BMJ open diabetes research & care · 2021
Impaired exocrine pancreatic function in different stages of type 1 diabetes.
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Dozio Nicoletta, Indirli Rita, Giamporcaro Gian Maria, Frosio Laura, Mandelli Alessandra, Laurenzi Andrea, Bolla Andrea Mario, Stabilini Angela, Valle Andrea, Locatelli Massimo, Cavestro Giulia Martina, Scavini Marina, Battaglia Manuela, Bosi Emanuele
Аннотация
INTRODUCTION: Aim of this study was to investigate the pancreatic exocrine function in patients with type 1 diabetes (T1D) by multiple non-invasive tests.
RESEARCH DESIGN AND METHODS: The study is a single-center, cross-sectional study of pancreatic exocrine function in adult patients with new-onset or long-standing T1D and healthy controls.
RESULTS: Healthy controls, new-onset T1D, and long-standing T1D were similar for age at the time of the study, gender and body mass index (BMI) categories. Age of onset of T1D patients with long-standing disease was younger than that of patients with new-onset T1D (p<0.001). As expected, the three groups differed for C-peptide and hemoglobin A1c (HbA1c) levels. Lipase activity measured by 13C-mixed triglyceride breath test was reduced progressively, although not significantly, from controls to recent-onset T1D and long-standing T1D participants. Fecal elastase-1 was significantly lower in participants with T1D, either new onset or long standing. Pancreatic amylase, lipase, retinol binding protein and prealbumin were significantly different across the groups, with a significant trend toward lower values in long-standing T1D and intermediate values in new-onset T1D, while no differences were observed for total amylase. The markers of impaired exocrine function tests (fecal elastase-1, serum pancreatic amylase and lipase) and of nutritional status (retinol binding protein and prealbumin levels) correlated with the reduction of fasting and urinary C-peptide.
CONCLUSIONS: Our results confirm that exocrine pancreatic impairment is a feature of T1D, with low fecal elastase-1, serum pancreatic amylase and lipase as specific markers, associated with reduced levels of nutritional indexes. Moreover, the evidence of more advanced insufficiency in long-standing disease reflects the chronic nature of this process, and its correlation with the residual β-cell function suggests parallel pathways for the impairment of the endocrine and exocrine pancreatic function.
RESEARCH DESIGN AND METHODS: The study is a single-center, cross-sectional study of pancreatic exocrine function in adult patients with new-onset or long-standing T1D and healthy controls.
RESULTS: Healthy controls, new-onset T1D, and long-standing T1D were similar for age at the time of the study, gender and body mass index (BMI) categories. Age of onset of T1D patients with long-standing disease was younger than that of patients with new-onset T1D (p<0.001). As expected, the three groups differed for C-peptide and hemoglobin A1c (HbA1c) levels. Lipase activity measured by 13C-mixed triglyceride breath test was reduced progressively, although not significantly, from controls to recent-onset T1D and long-standing T1D participants. Fecal elastase-1 was significantly lower in participants with T1D, either new onset or long standing. Pancreatic amylase, lipase, retinol binding protein and prealbumin were significantly different across the groups, with a significant trend toward lower values in long-standing T1D and intermediate values in new-onset T1D, while no differences were observed for total amylase. The markers of impaired exocrine function tests (fecal elastase-1, serum pancreatic amylase and lipase) and of nutritional status (retinol binding protein and prealbumin levels) correlated with the reduction of fasting and urinary C-peptide.
CONCLUSIONS: Our results confirm that exocrine pancreatic impairment is a feature of T1D, with low fecal elastase-1, serum pancreatic amylase and lipase as specific markers, associated with reduced levels of nutritional indexes. Moreover, the evidence of more advanced insufficiency in long-standing disease reflects the chronic nature of this process, and its correlation with the residual β-cell function suggests parallel pathways for the impairment of the endocrine and exocrine pancreatic function.