Manoukian M A, Foote J A, Crapo L M
Department of Medicine, Santa Clara Valley Medical Center, San Jose, Calif 95128, USA.
Arch Intern Med. 1999 Mar 22;159(6):601-6. doi: 10.1001/archinte.159.6.601.
Hypokalemia is a well-known, consistent finding in thyrotoxic periodic paralysis (TPP). It is less well known that hypophosphatemia and mild hypomagnesemia are often present in TPP and that rebound hyperkalemia can occur as a result of potassium therapy.
To report the prevalence of these electrolyte abnormalities in 24 episodes of TPP in 19 patients admitted to a single university-affiliated public hospital during a 15-year period.
The medical records of all patients admitted to the Santa Clara Valley Medical Center in San Jose, Calif, between August 1, 1982, and June 1, 1997, with any type of hypokalemic periodic paralysis were reviewed. In patients with TPP, serum potassium, phosphorus, and magnesium levels were evaluated during and after episodes of paralysis. The administered dose of potassium chloride, recovery time from hypokalemia, and prevalence of rebound hyperkalemia after recovery were also ascertained. Data are presented as mean +/- SD.
Hypokalemia was present in all 24 initial episodes of TPP, with serum potassium levels ranging from 1.1 to 3.4 mmol/L (mean, 1.9+/-0.5 mmol/L). After recovery from hypokalemia, the maximum serum potassium level significantly increased, ranging from 4.0 to 6.6 mmol/L (mean, 4.9+/-0.5 mmol/L; P<.001). In 10 (42%) of 24 episodes, rebound hyperkalemia (serum potassium level >5.0 mmol/L) was present. Recovery time did not correlate with the potassium chloride dose administered (r = 0.17). Initial serum phosphorus levels ranged from 0.36 to 0.97 mmol/L (mean, 0.61+/-0.23 mmol/L) (1.1-3.0 mg/dL [mean, 1.9+/-0.7 mg/dL]), with hypophosphatemia present in 12 (80%) of 15 episodes. Serum phosphorus levels significantly increased (P<.01), to 1.26 to 1.74 mmol/L (mean, 1.48+/-0.16 mmol/L) (3.9-5.4 mg/dL [mean, 4.6+/-0.5 mg/dL]), with or without phosphorus replacement therapy. A slight increase in serum magnesium levels after paralysis resolved was observed in all patients (P<.07). No further episodes of paralysis occurred in any patients after they became euthyroid.
Hypokalemia, hypophosphatemia, and mild hypomagnesemia are characteristic features of TPP. Hypokalemia occurred in 100% and hypophosphatemia in 80% of the episodes in our study. Rebound hyperkalemia is a potential hazard of potassium administration and occurred in 42% of 24 episodes.
低钾血症是甲状腺毒症性周期性瘫痪（TPP）中一个广为人知的常见表现。但鲜为人知的是，TPP患者常伴有低磷血症和轻度低镁血症，并且补钾治疗可能导致反弹性高钾血症。
报告一所大学附属医院在15年期间收治的19例患者24次TPP发作时这些电解质异常的发生率。
回顾了1982年8月1日至1997年6月1日期间加利福尼亚州圣何塞市圣克拉拉谷医疗中心收治的所有低钾性周期性瘫痪患者的病历。对于TPP患者，在瘫痪发作期间及之后评估血清钾、磷和镁水平。还确定了氯化钾的给药剂量、低钾血症的恢复时间以及恢复后反弹性高钾血症的发生率。数据以均值±标准差表示。
所有24次TPP初始发作均存在低钾血症，血清钾水平为1.1至3.4 mmol/L（均值为1.9±0.5 mmol/L）。低钾血症恢复后，血清钾最高水平显著升高，范围为4.0至6.6 mmol/L（均值为4.9±0.5 mmol/L；P<0.001）。24次发作中有10次（42%）出现反弹性高钾血症（血清钾水平>5.0 mmol/L）。恢复时间与氯化钾给药剂量无关（r = 0.17）。初始血清磷水平为0.36至0.97 mmol/L（均值为0.61±0.23 mmol/L）（1.1 - 3.0 mg/dL[均值为1.9±0.7 mg/dL]），15次发作中有12次（80%）存在低磷血症。无论是否进行补磷治疗，血清磷水平均显著升高（P<0.01），升至1.26至1.74 mmol/L（均值为1.48±0.16 mmol/L）（3.9 - 5.4 mg/dL[均值为4.6±0.5 mg/dL]）。所有患者瘫痪缓解后血清镁水平均有轻微升高（P<0.07）。所有患者甲状腺功能恢复正常后均未再出现瘫痪发作。
低钾血症、低磷血症和轻度低镁血症是TPP的特征性表现。在我们的研究中，低钾血症在所有发作中发生率为100%，低磷血症为80%。反弹性高钾血症是补钾治疗的潜在风险，24次发作中有42%出现。
