Relationship between clinical features and gastric emptying disturbances in diabetes mellitus.

BACKGROUND AND OBJECTIVES: Gastric emptying (GE) may be delayed or rapid in diabetes mellitus. We sought to ascertain differences in risk factors or associated features (i.e. diabetic 'phenotype') among patients with diabetes who have rapid, slow or normal GE. METHODS: From a database of patients in whom gastrointestinal transit was assessed by scintigraphy, we compared the diabetic phenotype in diabetic patients with rapid, slow and normal GE. RESULTS: Of 129 patients, 55 (42%) had normal, 46 (36%) had delayed and 28 (22%) patients had rapid GE. In each GE category, there was an approximately equal number of type 1 and type 2 diabetes. In multivariable analyses, significant weight loss (OR, 2.81; 95% CI, 1.09-7.23) and neuropathy (OR, 3.60; 95% CI, 1.007-12.89) were the risk factors for delayed and rapid GE, respectively. Insulin therapy (OR, 0.08; 95% CI, 0.01-0.53) was associated with a lower risk of rapid compared to normal GE. However, other manifestations or characteristics of the diabetes 'phenotype' (i.e. type and duration of diabetes, glycosylated haemoglobin levels, and extraintestinal complications) were not useful for discriminating normal from delayed or rapid GE. At a specificity of 60%, clinical features were 73% sensitive for discriminating between normal and delayed GE and 80% sensitive for discriminating normal from rapid GE. CONCLUSIONS: Diabetes is associated with slow and rapid GE. Because the diabetic phenotype is of limited utility for identifying disordered GE, GE should be assessed in patients with diabetes and gastrointestinal symptoms.

Biodistribution and dosimetry of [(18)F]fluorodeoxyglucose labelled leukocytes in normal human subjects.

SUMMARY: This study was performed in order to assess [(18)F]fluorodeoxyglucose white blood cell ((18)F-FDG WBC) dosimetry in normal human subjects. Using previously reported methods, mixed cell suspensions of autologous leukocytes were prepared from four normal volunteers. Leukocytes were labelled in heparin-saline by incubation with (18)F-FDG at 37 degrees C for 20 min. After washing and resuspension, (18)F-FDG WBCs (225-315 MBq) were administered by intravenous injection. Whole-body imaging was performed at 0.5, 1, 2, 4 and 6 h using a GE Varicam with 511 keV collimation. Blood samples were obtained at corresponding times as well as fractionated urinary collection. Whole-body anterior and posterior images were used for calculation of organ dosimetry. Uptake of (18)F-FDG WBCs occurred predominantly within the reticulo-endothelial system. Plasma activity, urinary excretion (9.9+/-2.3% at 6 h), and brain uptake (1.7+/-0.4%) were consistent with partial elution of (18)F-FDG. Positron emission tomography imaging performed at 5-6 h after injection yielded good quality images of reticulo-endothelial uptake. Whole-body and organ dosimetry for (18)F-FDG WBCs in doses of 225-250 MBq are comparable with reported results for conventional doses of (111)In oxine labelled leukocytes. Further studies of (18)F-FDG WBC as an agent for positron emission tomography imaging of inflammatory disease appear warranted.