These cases illustrate that patients with ileostomies can develop sudden acute electrolyte and acid-base disorders, usually in association with an increase in ileostomy output. The specific disorder that develops appears to depend on the nature of the ileostomy losses, but in all cases was sustained by the acute decrease in glomerular filtration rate that occurred in association with extra cellular fluid volume depletion. The 2 patients with metabolic alkalosis are of particular interest in this regard. The association of metabolic alkalosis with high-volume ileostomy drainage has been reported previously in only 2 patients. One was an infant with cystic fibrosis who rapidly developed severe metabolic alkalosis after placement of an ileostomy. The investigators noted a link between metabolic alkalosis and cystic fibrosis, but did not speculate on the cause in their patient. In that patient and the 2 patients reported here, ileal drainage was characterized by abnormally high chloride concentrations and high volume losses, likely accounting for the nature of the acid-base disorder . In 1 prior report in an adult, metabolic alkalosis(serum bicarbonate level. 32 mmol/L.) also developed rapidly after ileostomy placement, with recorded ileostomy volumes of 1.5-2L/d.

We presume the alkalosis in all these patients was caused by the selective loss of chloride in their ileostomy drainage. Selective chloride depletion is the most common cause of metabolic alkalosis. 12 The cause of the excessively high chloride concentrations in the ileal drainage in these patients is unclear. The patient with cysticfibrosis makes it unlikely that increased secretion of chloride into the gut lumen is responsible because this patient lacks cystic fibrosis transmembrane

regulator (CFTR), the major gut chloride secretory ion channel. 13 More likely, the chloride loss is caused by impaired chloride absorption as a result of rapid transit through the gut. It is possible that a high rate of gastrin chloride secretion (stimulated by high gastrin levels) could also be a contributing factor. We have no information about gastric acid secretion or serum gastrin levels in these patients, but it is note worthy that in both patients, proton pump inhibition was ineffective in reducing ileostomy output. Patient 2 had only 10 cm of ileum remaining, and it is likely that she was in a precarious balance with regard to ileal absorption at all times, so that any cause of increased ileal volume drainage tipped her into alkalosis and volume depletion. On the other hand, patient 1 had virtually all his ileum. He had presumed pancreaticin sufficiency, but this should not have affected his ability to absorb chloride from the smallbowel.

                                                            [J.AJKD,2008;(10)1053]

参考译文

这些病例说明做过回肠造痿术的患者，会迅速发展为急性水电解质紊乱和酸碱平衡失调，同时伴随回肠引流液增加。水电解质紊乱和酸碱平衡失调的程度，取决于切除部分的回肠的生理特性，但几乎在所有的病例中都持续存在伴有细胞外液量减少而发生的肾小球滤过率降低。2例伴有代谢性碱中毒的患者，与这个特别相关。之前仅报道过2例患者代谢性碱中毒与回肠造口术后大量引流的相关性。其中1例是有回肠纤维粪性病的婴儿，在进行回肠造口术后迅速发生代谢性碱中毒。研究者认为回肠纤维囊性病与代谢性碱中毒存在线性关系,但是没有推测出它的原因。在上面提到的病例和本文的2例病例中,回肠引流物不但量很大，而且有异常高的氯化物，也许可以说明的酸碱平衡失调的本质。在此前报道的1例成人回肠造口术后,日回肠引流量1.5~2L.并迅速发生代谢性碱中毒(血清碳酸氢盐32mmol/L)。

我们推测所有患者的代谢性碱中毒,都是由于回肠造口引流选择性的丢失氯化物。选择性氯化物丢失是最为常见的代谢性碱中毒原因。目前尚不清楚是什么原因导致回肠引流液中大量高氯化合物丢失。患者不大可能大量分泌氯化物到肠道中,因为这些患者缺乏纤维囊性细胞膜调节因子,而这些因子是肠道氯离子分泌的主要离子通道。氯化物的大量丢失更有可能是氯离子快速通过肠道时的吸收障碍。另外有一种可能是氯化物的大量分泌(由于高水平胃泌素刺激)。我们虽然没有胃酸和血清胃泌素的数据,这也是没有价值的,因为我们使用质子泵抑制药并没有减少回肠引流物。病例2只保留了10cm长的回肠,这极有可能是她在任何时候都不能保持回肠吸收的平衡，以至于大量回肠液丢失，导致代谢性碱中毒和血容量下降。另一方面，病例1事实上是保留了他的全部回肠，我们推测他的大量分泌胰岛素，但这不足以促使从小肠吸收氯化物。

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