Malabsorption syndrome due to various causes is associated with antroduodenal hypomotility.

BACKGROUND: Patients with celiac disease who present with symptoms of gastrointestinal hypomotility have abnormal antroduodenal manometry. There are no data on antroduodenal manometry in malabsorption syndrome (MAS) due to causes other than celiac disease. METHODS: Fasting, post-prandial and post-octreotide antroduodenal motility parameters were compared in 18 untreated patients with MAS presenting with chronic diarrhea (tropical sprue 10, small bowel bacterial overgrowth 3, celiac disease 2, common variable immunodeficiency 1, AIDS with isosporidiasis and bacterial overgrowth 1, giardiasis 1) and 8 healthy subjects. RESULTS: Number of patients with MAS and controls having spontaneous migratory motor complexes (MMC) during fasting was comparable (11/18 vs 7/8; p=ns). Fasting contraction amplitude was weaker in MAS than in controls in the gastric antrum (median 42 [range 17-90] vs 80 [31-120] mmHg; p=0.001), proximal duodenum (50 [18-125] vs 72 [48-107]; p=0.013) and distal duodenum (45 [20-81] vs 76 [51-98]; p=0.001). In the fed state too, contraction amplitudes were weaker in patients with MAS in the antrum (32 [15-110] vs 76 [61-103] mmHg, p=0.002), proximal duodenum (57 [20-177] vs 73 [56-113]; p=0.07) and distal duodenum (45 [24-87] vs 75 [66-97]; p<0.0001). Patients with MAS had lower fasting and post-prandial antral and duodenal motility indices than healthy subjects. Intravenous octreotide induced MMC in all patients and controls. CONCLUSIONS: MAS due to various causes is associated with antroduodenal hypomotility typical of myopathic disorders.

Lower density of antral somatostatin-immunoreactive cells in the digestive form of chronic Chagas' disease

Patients with the digestive form of chronic Chagas' disease exhibit abnormally increased gastrin release, possibly caused by antral gastrin cell (G cell) hyperfunction. In order to identify the mechanisms underlying this abnormality, we used an immunohistochemical method to assess the population of antral somatostatin-producing cells (D cells) in chagasic patients, since somatostatin is known to be the main inhibitory factor of gastrin secretion. Samples (N = 11) of endoscopic antral biopsies taken from 16 Chagas' disease patients and 13 control subjects were studied. Antral D and G cell populations were determined by an immunohistochemical technique using highly specific antibodies against somatostatin and gastrin. There was no significant difference between Chagas' disease and control groups regarding G cell population (number of cells/mm reported as median (range): 70.0 (23.7-247.0) vs 98.1 (52.7-169.4), P>0.10). In contrast, the number of antral D cells in Chagas' disease patients was significantly lower than in controls (l6.4 (6.9-54.4) vs 59.3 (29.6-113.8), P<0.05). Chronic superficial gastritis and infection with Helicobacter pylori were more frequent in chagasic patients than in controls, but there was no demonstrable association between these factors and the reduction of the number of antral D cells. These data suggest that reduction in the number of antral somatostatin-producing cells, which should lead to reduced inhibition of gastrin cell activity, may play a role in the increased gastrin secretion observed in Chagas' disease patients.