Fine K D, Santa Ana C A, Fordtran J S
Department of Internal Medicine, Baylor University Medical Center, Dallas, TX 75246.
N Engl J Med. 1991 Apr 11;324(15):1012-7. doi: 10.1056/NEJM199104113241502.
There is no specific method of diagnosing magnesium-induced diarrhea. Therefore, the frequency and clinical importance of diarrhea caused by magnesium are unknown. The purposes of this study were to establish a method for diagnosing magnesium-induced diarrhea and to apply it to patients with chronic diarrhea.
We measured fecal output of soluble magnesium and fecal magnesium concentration in 19 normal subjects with formed stools (15 collection periods), with non-magnesium-induced diarrhea (36 collection periods), and with diarrhea induced by magnesium hydroxide alone (11 collection periods) or in combination with phenolphthalein (3 collection periods), and in 359 patients with chronic diarrhea.
The upper limits of fecal output of soluble magnesium and fecal magnesium concentration in normal subjects were 14.6 mmol per day and 45.2 mmol per liter, respectively. When normal subjects had diarrhea due to the ingestion of magnesium hydroxide alone or in combination with phenolphthalein, fecal magnesium output was always abnormally high. For each millimole increase in fecal magnesium output, fecal weight increased by approximately 7.3 g. The fecal magnesium concentration was very high when magnesium was the only cause of diarrhea but only moderately elevated when diarrhea was induced by magnesium hydroxide plus phenolphthalein. Biochemical and clinical evidence indicated that excessive ingestion of magnesium was an important cause of chronic diarrhea in 15 of the 359 patients with chronic diarrhea (4.2 percent), if not the only cause.
Quantitative fecal analysis for soluble magnesium is an accurate method of diagnosing magnesium-induced diarrhea. Some patients with chronic diarrhea ingest excessive amounts of magnesium (in antacids or food supplements), and physicians may fail to discover this before embarking on an expensive and invasive diagnostic evaluation.
目前尚无诊断镁所致腹泻的特异性方法。因此,镁引起腹泻的频率及临床重要性尚不清楚。本研究的目的是建立一种诊断镁所致腹泻的方法,并将其应用于慢性腹泻患者。
我们测量了19名大便成形的正常受试者(15个收集期)、非镁所致腹泻患者(36个收集期)、仅由氢氧化镁或与酚酞联合引起腹泻的患者(11个收集期)以及359例慢性腹泻患者的粪便可溶性镁排出量和粪便镁浓度。
正常受试者粪便可溶性镁排出量和粪便镁浓度的上限分别为每天14.6 mmol和每升45.2 mmol。当正常受试者因单独摄入氢氧化镁或与酚酞联合摄入而出现腹泻时,粪便镁排出量总是异常升高。粪便镁排出量每增加1 mmol,粪便重量增加约7.3 g。当镁是腹泻的唯一原因时,粪便镁浓度非常高,但当腹泻由氢氧化镁加酚酞引起时,粪便镁浓度仅中度升高。生化和临床证据表明,在359例慢性腹泻患者中,有15例(4.2%)过量摄入镁是慢性腹泻的一个重要原因,即便不是唯一原因。
对可溶性镁进行定量粪便分析是诊断镁所致腹泻的准确方法。一些慢性腹泻患者摄入了过量的镁(在抗酸剂或食品补充剂中),而医生在进行昂贵且有创的诊断评估之前可能未能发现这一点。