BACKGROUND: Concurrent exocrine pancreatic dysfunction may be one of the factors implicated in malabsorption in untreated celiac disease, as shown by studies on bicarbonate and pancreatic enzyme secretion. The purpose of this study was to evaluate exocrine pancreatic function in relation to jejunal morphology in celiac disease. METHODS: Thirty-six patients fulfilling the ESPGHAN criteria for celiac disease, aged 3 to 18 years and 36 control subjects matched for age and sex were investigated. The design of the study included measurement of serum pancreatic isoamylase by a chromogenic method after selective inhibition of sialic isoamylase in the untreated phase in patients consuming a gluten-containing diet and after gluten elimination for a period of 1 year; fecal human elastase activity determined by enzyme-linked immunosorbent assay in patients consuming a gluten-free diet and again after gluten challenge for 6 months; correlation of serum pancreatic isoamylase and fecal elastase to the jejunal morphology, classified by criteria described by Marsch; the enzymes in the control group; and ultrasonography of the pancreas in both groups. RESULTS: Enzyme values obtained from celiac disease patients with normal mucosa were significantly higher than those obtained from patients with villous atrophy (p < 0.001) and comparable to those obtained from the control group. Serum pancreatic isoamylase activity increased to normal after gluten elimination, and human elastase activity decreased to values below 200 microg/g of stool after gluten challenge. Enzyme activity was related inversely to the degree of intestinal damage. The echogenicity of the pancreas was normal, regardless of enzyme activity or gut morphology. CONCLUSIONS: Exocrine pancreatic function is abnormal in celiac disease when mucosal atrophy is present. Exocrine pancreatic function parameters are associated with the changes of intestinal mucosal morphology in three consecutive phases of the disease.
BACKGROUND: Concurrent exocrine pancreatic dysfunction may be one of the factors implicated in malabsorption in untreated celiac disease, as shown by studies on bicarbonate and pancreatic enzyme secretion. The purpose of this study was to evaluate exocrine pancreatic function in relation to jejunal morphology in celiac disease. METHODS: Thirty-six patients fulfilling the ESPGHAN criteria for celiac disease, aged 3 to 18 years and 36 control subjects matched for age and sex were investigated. The design of the study included measurement of serum pancreatic isoamylase by a chromogenic method after selective inhibition of sialic isoamylase in the untreated phase in patients consuming a gluten-containing diet and after gluten elimination for a period of 1 year; fecal human elastase activity determined by enzyme-linked immunosorbent assay in patients consuming a gluten-free diet and again after gluten challenge for 6 months; correlation of serum pancreatic isoamylase and fecal elastase to the jejunal morphology, classified by criteria described by Marsch; the enzymes in the control group; and ultrasonography of the pancreas in both groups. RESULTS: Enzyme values obtained from celiac disease patients with normal mucosa were significantly higher than those obtained from patients with villous atrophy (p < 0.001) and comparable to those obtained from the control group. Serum pancreatic isoamylase activity increased to normal after gluten elimination, and human elastase activity decreased to values below 200 microg/g of stool after gluten challenge. Enzyme activity was related inversely to the degree of intestinal damage. The echogenicity of the pancreas was normal, regardless of enzyme activity or gut morphology. CONCLUSIONS:Exocrine pancreatic function is abnormal in celiac disease when mucosal atrophy is present. Exocrine pancreatic function parameters are associated with the changes of intestinal mucosal morphology in three consecutive phases of the disease.
Authors: David C Dallas; Megan R Sanctuary; Yunyao Qu; Shabnam Haghighat Khajavi; Alexandria E Van Zandt; Melissa Dyandra; Steven A Frese; Daniela Barile; J Bruce German Journal: Crit Rev Food Sci Nutr Date: 2017-10-13 Impact factor: 11.176
Authors: Omid Sadr-Azodi; David S Sanders; Joseph A Murray; Jonas F Ludvigsson Journal: Clin Gastroenterol Hepatol Date: 2012-07-16 Impact factor: 11.382