Maton P N, Selden A C, Fitzpatrick M L, Chadwick V S
Gastroenterology. 1985 Feb;88(2):391-6. doi: 10.1016/0016-5085(85)90497-4.
Normal volunteers (n = 6), patients with untreated celiac disease and subtotal villous atrophy (n = 6), patients with nonresponsive celiac disease (n = 2), and patients with celiac disease on a gluten-free diet with a virtually normal biopsy specimen (n = 6) drank a liquid fat meal after an overnight fast. Gallbladder emptying was monitored by using 99mTc-eHIDA, and blood samples were taken for cholecystokinin estimation by radioimmunoassay after high-performance liquid chromatography. The half-times of gallbladder emptying were 20.4 +/- 2.9 min (mean +/- SEM) for normals and 22.1 +/- 2.8 min in treated patients with celiac disease (NS). In patients with untreated celiac disease half-times were 154.3 +/- 10.3 min (p less than 0.02 vs. normals and treated patients with celiac disease), and in 2 nonresponsive patients, half-times were 40.7 and 37.3 min. Integrated plasma cholecystokinin responses were 473 +/- 87 and 436 +/- 137 pmol X L-1 X 30 min-1 in normals and treated patients with celiac disease (NS). In untreated patients with celiac disease values were 16 +/- 9 pmol X L-1 X 30 min-1 (p less than 0.001 vs. normals and treated patients with celiac disease), and in nonresponsive patients values were 442 and 322 pmol X L-1 X 30 min-1. In 2 patients studied before and during gluten-free diet half-times for gallbladder emptying changed from 168.9 and 302.4 min to 20.1 and 23.4 min, and cholecystokinin responses changed from 0 and 45 to 623 and 298 pmol X L-1 X 30 min-1. Cholecystokinin immunoreactivity cochromatographing with cholecystokinin-octapeptide was responsible for 50%-60% of circulating cholecystokinin in normals and in treated patients but the small amount of cholecystokinin that was released in untreated patients with celiac disease cochromatographed with cholecystokinin-33/39. We conclude that there is a reversible defect of gallbladder emptying and cholecystokinin release in celiac disease.
正常志愿者(n = 6)、未经治疗的乳糜泻合并绒毛萎缩患者(n = 6)、难治性乳糜泻患者(n = 2)以及采用无麸质饮食且活检标本基本正常的乳糜泻患者(n = 6)在禁食过夜后饮用了液体脂肪餐。通过使用99mTc - eHIDA监测胆囊排空情况,并在高效液相色谱后通过放射免疫分析法采集血样以测定胆囊收缩素。正常组胆囊排空半衰期为20.4±2.9分钟(均值±标准误),接受治疗的乳糜泻患者为22.1±2.8分钟(无显著差异)。未经治疗的乳糜泻患者半衰期为154.3±10.3分钟(与正常组及接受治疗的乳糜泻患者相比,p<0.02),2例难治性患者的半衰期分别为40.7分钟和37.3分钟。正常组和接受治疗的乳糜泻患者血浆胆囊收缩素综合反应分别为473±87和436±137 pmol·L-1·30分钟-1(无显著差异)。未经治疗的乳糜泻患者的值为16±9 pmol·L-1·30分钟-1(与正常组及接受治疗的乳糜泻患者相比,p<0.001),难治性患者的值分别为442和322 pmol·L-1·30分钟-1。在2例接受无麸质饮食前后研究的患者中,胆囊排空半衰期从168.9分钟和302.4分钟变为20.1分钟和23.4分钟,胆囊收缩素反应从0和45变为623和298 pmol·L-1·30分钟-1。与胆囊收缩素八肽共色谱的胆囊收缩素免疫反应性在正常组和接受治疗的患者中占循环胆囊收缩素的50% - 60%,但在未经治疗的乳糜泻患者中释放的少量胆囊收缩素与胆囊收缩素 - 33/39共色谱。我们得出结论,乳糜泻存在胆囊排空和胆囊收缩素释放的可逆性缺陷。