Medical therapy of malabsorption in patients with head pancreatic resection.

Exocrine pancreatic insufficiency caused by pancreatic resection results from various factors which regulate digestion and absorption of nutrients. Pancreatic function has been extensively studied in the last 40 years even if some aspects of secretion and gastrointestinal adaptation after pancreatic resection are not completely understood. The pancreatic gland normally secretes more than 2 liters of juice per day which is constituted of water, bicarbonates and enzymes [1]; protein secretion per gram of pancreatic tissue is more elevated than that of any other organ [2] and more than 85% of the protein content is constituted of enzymes which are able to digest lipids, proteins and carbohydrates [3]. The pancreas normally produces more enzymes than are necessary for food digestion [1] and normal digestion is guaranteed up to a loss of 95% of pancreatic secretive capacity [4]. Recently, French authors [5] have demonstrated that gastric lipase can compensate pancreatic lipase even if it is not capable of complete lipolytic activity. Enzyme degradation in the intestinal lumen is the main factor for controlling nutrient absorption. The activity of pancreatic enzymes progressively decreases during their progression in the intestinal lumen: 60% of active trypsin and chymotrypsin are present in the jejunum whereas only 20 % are present in the ileum; on the other hand, amylases and lipases are more stable [6, 7, 8]. There are various explanations for the loss of enzymatic action of the enzymatic activity during progression in the intestinal lumen: proteolytic degradation (chymotrypsin is the main lipase degradation factor) [9], lipase acid inactivation (lipase is particularly sensitive to acid inactivation) [10], and the brief half life of some enzymes, particularly lipase [11]. This is the reason why, in patients with exocrine pancreatic insufficiency, fat maldigestion is more severe than that of carbohydrates and proteins. In addition to an optimal concentration of biliary acids and colipases in the intestinal lumen, good fat digestion requires an adequate blending of nutrients with the pancreatic juice and optimal intestinal motility. In pathologic conditions, such as chronic pancreatitis, there is a deficit in bicarbonate production; a low duodenal pH determines biliary acid precipitation and the remaining lipase activity worsens. Finally, other causes of malabsorption may be an accelerated gastric emptying and a lower intestinal time of transit [12, 13].