In prospective, randomized trials which of the following agents or therapeutic measures has/have been demonstrated to accelerate recovery from acute pancreatitis?

e. None of the above

A variety of pharmacologic agents that directly or indirectly reduce acinar cell enzyme release or ductal secretion have undergone clinical evaluation for the treatment of acute pancreatitis—generally with unimpressive results. Among the first were anticholinergic drugs. Despite extensive experience over many years, no objective data have emerged to support their use. Clinical trials of glucagon and calcitonin based on the same principle have produced a similar lack of supportive data. More recently, a somatostatin analog has been subjected to clinical trials for patients with acute pancreatitis. Somatostatin inhibits pancreatic enzyme and bicarbonate secretion by preventing the normal release of cholecystokinin, secretin, and other gut peptides. Despite the theoretical appeal, it has not been possible to demonstrate that somatostatin alters the natural history or prognosis of simple acute pancreatitis, although it does diminish pancreatic secretion.

Peritoneal lavage as a specific therapy for acute pancreatitis was proposed after experimental studies demonstrated improved survival in animals with fulminant pancreatitis. The concept was appealing in that activated proteases and other vasoactive substances identifiable in peritoneal aspirates from patients with pancreatitis would be removed, rather than systemically absorbed. Unfortunately, clinical trials using this approach have produced disappointing results, and the eventual overall mortality rate appears unchanged.