OBJECTIVE: Little data exist describing the change over time in islet function and glycemic control in patients with chronic pancreatitis (CP). METHODS: In 325 CP patients who underwent 2 mixed meal tolerance tests and/or glycated hemoglobin (HbA1c) levels, we estimated the rate of change in metabolic measures per 6 months and assessed the association between potential risk factors for diabetes and rate of change using multivariate regression models. RESULTS: Per 6-month time, HbA1c increased by 0.062% with a standard error of 0.029% (P = 0.037) and the ratio (area under the curve (AUC) C-peptide to AUC glucose from mixed meal tolerance testing) decreased by 0.0028 with a standard error of 0.0011 (P = 0.014). We observed more rapid decline in smokers (AUC C-peptide, P = 0.043) and patients with surgical drainage (AUC glucose, P = 0.001; ratio, P = 0.03) or with calcific pancreatitis (HbA1c, P = 0.003). In multivariate models, AUC C-peptide and ratio declined at a greater rate in smokers and HbA1c in those with pancreatic calcifications (both P < 0.05). CONCLUSIONS: We observed a measurable decline in β-cell function and glycemic control in patients with CP. Patients with a history of tobacco smoking, surgical drainage, or pancreatic calcification may be at highest risk.
OBJECTIVE: Little data exist describing the change over time in islet function and glycemic control in patients with chronic pancreatitis (CP). METHODS: In 325 CPpatients who underwent 2 mixed meal tolerance tests and/or glycated hemoglobin (HbA1c) levels, we estimated the rate of change in metabolic measures per 6 months and assessed the association between potential risk factors for diabetes and rate of change using multivariate regression models. RESULTS: Per 6-month time, HbA1c increased by 0.062% with a standard error of 0.029% (P = 0.037) and the ratio (area under the curve (AUC) C-peptide to AUC glucose from mixed meal tolerance testing) decreased by 0.0028 with a standard error of 0.0011 (P = 0.014). We observed more rapid decline in smokers (AUC C-peptide, P = 0.043) and patients with surgical drainage (AUC glucose, P = 0.001; ratio, P = 0.03) or with calcific pancreatitis (HbA1c, P = 0.003). In multivariate models, AUC C-peptide and ratio declined at a greater rate in smokers and HbA1c in those with pancreatic calcifications (both P < 0.05). CONCLUSIONS: We observed a measurable decline in β-cell function and glycemic control in patients with CP. Patients with a history of tobacco smoking, surgical drainage, or pancreatic calcification may be at highest risk.
Authors: Phil A Hart; Melena D Bellin; Dana K Andersen; David Bradley; Zobeida Cruz-Monserrate; Christopher E Forsmark; Mark O Goodarzi; Aida Habtezion; Murray Korc; Yogish C Kudva; Stephen J Pandol; Dhiraj Yadav; Suresh T Chari Journal: Lancet Gastroenterol Hepatol Date: 2016-10-12
Authors: H Schrader; B A Menge; C Zeidler; P R Ritter; A Tannapfel; W Uhl; W E Schmidt; J J Meier Journal: Diabetologia Date: 2010-03-09 Impact factor: 10.122
Authors: Tim Strate; Kai Bachmann; Philipp Busch; Oliver Mann; Claus Schneider; Jens P Bruhn; Emre Yekebas; Thomas Kuechler; Christian Bloechle; Jakob R Izbicki Journal: Gastroenterology Date: 2008-03-04 Impact factor: 22.682