Impaired gastric myoelectricity in patients with chronic pancreatitis： Role of maldigestion

AIM: To investigate whether gastric myoelectrical activity was impaired in patients with chronic pancreatitis (CP) and to explore the role of pancreatic enzyme in regulating gastric myoelectrical activity. METHODS: Twenty CP patients and 20 controls participated in the study. Gastric myoelectrical activity was recorded by a homemade electrogastrography (EGG) device. Two experiments were carried out. In experiment one, EGG was recorded in both controls and CP patients. While in experiment two, either pancreatic enzymes or placebo was given together with test meals. Spectral analysis was used to generate various EGG parameters. RESULTS: The control subjects, but not the CP patients, showed typically increased postprandial dominant frequency. The postprandial dominant power (DP) increment (2.24±1.13 vs 5.35±0.96 dB, P= 0.04) and the percentage of normal 2-4 cpm slow waves (63.0±3.8% vs 77.4±3.1%, P<0.05) were lower in CP patients when compared with the control. In the 20 CP patients, the DP increment (4.76±1.02 vs 2.53±1.20 dB, P<0.05) and the postprandial percentage of normal 2-4 cpm (74.4±2.8% vs 64.8±5.7%, P<0.05) were significantly higher with pancreatic enzyme replacement than the placebo. CONCLUSION: CP patients have an abnormal postprandial stomach myoelectricity showing poor response in dominant frequency/power and regularity, whereas these abnormalities are corrected after pancreatic enzyme replacement. Maldigestion is likely to be the factor leading to abnormal postprandial gastric myoelectricity of CP patients.

Impaired gastric myoelectricity in patients with chronic pancreatitis: role of maldigestion

AIM: To investigate whether gastric myoelectrical activity was impaired in patients with chronic pancreatitis (CP) and to explore the role of pancreatic enzyme in regulating gastric myoelectrical activity. METHODS: Twenty CP patients and 20 controls participated in the study. Gastric myoelectrical activity was recorded by a homemade electrogastrography (EGG) device. Two experiments were carried out. In experiment one, EGG was recorded in both controls and CP patients. While in experiment two, either pancreatic enzymes or placebo was given together with test meals. Spectral analysis was used to generate various EGG parameters. RESULTS: The control subjects, but not the CP patients, showed typically increased postprandial dominant frequency. The postprandial dominant power (DP) increment (2.24+/-1.13 vs 5.35+/-0.96 dB, P = 0.04) and the percentage of normal 2-4 cpm slow waves (63.0+/-3.8% vs 77.4 +/-3.1%, P<0.05) were lower in CP patients when compared with the control. In the 20 CP patients, the DP increment (4.76+/-1.02 vs 2.53+/-1.20 dB, P<0.05) and the postprandial percentage of normal 2-4 cpm (74.4+/-2.8% vs 64.8+/-5.7%, P<0.05) were significantly higher with pancreatic enzyme replacement than the placebo. CONCLUSION: CP patients have an abnormal postprandial stomach myoelectricity showing poor response in dominant frequency/power and regularity, whereas these abnormalities are corrected after pancreatic enzyme replacement. Maldigestion is likely to be the factor leading to abnormal postprandial gastric myoelectricity of CP patients.