Malnutrition and weight loss in patients with chronic pancreatitis mainly result from maldigestion and abdominal pain (Fig. 1). The loss of aci-
nar cells causes insufficient secretion of lipase, col-ipase, amylase, and proteases, which results in maldigestion of lipid, carbohydrates, and protein. Of these nutrients, fat maldigestion is the most clinically apparent. However, because the pancreas secretes a large surplus of enzymes, pancreatic enzyme output must be reduced to less than 10% of normal before fat absorption is appreciably impaired. Fat digestion depends not only on the amount of pancreatic lipase and colipase, but also on the activity of these enzymes. Since lipase has maximal enzymatic activity in the range of pH 6.5-8, decreased bicarbonate delivery to the duodenum leads to inactivation of lipase through a pH drop. In addition, since duodenal acidification precipitates bile salts, mixed micelle formation is impaired, resulting in the malabsorption of fat. All these pathophysiological events contribute to massive steatorrhoea, leading to malnutrition and weight loss in chronic pancreatitis patients.
Moreover, abdominal pain induced by food ingestion is common in these patients and results in decreased oral intake leading to weight loss. Inadequate food intake owing to recurrent or near continuous pain usually accounts for the initial 10-20% loss of body weight. However, the patho-physiology of this abdominal pain is poorly understood. Pancreatic hypertension, elevated interstitial fluid pressure, pancreatic ischaemia, damage to pancreatic nerves, tissue necrosis, pseudocyst formation, and common bile duct and/or duodenal obstruction may cause the abdominal pain .
Other factors may contribute to malnutrition in patients with chronic pancreatitis. Increased resting energy expenditure, small-bowel bacterial overgrowth, severe alcoholism, and poor control of associated diabetes may have a role. Hebuterne et al. reported that the measured REE was significantly higher than the predicted energy expenditure in underweight patients with chronic pancreatitis but not in control groups . Therefore, weight loss accompanied by hypermetabolism should be taken into consideration in patients with chronic pancreatitis. Small-bowel bacterial overgrowth deconjugates bile salt, impairing micelle formation. Almost 40% of patients with chronic pancreatitis have co-existent small-bowel bacterial overgrowth . The mechanisms for this association are not clear but may include small-bowel dysmotility induced by narcotics, shifts in hormone levels (especially cholecys-tokinin) induced by chronic pancreatitis, or previous surgery. In addition, in the majority of patients suffering from chronic pancreatitis, pancreatic endocrine insufficiency is correlated with exocrine dysfunction. The prevalence of impaired or diabetic glucose tolerance is 40-70%, and half of these patients suffer from an insulin-dependent diabetes mellitus. The aetiology of diabetes melli-tus that results from chronic pancreatitis includes a loss of p-cells secreting insulin, impaired p-cell responsiveness to glucose, and disturbances of the enteroinsular axis via diminished levels of incretins. The susceptibility to severe hypogly-caemia in patients with diabetes mellitus secondary to chronic pancreatitis is higher than in type I diabetics. This is mainly caused by impaired glucagon secretion and also influenced by malnutrition and concomitant hepatic dysfunction due to the alcoholic toxicity .
Although abnormalities can be identified on small-bowel function tests and deficiencies of fat-soluble vitamins, calcium, zinc, selenium, etc. may be demonstrated, the presence of clinical syndromes are rare, as with demonstrable low B12 uptake in some 10-15% of patients .
The absorption of fat-soluble vitamins (A, E, and K) is usually preserved [84, 88, 89] in patients with chronic pancreatitis, and, although vitamin D is not significantly reduced, osteopaenia and osteoporosis are much more common than previously thought . Deficiencies of water-soluble vitamin are often seen in chronic alcoholics, and impairment of copper, selenium, and zinc metabolism is particularly pronounced in patients with combined chronic pancreatitis and diabetes melli-tus .
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