Bakkeren J, Monnens L, van Os C
Acta Paediatr Scand. 1981 Jan;70(1):43-6. doi: 10.1111/j.1651-2227.1981.tb07171.x.
Congenital chloride diarrhoea is assumed to be caused by a defect in the coupled NaCl influx mechanism in the ileum. As a similar coupled NaCl transport mechanism has been postulated in the gallbladder, the concentrating ability of the gallbladder was studied in a patient with congenital chloride diarrhoea. Bile acid concentrations were measured in the duodenal fluid before and after stimulation of gallbladder contraction by cholecystokinin. In the chloride-diarrhoea patient no increase in bile acid concentration was established after cholecystokinin injection, in contrast to a pronounced increase in three control children, suggesting that the absorption of salt and water by the gallbladder may be disturbed in the patient. The results support the postulated similarity of the NaCl transport mechanisms in the ileum and gallbladder. In congenital chloride diarrhoea one defect in a NaCl transport protein could explain the disturbances in electrolyte absorption.
先天性氯腹泻被认为是由回肠中耦合的氯化钠流入机制缺陷引起的。由于胆囊中也假定存在类似的耦合氯化钠转运机制，因此对一名先天性氯腹泻患者的胆囊浓缩能力进行了研究。通过胆囊收缩素刺激胆囊收缩前后，测量十二指肠液中的胆汁酸浓度。与三名对照儿童的显著增加相反，注射胆囊收缩素后，氯腹泻患者的胆汁酸浓度没有增加，这表明该患者胆囊对盐和水的吸收可能受到干扰。结果支持了回肠和胆囊中氯化钠转运机制假定的相似性。在先天性氯腹泻中，一种氯化钠转运蛋白的缺陷可以解释电解质吸收的紊乱。
