ACUTE-PANCREATITIS

Experimental models suggest that oxygen-derived free radicals and impairment of the pancreatic microcirculation may be important determinants of the severity of acute pancreatitis. Lipid intolerance does not appear to be a predisposing factor in alcoholic or gallstone pancreatitis; however, estrogen replacement therapy can produce acute pancreatitis in women with familial hypertriglyceridemia. Use of the lipase-to-amylase ratio is not effective in identifying the etiology of pancreatitis, but a threefold elevation of the serum alanine aminotransferase suggests gallstone disease. Serum measurements of neutrophil elastase, C-reactive protein, and pancreatitis-associated protein look promising as simple, inexpensive indicators of severity. Therapeutic studies using either intravenous octreotide or protease inhibitors in peritoneal lavage have been inconclusive. After operative therapy for complicated acute pancreatitis, patients may develop cutaneous fistulas or Candida sepsis.