Table 2: Relation of Gastroparesis Symptom Severity to Regional GI Contractility
AGA Abstracts
Table 2
Mo1600 Obstructive Gastroparesis: Effect of Laparoscopic Pyloroplasty on Symptoms, Gastric Emptying and Gastric Myoelectrical Activity After Successful Endoscopic Pyloric Therapies Jennifer Wellington, Kenneth L. Koch, Paula S. Stuart
Mo1599
Subtypes of gastroparesis (GP) may respond to different treatment approaches. We hypothesized that a subset of patients with GP, normal 3 cpm gastric myoelectrical activity (GMA), and normal upper endoscopy had GP related to pyloric dysfunction, termed obstructive gastroparesis. Aims: 1. To determine the effect of pyloric therapies [botulinum toxin A (btA), pyloric balloon dilation (BD), and pyloroplasty] on symptoms and body weight in these patients. 2. To evaluate the effect of pyloroplasty on symptoms, gastric emptying (GE) and GMA in patients who had successful endoscopic pyloric therapies. Methods: Patients were identified who had GP, normal 3 cpm GMA, and normal endoscopy that excluded mechanical obstruction of the pylorus. Electrogastrography (EGG) with water load tests (WLT) were performed using standard methods to determine GMA. GE was measured with 4hr scintigraphy. Patients had failed medical treatments for GP. Each patient underwent up to three pyloric treatments with btA or BD. Changes in major symptoms and weight were measures of treatment effect. EGG and gastric emptying studies were repeated six months after pyloroplasty. Results: 33 patients (29 women) met inclusion criteria. Median age was 42 years. Twenty-six patients had idiopathic GP and seven had diabetic GP. The average percent meal retained at four hours was 42% (range 16% to 68%). Complete or partial symptom response occurred in 75%, 72%, and 88% of patients after the first, second, or third endoscopic pyloric treatment respectively. Weight increased significantly after the second and third treatment (p<0.04). Eight patients (8 women; average age 36 years) of the original 33 patients elected to undergo laparoscopic pyloroplasty after multiple successful pyloric btA or BD therapies. At six months post pyloroplasty, 7 of the 8 patients (87%) reported improved symptoms and weight increased an average of 2.5 lbs (range -5lbs to +9lbs) . Percentage of meal retained at 4 hrs improved from 50% (range 24% to 90%) pre-pyloroplasty to 13% (range 1% to 64%) post-pyloroplasty (p<0.01). GMA activity (% time in 3 cpm range) before the WLT decreased from 54 +/- 12 % before to 24 +/- 16 % after pyloroplasty (p<0.03) and at 20 min after the WLT the % time in 3 cpm decreased from 64 +/- 14 % before pyloroplasty to 20 +/- 14% after pyloroplasty (p=0.03).WLT volumes were similar before and after pyloroplasty at 421ml +/- 133ml vs. 404ml +/- 175ml water (P= 0.75). Conclusions: 1. Pyloric dysfunction is a key factor in delayed emptying in patients with GP and normal 3 cpm GMA. 2. Pyloroplasty in patients with severe GP who had responded to btA or BD resulted in normalization of gastric emptying and decreased 3 cpm GMA, consistent with relief of obstructive pathophysiology.
Relation of Gastroparesis Symptom Severity to Gastric, Small Bowel, and Colon Transit and Contraction Profiles on Wireless Motility Capsule Testing in a Large Multicenter Cohort William L. Hasler, Kevin P. May, Pankaj J. Pasricha, Henry P. Parkman, Thomas L. Abell, Kenneth L. Koch, Richard W. McCallum, Linda Anh B. Nguyen, William J. Snape, Irene Sarosiek, John O. Clarke, Gianrico Farrugia, Jorge Calles-Escandon, James Tonascia, Laura Miriel, Linda A. Lee, Frank A. Hamilton Background: Most gastroparesis symptoms correlate poorly with delayed gastric emptying. A related disorder, chronic unexplained nausea and vomiting, has similar symptoms but with normal gastric emptying suggesting that symptoms result from other pathogenic factors or are non-specific. Subsets of patients with presumed gastroparesis also show delays in small bowel (SB) or colon transit on indigestible wireless motility capsule (WMC) testing, raising the possibility that some symptoms (e.g. bloating, pain) originate from extragastric transit or contractile abnormalities. We aimed to (i) determine if delayed WMC gastric emptying times (GETs), SB transit times (SBTTs), or colon transit times (CTTs) correlate with any symptom of gastroparesis and (ii) define if WMC regional contraction profiles relate better than transit to any symptom. Methods: WMCs were performed in 147 patients with suspected gastroparesis at 8 centers of the NIDDK Gastroparesis Consortium. Delayed vs. normal GET (>5 vs. <5 hr), SBTT (>6 vs. <6 hr), and CTT (>59 vs. <59 hr) were defined as stated. Patients were divided into groups with high vs. low contractility based on numbers of gastric (1 hr before GET), SB (1 hr after GET), and colon (per hr) contractions. WMC data were related to overall Gastroparesis Cardinal Symptom Index (GCSI) scores, nausea/ vomiting, early satiety/fullness, bloating/distention, upper abdominal pain/discomfort subscores, and individual GI scores from PAGI-SYM surveys (0=none, 5=very severe). Results: WMC delays in GET (56/140, 40%), SBTT (16/116, 14%), and CTT (40/110, 36%) were defined. Overall GCSI scores were similar with delayed vs. normal GET (2.8+1.1 vs. 2.8+1.1, P=0.88), SBTT (3.0+0.8 vs. 2.7+1.1, P=0.26), and CTT (2.7+1.0 vs. 2.8+1.1, P=0.59). Nausea/ vomiting, early satiety/fullness, bloating/distention, and upper abdominal pain/discomfort subscores showed no relation to any regional transit delay (Table 1). These subscores also were similar with high vs. low gastric, SB, and colon contraction counts (Table 2). Most individual PAGI-SYM scores were not different in those with delayed vs. normal GET, SBTT, and CTT and with high vs. low gastric, SB, and colon contraction counts. Scores for inability to finish meals and constipation were higher with delayed SBTT (P<0.05). Diarrhea and lower abdominal pain scores were lower with delayed CTT; diarrhea scores were less with high colon contraction counts (P<0.05). Conclusions: Symptoms of gastroparesis, including those potentially of extragastric origin, show little association with any regional GI transit delay or contractile profile as defined by WMC testing, although diarrhea and lower abdominal pain relate to SB or colon abnormalities. These findings indicate that factors other than gut transit or phasic contractile abnormalities as measured by WMCs are major contributors to gastroparesis symptom severity. Table 1: Relation of Gastroparesis Symptom Severity to Regional GI Transit
Mo1601 Relationship Between Gastric Emptying and Glycemic Variability in Type 1 Diabetes Mellitus Gopanandan Parthasarathy, Yogish C. Kudva, Michael Camilleri, Adil E. Bharucha Background. In type 1 DM (T1DM), delayed gastric emptying (GE) may predispose to a mismatch between insulin delivery and glucose absorption. However, the effect of GE disturbances on glycemic control in T1DM is unclear. Aims. To understand the effects of accelerating GE on glycemia in T1DM. Methods. GE was evaluated with a 13C-spirulina GE breath test (GEBT, 223 kcal, AB Diagnostics), in 30 T1DM patients (47 ± 18 years[mean ± SD]) on an insulin pump on 3 occasions - baseline (GEBT1), after iv saline or erythromycin (2 or 3 mg/kg) (GEBT2), and then (GEBT3) after erythromycin (250 mg oral suspension tid) or placebo for 7 days. During GEBT, 13C breath samples were collected at baseline, 15, 30, 45, 60, 90, 120, 180, and 240 minutes after a meal. The cumulative kPCD (cumkPCD, cumulative % 13C dose recovered) for all breath samples was analyzed (AUC). A weight maintaining diet with 30, 30 and 40 % of the calories to be consumed during each of 3 daily meals was provided. Continuous glucose monitoring (CGM) throughout the study provided blood glucose values. Insulin was summarized as the insulin dose(U)/time gap (minutes) between insulin administration and blood glucose measurement. Mixed effects models evaluated the relationship between GE, glucose, and erythromycin; parameter estimates represented their contributions. Because GE was perturbed with erythromycin, the GE(cumkPCD) was the dependent variable in 3 models i.e., GEBT1, GEBT2, and GEBT3. Results. The duration of DM was 26 ± 13 years. Mean HbA1c was 7.6 ± 0.8 %. Fasting blood glucose before GEBT was 155 ± 67 (GEBT1), 183 ± 50 (GEBT2), and 201 ± 81 (GEBT3). GEBT data were analyzed based on kPCD values, which is the metric approved by the FDA for GEBT reports. Greater kPCD values reflect faster GE. In model 1, (Table) the dependent variable (cumkPCD during GEBT1) was associated with (i) higher blood glucose concentration and (ii) a lower insulin dose or a longer time gap. Because both the dependent and predictor variables were log transformed, the parameter estimates reflect the % change in cumkPCD per unit % change of the predictor. Hence, for model 1, each doubling, (100% increase) in blood glucose values was associated on average with a 89% increase in cumkPCD. Baseline GEBT (GEBT1) predicted GEBT2 and GEBT3. In addition,
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AGA Abstracts