Kenneth L Koch1, William L Hasler2, Mark Van Natta3, Jorge Calles-Escandon4, Madhusudan Grover5, Pankaj J Pasricha6, William J Snape7, Henry P Parkman8, Thomas L Abell9, Richard W McCallum10, Linda A Nguyen11, Irene Sarosiek10, Gianrico Farrugia12, James Tonascia3, Linda Lee3, Laura Miriel3, Frank Hamilton13. 1. Section on Gastroenterology, Wake Forest University, Winston-Salem, North Carolina. 2. Division of Gastroenterology, University of Michigan, Ann Arbor, Michigan. 3. Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland. 4. Endocrinology Section, MetroHealth Medical Center, Cleveland, Ohio. 5. May Clinic, Rochester, Minnesota. 6. Center for Neurogastroenterology, Johns Hopkins Bayview Medical Center, Baltimore, Maryland. 7. California Pacific Medical Center, San Francisco, California. 8. Section of Gastroenterology, Temple University, Philadelphia, Pennsylvania. 9. Digestive and Liver Health, University of Louisville, Louisville, Kentucky. 10. Division of Gastroenterology, Texas Tech University, El Paso, Texas. 11. Division of Gastroenterology, Stanford University, Palo Alto, California. 12. Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota. 13. National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland.
Abstract
BACKGROUND: Symptoms induced by caloric or non-caloric satiety test meals and gastric myoelectrical activity (GMA) have not been studied in patients with diabetic gastroparesis (DGP) before and after intense glucose management. AIMS: We determined the effects of continuous subcutaneous insulin infusion (CSII) with continuous glucose monitoring (CGM) on GI symptoms, volume consumed, and GMA induced by the caloric meal satiety test (CMST) and water load satiety test (WLST) in DGP. METHODS: Forty-five patients with DGP underwent CMST and WLST at baseline and 24 weeks after CSII with CGM. Subjects ingested the test meals until they were completely full. Visual analog scales were used to quantify pre- and postmeal symptoms, and GMA was recorded with cutaneous electrodes and analyzed visually and by computer. KEY RESULTS: At baseline and 24-week visits, nausea, bloating, abdominal discomfort, and fullness were immediately increased after CMST and WLST (Ps < 0.01). The meal volumes ingested were significantly less than normal controls at both visits in almost one-third of the subjects. After the CMST, the percentage 3 cycle per minute GMA increased and bradygastria decreased compared with WLST (Ps < 0.05). After treatment for 24 weeks meal volumes ingested, postmeal symptoms and GMA were no different than baseline. CONCLUSIONS AND INFERENCES: (a) Satiety test meals elicited symptoms of nausea, bloating, and abdominal discomfort; (b) CMST stimulated more symptoms and changes in GMA than WLST; and (c) CSII with CGM for 24 weeks did not improve symptoms, volumes ingested, or GMA elicited by the two satiety test meals in these patients with diabetic GP. Satiety tests in diabetic gastropresis are useful to study acute postprandial symptoms and GMA, but these measures were not improved by intensive insulin therapy.
BACKGROUND: Symptoms induced by caloric or non-caloric satiety test meals and gastric myoelectrical activity (GMA) have not been studied in patients with diabetic gastroparesis (DGP) before and after intense glucose management. AIMS: We determined the effects of continuous subcutaneous insulin infusion (CSII) with continuous glucose monitoring (CGM) on GI symptoms, volume consumed, and GMA induced by the caloric meal satiety test (CMST) and water load satiety test (WLST) in DGP. METHODS: Forty-five patients with DGP underwent CMST and WLST at baseline and 24 weeks after CSII with CGM. Subjects ingested the test meals until they were completely full. Visual analog scales were used to quantify pre- and postmeal symptoms, and GMA was recorded with cutaneous electrodes and analyzed visually and by computer. KEY RESULTS: At baseline and 24-week visits, nausea, bloating, abdominal discomfort, and fullness were immediately increased after CMST and WLST (Ps < 0.01). The meal volumes ingested were significantly less than normal controls at both visits in almost one-third of the subjects. After the CMST, the percentage 3 cycle per minute GMA increased and bradygastria decreased compared with WLST (Ps < 0.05). After treatment for 24 weeks meal volumes ingested, postmeal symptoms and GMA were no different than baseline. CONCLUSIONS AND INFERENCES: (a) Satiety test meals elicited symptoms of nausea, bloating, and abdominal discomfort; (b) CMST stimulated more symptoms and changes in GMA than WLST; and (c) CSII with CGM for 24 weeks did not improve symptoms, volumes ingested, or GMA elicited by the two satiety test meals in these patients with diabetic GP. Satiety tests in diabetic gastropresis are useful to study acute postprandial symptoms and GMA, but these measures were not improved by intensive insulin therapy.
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