Beta-cell function of the pancreas after necrotizing pancreatitis

To investigate the late sequellae of necrotizing pancreatitis on the endocrine function of the pancreas.

Twenty patients, 15 men (mean +/- SEM age 52.2+/-2.6 years and BMI 26.8+/-0.8 kg/m2) and 5 women (age 51.0+/-7.6 years and BMI 26.7+/-0.8 kg/m2) were submitted to a glucagon stimulation test 63 (range 8-136) months after an attack of pancreatitis. All nondiabetic patients (n = 15) were also submitted to an oral glucose tolerance test. For comparison, 16 healthy volunteers, 8 men (age 56.0+/-0.9 years and BMI 26.3+/-0.4 kg/m2) and 8 women (age 50.5+/-1.0 years and BMI 28.2+/-0.6 kg/m2), were also studied.

Five patients (25%) had diabetes mellitus and needed insulin treatment, 6 patients (30%) had an impaired glucose tolerance (IGT). Nondiabetic patients (IGT included) had a significantly higher basal insulin level (15.8+/-1.9 vs. 10.9 +/-2.2 mU/l, p < 0.05) and a lower glucose/insulin ratio (p < 0.05) compared with controls. The serum concentrations of insulin and C peptide, after stimulation with glucagon, calculated as peak value, maximal increment and as area under the curve were not significantly different in the nondiabetic patients compared to controls. The subgroup of IGT patients had a significantly higher basal C peptide (p < 0.05) and a reduced maximal increment (p < 0.05).

After nonresectional therapy for necrotizing pancreatitis, there is a high prevalence of disturbances in glucose metabolism. Patients with IGT have signs of both loss of beta-cell function and insulin resistance.