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This Article Full Text Full Text (PDF) All Versions of this Article: 294/6/G1384    most recent 00023.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Hasler, W. L. Articles by Parkman, H. P. PubMed PubMed Citation Articles by Hasler, W. L. Articles by Parkman, H. P.

NEUROREGULATION AND MOTILITY

Differences in intragastric pH in diabetic vs. idiopathic gastroparesis: relation to degree of gastric retention

¹Division of Gastroenterology, University of Michigan Health System, Ann Arbor, Michigan; ²Wake Forest Baptist Medical Center, Winston-Salem, North Carolina; ³University of Kansas Medical Center, Kansas City, Kansas; ⁴University of Louisville Medical Center, Louisville, Kentucky; ⁵Massachusetts General Hospital, Boston, Massachusetts; ⁶Buffalo Veterans Administration Hospital, Buffalo; ⁷University of Buffalo School of Medicine, Buffalo; ⁸SmartPill Corporation, Buffalo, New York; and ⁹Temple University Medical Center, Philadelphia, Pennsylvania

Submitted 16 January 2008 ; accepted in final form 10 April 2008

Evidence suggests that distinct mechanisms underlie diabetic and idiopathic gastroparesis. Differences in gastric acid in gastroparesis of different etiologies and varying degrees of gastric stasis are uninvestigated. We tested the hypotheses that 1) gastric pH profiles show differential alteration in diabetic vs. idiopathic gastroparesis and 2) abnormal pH profiles relate to the severity of gastric stasis. Sixty-four healthy control subjects and 44 gastroparesis patients (20 diabetic, 24 idiopathic) swallowed wireless transmitting capsules and then consumed ^99mTc-sulfur colloid-labeled meals for gastric scintigraphy. Gastric pH from the capsule was recorded every 5 s. Basal pH was higher in diabetic (3.64 ± 0.41) vs. control subjects (1.90 ± 0.18) and idiopathic subjects (2.41 ± 0.42; P < 0.05). Meals evoked initial pH increases that were greater in diabetic (4.98 ± 0.32) than idiopathic patients (3.89 ± 0.39; P = 0.03) but not control subjects (4.48 ± 0.14). pH nadirs prior to gastric capsule evacuation were higher in diabetic patients (1.50 ± 0.23) than control subjects (0.58 ± 0.11; P = 0.003). Four-hour gastric retention was similar in diabetic (18.3 ± 0.5%) and idiopathic (19.4 ± 0.5%) patients but higher than control subjects (2.2 ± 0.5%; P < 0.001). Compared with control subjects, those with moderate-severe stasis (>20% retention at 4 h) had higher basal (3.91 ± 0.55) and nadir pH (2.23 ± 0.42) values (P < 0.05). In subgroup analyses, both diabetic and idiopathic patients with moderate-severe gastroparesis exhibited increased pH parameters vs. those with mild gastroparesis. In conclusion, diabetic patients with gastroparesis exhibit reduced gastric acid, an effect more pronounced in those with severely delayed gastric emptying. Idiopathic gastroparetic subjects exhibit nearly normal acid profiles, although those with severely delayed emptying show reduced acid vs. those with mild delays. Thus both etiology and degree of gastric stasis determine gastric acidity in gastroparesis.

gastric emptying; diabetes mellitus; gastric acid