title: Decreased counterregulatory hormone responses to insulin-induced hypoglycemia in patients with pancreatic diabetes having autonomic neuropathy.
abstract: Thirteen patients with pancreatic diabetes caused by calcifying pancreatitis were divided into 2 groups; 5 with diabetic autonomic neuropathy [AN(+) group] and 8 without [AN(-) group]. They were subjected to an insulin-induced hypoglycemic stress test to evaluate their blood pancreatic glucagon, adrenalin, and cortisol responses. When a blood glucose level below 45 mg/100 ml was defined to be hypoglycemia, all the patients in the AN(-) group exhibited peripheral adrenalin responses, with a significant increase (mean, 19.0 times the basal level) in the blood adrenalin level. Among the AN(+) group, on the other hand, central nervous symptoms became evident rather than the peripheral adrenalin response (the blood adrenalin level hardly exceeded the basal level). With the exception of a single patient, none exhibited responses in the blood pancreatic glucagon levels. Only one patient showed a minimal cortisol response but the remaining 12 reacted normally in the cortisol release. The findings are summarized as follows: in pancreatic diabetes, insulin-induced hypoglycemia causes little change in pancreatic glucagon secretion; when the condition is complicated with autonomic neuropathy, central nervous symptoms develop while the blood adrenalin level hardly increases. These findings indicated that patients with pancreatic diabetes complicated with diabetic autonomic neuropathy have a risk of lapsing into an acute hypoglycemic coma and difficulty in recovering from the hypoglycemic state.
authors.affiliation: Third Department of Internal Medicine, Hirosaki University School of Medicine.
authors.forename: T
authors.initials: T
authors.lastname: Nakamura
authors.forename: K
authors.initials: K
authors.lastname: Takebe
authors.forename: K
authors.initials: K
authors.lastname: Kudoh
authors.forename: M
authors.initials: M
authors.lastname: Ishii
authors.forename: K
authors.initials: K
authors.lastname: Imamura
authors.forename: H
authors.initials: H
authors.lastname: Kikuchi
authors.forename: F
authors.initials: F
authors.lastname: Kasai
authors.forename: Y
authors.initials: Y
authors.lastname: Tandoh
authors.forename: N
authors.initials: N
authors.lastname: Yamada
authors.forename: Y
authors.initials: Y
authors.lastname: Arai
mesh_terms: D000437:Alcoholism / Q000150:complications; D001786:Blood Glucose / Q000032:analysis; D002114:Calcinosis / Q000150:complications* / Q000473:pathology; D002908:Chronic Disease; D003645:Death, Sudden; D003920:Diabetes Mellitus / Q000209:etiology / Q000503:physiopathology*; D003929:Diabetic Neuropathies / Q000209:etiology / Q000503:physiopathology*; D004198:Disease Susceptibility; D004837:Epinephrine / Q000378:metabolism*; D005934:Glucagon / Q000378:metabolism*; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism*; D007003:Hypoglycemia / Q000139:chemically induced* / Q000209:etiology / Q000503:physiopathology; D007328:Insulin; D010195:Pancreatitis / Q000150:complications* / Q000473:pathology
chemical_list: D001786:Blood Glucose; D007328:Insulin; D005934:Glucagon; D006854:Hydrocortisone; D004837:Epinephrine