In vitro and in vivo evidences that the malabsorption of cobalamin is related to its binding on haptocorrin (R binder) in chronic pancreatitis1

The intraluminal transport of cobalamin (Cbl) remains controversial in chronic pancreatitis. We have determined the ability ofintestinal juice to degrade the digestive holohaptocorrin (R binder) and the binding of endogenous Cbl in basal intestinal juice from 22 chronic pancreatitis patients and 22 controls. The intestinal juice from patients and controls degraded 34.7 ± 32.3% and 95.2 ± 7.2% of holophatocorrin, respectively. This percentage was correlated with the trypsin output but not with the Schilling test. The unsaturated Cbl-binding capacity was similar in both groups. Respectively, 62.5 ± 26.6% and 19.6 ± 11.7% of endogenous Cbl was bound to haptocorrin in intestinal juice from patients and controls. These percentages were correlated with the Schilling test and with the ability of intestinal juice to degrade haptocorrin. We concluded that 1) the sequestration of Cbl to haptocorrin is one of the factors responsible for the malabsorption of crystalline Cbl in patients with chronic pancreatitis and 2) enterohepatic circulation of Cbl can be interrupted in some cases of chronic pancreatitis. Am iC/in NuIr l986;44:265-277.