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This month’s selection of EPI research includes a few very clinically relevant and high-quality studies. The first of which comes out of University of Miami, by father and son authors Barkin. The authors suggest that the approach of relying solely on symptoms regarding the adequacy of pancreatic enzyme replacement therapy in chronic pancreatitis remains controversial. In a post-hoc pooled analysis of two studies, the authors aimed to answer whether improvement in objective measures of fat absorption is associated with changes in clinical symptoms. Indeed, they showed that mean change in CFA (coefficient of fat absorption) from baseline was significantly greater with pancrelipase vs. placebo at week 1 (24.7% vs. 6.4%; P less than .001), and improvements in stool consistency and frequency did in fact correlate with CFA. They conclude this provides the rationale for using these clinical symptoms as surrogate markers for the efficacy of PERT in patients with EPI, which while it may not be practicing changing should certainly be practice reassuring.
The following two studies are related to additional at-risk patient populations for exocrine pancreatic insufficiency. In a single-center cross-sectional study out of Italy, researchers demonstrated that EPI is a feature of type 1 diabetes—compared with healthy individuals, fecal elastase-1 levels were significantly lower in participants with new-onset and long-standing T1D (P = .0070 and .0010, respectively). Notably the study showed correlation between progressive exocrine and endocrine function throughout the natural history of disease. Certainly, further research is needed to clarify the pathogenesis and role of EPI in type 1 diabetes.
Lastly the final selection comes from AIIMS in India, where they assessed endocrine and exocrine function in patients following pancreatic trauma. Notably, of the 20 patients studied with trauma, 11 of them (55%) had evidence of pancreatic exocrine insufficiency by fecal elastase measurement. 4 patients had severe pancreatic insufficiency, 3 of which had partial pancreatectomy (with mean pancreatic volume of 48.65cm3 following surgery). Classic teaching is that EPI develops when exocrine function is impaired by ~90%, however in the resection groups, they have demonstrated severe EPI in patients with roughly 50% retained pancreatic volume.
This month’s selection of EPI research includes a few very clinically relevant and high-quality studies. The first of which comes out of University of Miami, by father and son authors Barkin. The authors suggest that the approach of relying solely on symptoms regarding the adequacy of pancreatic enzyme replacement therapy in chronic pancreatitis remains controversial. In a post-hoc pooled analysis of two studies, the authors aimed to answer whether improvement in objective measures of fat absorption is associated with changes in clinical symptoms. Indeed, they showed that mean change in CFA (coefficient of fat absorption) from baseline was significantly greater with pancrelipase vs. placebo at week 1 (24.7% vs. 6.4%; P less than .001), and improvements in stool consistency and frequency did in fact correlate with CFA. They conclude this provides the rationale for using these clinical symptoms as surrogate markers for the efficacy of PERT in patients with EPI, which while it may not be practicing changing should certainly be practice reassuring.
The following two studies are related to additional at-risk patient populations for exocrine pancreatic insufficiency. In a single-center cross-sectional study out of Italy, researchers demonstrated that EPI is a feature of type 1 diabetes—compared with healthy individuals, fecal elastase-1 levels were significantly lower in participants with new-onset and long-standing T1D (P = .0070 and .0010, respectively). Notably the study showed correlation between progressive exocrine and endocrine function throughout the natural history of disease. Certainly, further research is needed to clarify the pathogenesis and role of EPI in type 1 diabetes.
Lastly the final selection comes from AIIMS in India, where they assessed endocrine and exocrine function in patients following pancreatic trauma. Notably, of the 20 patients studied with trauma, 11 of them (55%) had evidence of pancreatic exocrine insufficiency by fecal elastase measurement. 4 patients had severe pancreatic insufficiency, 3 of which had partial pancreatectomy (with mean pancreatic volume of 48.65cm3 following surgery). Classic teaching is that EPI develops when exocrine function is impaired by ~90%, however in the resection groups, they have demonstrated severe EPI in patients with roughly 50% retained pancreatic volume.
This month’s selection of EPI research includes a few very clinically relevant and high-quality studies. The first of which comes out of University of Miami, by father and son authors Barkin. The authors suggest that the approach of relying solely on symptoms regarding the adequacy of pancreatic enzyme replacement therapy in chronic pancreatitis remains controversial. In a post-hoc pooled analysis of two studies, the authors aimed to answer whether improvement in objective measures of fat absorption is associated with changes in clinical symptoms. Indeed, they showed that mean change in CFA (coefficient of fat absorption) from baseline was significantly greater with pancrelipase vs. placebo at week 1 (24.7% vs. 6.4%; P less than .001), and improvements in stool consistency and frequency did in fact correlate with CFA. They conclude this provides the rationale for using these clinical symptoms as surrogate markers for the efficacy of PERT in patients with EPI, which while it may not be practicing changing should certainly be practice reassuring.
The following two studies are related to additional at-risk patient populations for exocrine pancreatic insufficiency. In a single-center cross-sectional study out of Italy, researchers demonstrated that EPI is a feature of type 1 diabetes—compared with healthy individuals, fecal elastase-1 levels were significantly lower in participants with new-onset and long-standing T1D (P = .0070 and .0010, respectively). Notably the study showed correlation between progressive exocrine and endocrine function throughout the natural history of disease. Certainly, further research is needed to clarify the pathogenesis and role of EPI in type 1 diabetes.
Lastly the final selection comes from AIIMS in India, where they assessed endocrine and exocrine function in patients following pancreatic trauma. Notably, of the 20 patients studied with trauma, 11 of them (55%) had evidence of pancreatic exocrine insufficiency by fecal elastase measurement. 4 patients had severe pancreatic insufficiency, 3 of which had partial pancreatectomy (with mean pancreatic volume of 48.65cm3 following surgery). Classic teaching is that EPI develops when exocrine function is impaired by ~90%, however in the resection groups, they have demonstrated severe EPI in patients with roughly 50% retained pancreatic volume.