. The aetiology was biliary (39 patients), alcoholic (32), biliary-alcoholic (18) and miscellaneous (29). After oedematous pancreatitis, ERCP was normal in 31 showed obstructive pancreatitis in 2 and a slight localized and smooth stricture of the main duct in 2 patients. After necrotizing pancreatitis, 29 patients showed ductal changes without features of chronic pancreatitis, 7 obstructive, 3 chronic calcifying pancreatitis and 44 normal pictures. In 17 patients submitted to two or three ERCPs during a mean 10-year follow-up, the ductal appearance was unchanged in 12, worsened in 3, and improved in 2 patients. The aetiology of pancreatitis and frequency of recurrences was similar in patients with or without scarring lesions. We conclude that residual ductal lesions are common after acute necrotizing pancreatitis.

Endocrine pancreatic insufficiency in chronic pancreatitis

“…Changes in hydrocarbonate metabolism described in AP are characterized by the presence of hyperglycemia and changes in insulin and glucagon secretion in up to 50% of the cases [26,27] after an acute episode. Although there are poor data concerning the endocrine function, biliary pancreatitis seems to have fewer adverse longterm effects on the endocrine pancreas [25] .…”

Exocrine pancreatic changes following acute attack of biliary pancreatitis

“…Some authors report progressive recovery of the function [4,7,11] and others report a functional deficit [8,13,15,30]. In 1962, Lundh [5] put forward the idea in his paper that the pancreatic function recovered with the passage of time, and these results were corroborated subsequently by other authors [9][10][11].…”

“…For some authors, there appears to be a difference in functional change between episodes of alcoholic and bili-Pareja/Artigues/Aparisi/Fabra/Martínez/ Trullenque ary origin. In this respect, more acute and persistent pancreatic dysfunction is reported after episodes of alcoholic pancreatitis, without a return to the previous level of functioning in some cases [13,14,28,29], while greater recovery functional is observed in cases of biliary etiology [7,13,14,[29][30][31]. Our study is homogeneous and includes only cases of biliary etiology, and we made a precise assessment of changes and of the state of exocrine pancreatic function 1 year after the acute episode, when the patient is no longer affected by the original cause or by possible complications arising from this cause.…”

“…when a clinical and analytical return to normal occurs and oral feeding is resumed [6-13, 15, 27-29], but differing results are reported on recovery of the function after the acute episode. Some authors report progressive recovery of the function back to its normal level over a varying period of time [7][8][9][10][11][12]27], while others have found a persisting functional deficit [13,28,30].…”

“…Büchler [13] and Angelini [7,14] found that there is a functional deficit after an acute attack, the degree of which depends on the severity and etiology of the attack. Büchler included patients whose acute pancreatitis episode was of largely alcoholic origin and found that most patients showed impaired functioning in the year following an acute necrohemorrhagic episode.…”