Assessment of colon motility using simultaneous manometric and functional cine-MRI analysis: preliminary results.

PURPOSE: Gastrointestinal functional disorders are common symptoms. The evaluation of underlying colonic motility dysfunction is difficult due to lacking adequate examination techniques. Recently cine-magnetic resonance imaging (MRI) was introduced as imaging technique for visualizing colon motility. However, the correlation of MR-visible colonic-movements and real intraluminal movements was not demonstrated yet. Therefore, this feasibility study's purpose was to stimulate high amplitude propagated pressure waves (HAPPWs) by bisacodyl application under manometric control and to simultaneously identify them with cine-MRI. MATERIALS AND METHODS: Colonoscopically, a water-perfused 8-lumen-probe was placed in descending colon. Intraluminal pressure was recorded over time. After 90 min equilibration phase, MR exam at rest (HASTE-sequence, 1.5Tesla-Avanto(®), Siemens-Medical-Solutions) was performed. Consecutively, 10 mg bisacodyl were instilled via colonic probe to induce HAPPWs. Cine-MRI and manometry were performed simultaneously over 24 min. HAPPWs were defined as pressure waves with amplitude >50 mmHg and propagation over min. three side-holes. MRI was analyzed for corresponding luminal changes of the referring colonic segment propagated aborally. RESULTS: Ten healthy volunteers (age:19-62 years, 4 females, 6 males) were enrolled. Manometry identified 11 HAPPWs, most 9-16 min post-stimulation. All HAPPWs were identified on MRI with corresponding luminal changes (100% sensitivity). CONCLUSIONS: In accordance with our study group's previous publications, these results show that cine-MRI allows not only for reliable HAPPWs' visualization using pharmalogical stimuli, but visualized colonic movements have 100% correlation to intraluminal pressure changes in manometry (gold-standard). This may be a first step to introduce cine-MRI for non-invasive colon motility assessment in patients with functional gastro-intestinal disorders.

[Cannabinoid-induced hyperemesis]. / Cannabinoidinduzierte Hyperemesis.

In this case report, we describe a 29 year-old male patient with a history of chronic cannabis abuse presenting with recurrent vomiting, intense nausea and abdominal pain. Abstinence from cannabis resolved both vomiting and abdominal pain. We conclude that in case of chronic cannabis abuse, patients presenting with severe and chronic nausea, vomiting, accompanied by abdominal pain and compulsive behaviour (hot bathing), in the absence of other obvious causes, the diagnosis of cannabinoid-induced hyperemesis syndrome should be considered.

Endogenous GLP-1 regulates postprandial glycemia in humans: relative contributions of insulin, glucagon, and gastric emptying.

OBJECTIVE: Synthetic glucagon-like peptide-1 (7-36)amide (GLP-1) lowers postprandial (pp) glycemia by stimulating insulin and inhibiting glucagon release and delaying gastric emptying (GE). However, the biological effects of the endogenous peptide and their relative contributions to pp glycemia remain to be defined in detail. Using the specific GLP-1 receptor antagonist exendin(9-39)amide [Ex(9-39)], we studied the exact impact of GLP-1 after an oral meal in humans. RESEARCH DESIGN AND METHODS: After a 50-min basal period, 12 healthy subjects ingested a 412-kcal mixed semisolid meal containing 30 g oatmeal, labeled with 99mTc-Sn-colloid. GE was measured by high-resolution scintigraphy until 210 min after meal ingestion. In random order, saline or Ex(9-39) at 900 pmol/kg·min was infused iv. Additionally, in six subjects gastric motility was measured by antroduodenal manometry and a gastric barostat in parallel. RESULTS: Ex(9-39) increased pp blood glucose excursions during the first 60 min after the meal (43.9 ± 5.4 vs. 35.9 ± 3.6 mg/dl, P = 0.008; pp peak glucose 154.0 ± 5.5 vs.141.0 ± 4.7 mg/dl, P = 0.009). Insulin increased slightly with Ex(9-39), whereas the insulin to glucose ratio was unchanged. pp glucagon was significantly increased with Ex(9-39) (7.5 ± 2.4 vs. 3.2 ± 2.1 pg/ml, P = 0.024). GE and accordingly gastric motility did not change with Ex(9-39). Multiple linear regression analysis revealed only changes of pp glucagon to be significantly associated with increased pp glycemia under Ex(9-39) (R = 0.678, P = 0.015). CONCLUSIONS: Released after an oral meal, GLP-1 lowers pp glycemia. In this study, the inhibition of glucagon release was a major determinant of the acute GLP-1 action in healthy subjects. In contrast, gastric emptying was not changed by GLP-1 receptor antagonism.

Impaired hyperglycemia-induced delay in gastric emptying in patients with type 1 diabetes deficient for islet amyloid polypeptide.

OBJECTIVE: Slowing of gastric emptying by hyperglycemia, a physiological response to minimize postprandial hyperglycemia, may be impaired in patients with type 1 diabetes. The causes and consequences on glucose homeostasis are unknown. RESEARCH DESIGN AND METHODS: Consequences of euglycemia- and hyperglycemia-induced changes in gastric emptying on postprandial glucose fluxes and excursions were studied in 10 healthy subjects and 15 type 1 diabetic subjects after ingestion of a mixed meal using the double isotope approach ([6,6-(2)H(2)] and [1-(13)C]glucose) and scintigraphic measurements of gastric emptying. RESULTS: Gastric emptying was greater in type 1 diabetic subjects (90-120 min, P < 0.03), and 50% retention times were comparable in healthy subjects and type 1 diabetic subjects (167 +/- 8 vs. 152 +/- 10, P = 0.32). Hyperglycemia markedly delayed gastric emptying in healthy subjects but did not alter it in type 1 diabetic subjects (50% retention time 222 +/- 18 vs. 167 +/- 8 min, P = 0.003 and 148 +/- 9 vs. 152 +/- 10 min, P = 0.51). Plasma islet amyloid polypeptide (IAPP) increased approximately fourfold in healthy subjects (P < 0.001), whereas it was undetectable in type 1 diabetic subjects. IAPP replacement, using the analog pramlintide, in type 1 diabetic subjects slowed gastric emptying to a comparable extent, as did hyperglycemia in healthy subjects (P < 0.14), and greatly reduced postprandial hyperglycemia (P < 00.1). Meal-derived glucose appearance in plasma (10.7 +/- 0.5 vs. 6.8 +/- 0.7 mumol . kg(-1) . min(-1), P < 0.001) was reduced, and splanchnic glucose sequestration increased (14.0 +/- 3.0 vs. 25.0 +/- 6.0%, P = 0.04). CONCLUSIONS: In patients with type 1 diabetes the ability to delay gastric emptying in response to hyperglycemia is impaired. This impairment contributes to exaggerated rates of meal-derived glucose appearance and, ultimately, postprandial glucose excursions.