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Correction to Mehler, N Engl J Med 349(9):875-881 August 28, 2003.

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Volume 349:2363-2364 December 11, 2003 Number 24
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Bulimia Nervosa

 

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To the Editor: In Dr. Mehler's discussion of the physiological complications of bulimia nervosa (Aug. 28 issue),1 he emphasizes the diagnostic usefulness of urinary electrolyte measurements and concludes that low urinary potassium and sodium concentrations are compatible with vomiting. The amount of potassium in gastric secretions is actually trivial, and the mechanism of hypokalemia in such persons is urinary potassium loss, which occurs as high distal delivery of bicarbonate enhances potassium secretion in the cortical collecting duct.2,3,4 In addition, there is an obligatory loss of sodium with bicarbonate after each bout of vomiting. Therefore, the urinary hallmarks of active vomiting are an elevated potassium concentration, a low urinary chloride concentration, and depending on the degree of urinary bicarbonate, sodium loss. Only urinary electrolyte measurements performed at a time that is remote from the episode of vomiting and in the absence of distal bicarbonate delivery might show low urinary potassium and sodium concentrations.


Jordan J. Weinstein, M.D.
University of Toronto
Toronto, ON M5B 1W8, Canada
j.weinstein{at}utoronto.ca

References

  1. Mehler PS. Bulimia nervosa. N Engl J Med 2003;349:875-881. [Free Full Text]
  2. Kassirer JP, Schwartz WB. Correction of metabolic alkalosis in man without repair of potassium deficiency. Am J Med 1966;40:19-26. [CrossRef][Web of Science][Medline]
  3. Carlisle EJ, Donnelly SM, Ethier JH, et al. Modulation of the secretion of potassium by accompanying anions in humans. Kidney Int 1991;39:1206-1212. [Web of Science][Medline]
  4. Kamel KS, Ethier JH, Richardson RM, Bear RA, Halperin ML. Urine electrolytes and osmolality: when and how to use them. Am J Nephrol 1990;10:89-102. [Web of Science][Medline]

 
The author replies: Dr. Weinstein is concerned about the discussion of the role of urinary electrolytes in the diagnosis of bulimia. I agree with him that with vomiting, most of the potassium loss is in the urine as a result of metabolic alkalosis and the bicarbonate diuresis that ensues, resulting in loss of potassium as the accompanying cation. Rates of renal potassium secretion are further increased in the presence of an elevated aldosterone level secondary to volume contraction, causing worsening hypokalemia. My comment about the usefulness of finding a low urinary potassium level in a patient with bulimia was in reference to diarrheal states due to laxative abuse and to the differentiation of this mode of purging from vomiting, wherein the urinary potassium level is elevated. However, there is an error in Table 2 of the article: urinary levels of potassium are indeed increased with excessive vomiting, not decreased, as printed.

The key points of the paragraph to which Dr. Weinstein refers remain the same — namely, that hypokalemia is highly specific for the diagnosis of bulimia in otherwise healthy young women and that patients with strict nonpurging anorexia nervosa should not have metabolic disturbances.


Philip S. Mehler, M.D.
Denver Health and Hospitals
Denver, CO 80204
pmehler{at}dhha.org


 

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