Cherney DZ, Davids MR, Halperin ML (2002) Acute hyponatraemia and 'ecstasy': insights from a quantitative and integrative analysis. Qjm 95: 475-483.
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The authors examine possible causes of ecstasy-related hyponatremia through the device an Òimaginary consultationÓ with a physician who had published relevant research in the 1930s. The case of a woman with hyponatremia after ecstasy use is presented, and the ÒconsultationÓ is then described. Various proposed explanations for hyponatremia after ecstasy use are offered as questions, and answers are often provided in the form of quantitative analyses of water volume, sodium deposition, and factors relevant to water versus sodium dissipation in humans. The authors propose that the usual explanation for ecstasy-associated hyponatremia, that it is the result of drinking excessive amounts of water in combination with AVP release after MDMA, is insufficient. The authors support their arguments through calculations of the amount of water needed to significantly alter sodium levels, indicating that these are far too high to be reached through excessive water consumption, and by noting that previous studies in humans suggests that drinking large amounts of water is aversive. The authors present an alternative explanation, postulating that MDMA dilates the GI tract so that more water may be consumed and retained than would usually occur. This causes sodium within the body to diffuse into the lumen, and MDMA-induced vasoconstriction reduces hemodynamic effects. Greater susceptibility to hyponatremia in women is explained as the result of women having lower muscle mass, and less water within muscle cells, than men, but no mention is made of possible gender differences in CNS effects of hyponatremia. In examining humansÕ capacity to drink large amounts of water and relating these to hyponatremia after ecstasy use, the authors may not be considering the effects that ecstasy or other drugs might have on awareness of bodily discomfort. It is also uncertain as to whether MDMA can dilate the intestinal lumen. This paper explores issues relating to hyponatremia after ecstasy use in an unusual manner. Even if readers disagree with the authorsÕ conclusions concerning the causes of hyponatremia in ecstasy users, the questions posed in this paper are pertinent and clearly stated, and might serve as a springboard for further discussion of ecstasy-related hyponatremia.

 
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