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Background: We aimed to determine the cumulative rate of diabetes mellitus (DM) and the risk factors for DM in patients with chronic pancreatitis (CP) in Japan., Methods: We conducted a follow-up survey of CP in 2002 in patients registered as having CP in 1994, and confirmed 656 patients to be checked in regard to the survey items concerning diabetes. We analyzed the cumulative rate of DM and the risk factors for DM over an 8-year follow up period., Results: In 1994, 35.1% of 656 CP patients had DM, and the incidence of diabetes had increased to 50.4% in 2002. Of 418 patients without diabetes in 1994, 28.9% (121/418) were newly diagnosed with DM in 2002. Alcoholic CP was the most common type of CP in patients with newly developed diabetes, accounting for 67.8%. The incidence of DM was highest in those with alcoholic CP (34.3%) followed by idiopathic CP (23.0%). The risk of diabetes increased 1.32-fold after the onset of pancreatic calcification. Of 121 patients with newly diagnosed DM in 2002, 37 (30.6%) had pancreatic stones in 1994 and 49 (40.5%) had a stone in 2002. The highest incidence of newly diagnosed DM was observed in patients with continuous alcoholic intake (40.9%). Patients treated with camostat mesilate developed DM less frequently than those without camostat mesilate., Conclusions: The present study showed that the incidence of DM in patients with CP increased with time. Of 418 CP patients without DM in 1994, 28.9% developed DM over a period of 8 years. Continuous alcoholic intake aggravated CP and increased the risk of DM in those with CP.

Background: Differentiation between functional dyspepsia and early chronic pancreatitis is difficult because these diseases do not produce specific abnormalities in laboratory testing. The aim of this study was to examine the potential efficacy of camostat mesilate, a protease inhibitor, against functional dyspepsia and to characterize patients with favorable responses., Methods: Dyspeptic patients who exhibited no abnormalities on laboratory blood and urine testing, abdominal ultrasonography and upper gastrointestinal endoscopy were randomized to receive camostat mesilate 200 mg three times daily or famotidine 20 mg twice daily for 4 weeks. Symptoms severity was recorded before and at 2 and 4 weeks after starting treatment using a visual analog scale., Results: Epigastralgia was significantly improved after 2 and 4 weeks of treatment in both groups (P < 0.01); this improvement tended to be more marked in the camostat mesilate group (P < 0.05 at 2 weeks). The beneficial effect of camostat mesilate on epigastralgia was more prominent in chronic alcohol drinkers at 2 weeks (P < 0.05) and 4 weeks (P < 0.01)., Conclusions: Camostat mesilate is superior to famotidine for relieving epigastralgia in patients with functional dyspepsia. Its pain-relieving effect is greater in patients who habitually drink alcohol.

Our previous report stated that kikyo-to, a Japanese herbal medicine, consisting of the roots of Platycodon grandiflorum and Glycyrrhiza sp., stimulates the pancreatic exocrine secretion of conscious rats. The present study focused on the effective components of kikyo-to and the mechanism of stimuli to pancreatic secretion of rats. When 10 to 100 mg of platycodin D, a saponin from the root of Platycodon grandiflorum, was intragastrically administered, the pancreatic secretion of rats was stimulated. At the same time, the plasma CCK concentration increased. On the other hand, the stimulative effects of glycyrrhizin, a saponin from the root of Glycyrrhiza sp. were weak compared to platycodin D. The effects of 10 mg/kg of platycodin D on pancreatic secretion were inhibited by loxiglumide (50 mg/kg, i.g.), a CCK receptor antagonist. In contrast, the suppressive effect of atropine (300 micrograms/kg/h, i.v.) on pancreatic secretion was reduced by administering 10 mg/kg of platycodin D. In addition, up to 1 mM of platycodin D did not inhibit the trypsin activities in vitro. In conclusion, kikyo-to serves to stimulate pancreatic exocrine secretion mainly because platycodin D causes gastrointestinal hormones, particularly, CCK to be released from the duodenum.