Siegel Arthur J, Verbalis Joseph G, Clement Stephen, Mendelson Jack H, Mello Nancy K, Adner Marvin, Shirey Terry, Glowacki Julie, Lee-Lewandrowski Elizabeth, Lewandrowski Kent B
Department of Medicine, McLean Hospital, Belmont, Mass, USA.
Am J Med. 2007 May;120(5):461.e11-7. doi: 10.1016/j.amjmed.2006.10.027.
Exercise-associated hyponatremia (EAH), as defined by a blood sodium concentration [Na+] less than 135 mmol/L, may lead to hypotonic encephalopathy with fatal cerebral edema. Understanding the pathogenetic role of antidiuresis may lead to improved strategies for prevention and treatment.
Normonatremic marathon runners were tested pre- and post-race for creatine kinase, interleukin-6, cortisol, prolactin, and arginine vasopressin. Similar testing also was carried out in runners with encephalopathy caused by EAH, including 2 cases with fatal cerebral edema.
Normonatremic runners (n = 33; 2001) with a mean 3% decrease in body weight showed a 40-fold increase in interleukin-6 (66.6 +/- 11.9 pg/mL from 1.6 +/- 0.5 pg/mL, P = .001), which was significantly correlated with increases in creatine kinase (r = 0.88, P = <.0001), cortisol (r = 0.70, P = .0003), and prolactin (r = 0.67, P <.007), but not arginine vasopressin (r = 0.44, P = .07). Collapsed runners with EAH (n = 22; 2004) showed a mean blood urea nitrogen less than 15 mg/dL with measurable plasma levels of arginine vasopressin (>0.5 pg/mL) in 43% of cases. Two marathon runners with fatal cerebral edema additionally showed less than maximally dilute urines (>100 mmol/kg/H2O) and urine [Na+] greater than 25 mEq/L.
Cases of EAH fulfill the essential diagnostic criteria for the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Runners with hypotonic encephalopathy at subsequent races were treated with intravenous hypertonic (3%) saline on the basis of this paradigm, which resulted in rapid clinical improvement without adverse effects. Release of muscle-derived interleukin-6 may play a role in the nonosmotic secretion of arginine vasopressin, thereby linking rhabdomyolysis to the pathogenesis of EAH.
运动相关性低钠血症（EAH）定义为血钠浓度[Na⁺]低于135mmol/L，可导致低渗性脑病及致命性脑水肿。了解抗利尿的发病机制可能有助于改进预防和治疗策略。
对血钠正常的马拉松运动员在赛前和赛后进行肌酸激酶、白细胞介素-6、皮质醇、催乳素和精氨酸加压素检测。对因EAH导致脑病的运动员也进行了类似检测，包括2例致命性脑水肿患者。
血钠正常的运动员（n = 33；2001年）体重平均下降3%，白细胞介素-6升高40倍（从1.6±0.5pg/mL升至66.6±11.9pg/mL，P = 0.001），与肌酸激酶升高（r = 0.88，P <0.0001）、皮质醇升高（r = 0.70，P = 0.0003）和催乳素升高（r = 0.67，P <0.007）显著相关，但与精氨酸加压素无关（r = 0.44，P = 0.07）。EAH导致虚脱的运动员（n = 22；得04年）血尿素氮平均低于15mg/dL，43%的病例血浆精氨酸加压素水平可测（>0.5pg/mL）。2例致命性脑水肿的马拉松运动员尿液最大稀释度降低（>100mmol/kg/H₂O）且尿[Na⁺]大于25mEq/L。
EAH病例符合抗利尿激素分泌不当综合征（SIADH）的基本诊断标准。基于此模式，后续比赛中出现低渗性脑病的运动员接受静脉输注高渗（3%）盐水治疗，临床症状迅速改善且无不良反应。肌肉源性白细胞介素-6的释放可能在精氨酸加压素的非渗透性分泌中起作用，从而将横纹肌溶解与EAH的发病机制联系起来。
