Hasler William L, Coleski Radoslav, Chey William D, Koch Kenneth L, McCallum Richard W, Wo John M, Kuo Braden, Sitrin Michael D, Katz Leonard A, Hwang Judy, Semler John R, Parkman Henry P
Division of Gastroenterology, Univ. of Michigan Health System, Ann Arbor, MI 48109, USA.
Am J Physiol Gastrointest Liver Physiol. 2008 Jun;294(6):G1384-91. doi: 10.1152/ajpgi.00023.2008. Epub 2008 Apr 10.
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 (99m)Tc-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.
有证据表明，糖尿病性胃轻瘫和特发性胃轻瘫有着不同的发病机制。不同病因的胃轻瘫患者胃酸水平差异以及不同程度的胃潴留情况尚未得到研究。我们检验了以下假设：1）糖尿病性胃轻瘫与特发性胃轻瘫患者的胃pH值变化存在差异；2）异常的pH值变化与胃潴留的严重程度相关。64名健康对照者和44名胃轻瘫患者（20例糖尿病性胃轻瘫，24例特发性胃轻瘫）吞服无线传输胶囊，然后食用（99m）Tc - 硫胶体标记餐进行胃闪烁扫描。每隔5秒记录胶囊传输的胃pH值。糖尿病患者的基础pH值（3.64±0.41）高于对照者（1.90±0.18）和特发性胃轻瘫患者（2.41±0.42；P<0.05）。进食引起的初始pH值升高在糖尿病患者（4.98±0.32）中比特发性胃轻瘫患者（3.89±0.39；P = 0.03）更大，但与对照者（4.48±0.14）无差异。糖尿病患者胃胶囊排空前的pH值最低点（1.50±0.23）高于对照者（0.58±0.11；P = 0.003）。糖尿病患者（18.3±0.5%）和特发性胃轻瘫患者（19.4±0.5%）的4小时胃潴留情况相似，但高于对照者（2.2±0.5%；P<0.001）。与对照者相比，中度至重度胃潴留（4小时潴留>20%）患者的基础pH值（3.91±0.55）和最低点pH值（2.23±0.42）更高（P<0.05）。在亚组分析中，中度至重度胃轻瘫的糖尿病和特发性患者的pH参数均高于轻度胃轻瘫患者。总之，糖尿病性胃轻瘫患者胃酸分泌减少，在胃排空严重延迟的患者中这种影响更为明显。特发性胃轻瘫患者的胃酸情况接近正常，尽管排空严重延迟的患者与轻度延迟的患者相比胃酸分泌减少。因此，病因和胃潴留程度共同决定了胃轻瘫患者的胃酸水平。
