No abstract

Summary 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.

The 13C-octanoic acid breath test for gastric emptying of solids is as reproducible as scintigraphy. A subset of 11 sampling times provides sufficient information to characterize the whole breath-test curve, but the sampling period should be extended to 6 h after dosing.

No abstract

Summary.Anagrelide, an inhibitor of platelet aggregation, decreases the number of platelets in normal subjects and in patients with myeloproliferative disorders. We describe studies aimed at discovering the general mechanism(s) by which anagrelide acts. We examined three hypotheses:(1) anagrelide shortens platelet survival, (2) anagrelide inhibits the proliferation of megakaryocytic-committed progenitor cells (CFU-M), and (3) anagrelide inhibits maturation of megakaryocytes. We observed that anagrelide did not shorten platelet survival. Proliferation of CFU-M in vivo was not affected by anagrelide, although high concentrations of anagrelide inhibited CFU-M in vitro. In-vivo and in-vitro anagrelide altered the maturation of megakaryocytes, causing a decrease in their size and changing other morphometric features. We conclude that anagrelide decreases the number of platelets primarily by interfering with the maturation of megakaryocytes.