期刊文献+

低钾性周期性麻痹临床特点分析 被引量:16

Clinical features of hypokalemic periodic paralysis
在线阅读 下载PDF
导出
摘要 目的:探讨低钾性周期性麻痹的临床特点,比较原发性低钾周期性麻痹与甲状腺毒症继发周期性麻痹两组患者的异同点。方法:北京大学第一医院1996年12月至2008年12月住院治疗的低钾性周期性麻痹患者44例,回顾性分析其临床资料。结果:原发组和甲状腺毒症继发组各22例,两组患者共同的特点:(1)均好发于青壮年男性;(2)主要临床表现均为肢体活动障碍和乏力,大部分病例以反复多次发作为主;(3)部分病例(40.9%~68.2%)发病有明显诱因,诱因以饱餐、喝甜饮料和剧烈运动最常见;(4)发病时,两组患者血钾水平均明显低于正常水平;(5)原发组与甲状腺毒症继发组分别有20%和25%的患者肌酸激酶明显升高,补钾治疗后较快恢复正常,乳酸脱氢酶及α羟基丁酸脱氢酶均正常;(6)补钾剂量与发病时血钾水平无相关性。两组患者的不同点主要表现为:(1)甲状腺毒症继发组患者有高代谢症状,甲状腺功能提示T3、T4升高和促甲状腺激素(TSH)降低,原发组患者无此类症状,其甲状腺功能正常;(2)甲状腺毒症继发组血钾水平显著低于原发组[(2.25±0.67)vs(2.78±0.49)mmol/L,P=0.007];(3)甲状腺毒症继发周期性麻痹较原发性低钾性周期性麻痹在补钾治疗过程中更容易出现反跳性高钾血症。结论:低钾性周期性麻痹有其临床特点,早期诊断及时补钾治疗预后较好。补钾时不能仅根据发病时血钾水平决定补钾剂量,应密切监测血钾水平。甲状腺毒症继发周期性麻痹在补钾治疗过程中更容易出现反跳性高钾血症,在补钾治疗时应当密切监测血钾,并积极根治甲状腺毒症。 Objective:To explore the clinical features of hypokalemic periodic paralysis,and compare clinical features of primary group with those of thyrotoxicosis secondary group.Methods: Clinical data of 44 patients with hypokalemic periodic paralysis in Peking University First Hospital from 1996 December to 2008 December were retrospectively analyzed.Results: There were 22 patients in primary group,and 22 in thyrotoxicosis group.Identical clinical features of both the groups:(1)It had a predilection in young men.(2)Main symptoms were limb movement disorder and fatigue,and paralysis recurrent attacked in most patients.(3) 40.9% to 68.2% patients had obvious incentives,and the common ones were a heavy meal,sweet drinks,or strenuous exercise.(4) Serum potassium levels of the two groups were obviously lower than the normal range.(5)In 20% patients of primary group and 25% patients of thyrotoxicosis secondary group,CK levels were higher than normal,while LDH and HBDH levels were normal.(6)The doses of potassium replishment were not correlated to serum potassium levels at the onset.Diffe-rent clinical features of the two groups:(1) Patients of thyrotoxicosis group had hypermetabolism symptoms and thyroid dysfunction.Patients of primary group had no hypermetabolism symptoms,and all of them were euthyroid.(2)Serum potassium levels of thyrotoxicosis secondary group were lower than those of primary group significantly [(2.25±0.67) vs(2.78±0.49) mmol/L,P=0.007].(3) Hyperkalemia is easier than primary group to rebound in thyrotoxicosis secondary group,after replenishment of potassium.Conclusion: Hypokalemic periodic paralysis has its clinical features,and patients with early diagnosis and replenishment of potassium in time have good prognosis.The doses of potassium replenishment are not determined by serum potassium levels at the onset.Hyperkalemia is easier to rebound in thyrotoxicosis secondary group after replenishment of potassium,serum potassium levels should be monitored closely,and hyperthyrosis radically cured.
出处 《北京大学学报(医学版)》 CAS CSCD 北大核心 2009年第6期678-681,共4页 Journal of Peking University:Health Sciences
关键词 麻痹 家族周期性 低钾血症 甲状腺毒症 Paralysis familial Periodic Hypokalemia Thyrotoxicosis
  • 相关文献

参考文献7

  • 1Kung AW. Clinical review: Thyrotoxic periodic paralysis: A diagnostic challenge[ J ]. J Clin Endocrinol Metab, 2006, 91 (7) : 2490 - 2495.
  • 2Ko GT, Chow CC, Yeung VT, et al. Thyrotoxic periodic paralysis in a Chinese population[ J]. Q J Med, 1996, 89(6) : 463 -468.
  • 3沈宏锐,胡静,赵哲,李娜,袁军辉,邴琪.周期性瘫痪的临床与病理学特点[J].临床神经病学杂志,2009,22(4):265-267. 被引量:4
  • 4Lu KC, Hsu YJ, Chiu JS, et al. Effects of potassium supplementation on the recovery of thyrotoxic periodic paralysis [ J ].Am J Emerg Med, 2004, 22 (7) : 544 - 547.
  • 5Atienza Morales MP, Jimenez Garcia JA, Beato Perez JL, et al. Amiodarone as cause of periodic thyrotoxic hypokalaemic paralysis [J]. Rev Clin Esp, 2006, 206(11): 598 -599.
  • 6Chou HK, Tsao YT, Lin SH. An unusual cause of thyrotoxic periodic paralysis : triiodothyronine-containing weight reducing agents [J]. Am J Med Sci, 2009, 337(1): 71 -73.
  • 7Lin SH, Lin YF. Propranolol rapidly reverses paralysis, hypokalemia, and hypophosphatemia in thyrotoxie periodic paralysis [ J ]. Am J Kidney Dis, 2001, 37(3) : 620 -623.

二级参考文献16

  • 1沈定国.周期性麻痹诊断治疗中的几个问题[J].中华神经科杂志,2004,37(3):193-195. 被引量:48
  • 2Ahlawat SK, Sachdev A. Hypokalemic paralysis [J]. Postgrad Med J,1999, 75: 193.
  • 3Chesson AL Jr, Schochet SS Jr, Peters BH. Biphasic periodic paralysis [J]. Arch Neurol,1979,36: 700.
  • 4Lehmann-Horn F, Jurkat-Rott K, Rudel R. Periodic paralysis: understanding channelopathies [ J]. Curr Neurol Neurosci Rep, 2002, 2: 61.
  • 5Ptacek LJ, Tawil R, Griggs RC, et al. Dilhydropyridine receptor mutations cause hypokalemic periodic paralysis [ J ]. Cell, 1994, 77 : 863.
  • 6Wang Q, Liu M, Xu C, et al. Novel CACNA1S mutation causes autosomal dominant hypokalemic periodic paralysis in a Chinese family [J]. J Mol Med, 2005, 83: 203.
  • 7Bulman DE, Seoggan KA, van Oene MD, et al. A novel sodium channel mutation in a family with hypokalemic periodic paralysis [J]. Neurology, 1999, 53: 1932.
  • 8Jurkat-Rott K, Mitrovic N, Hang C, et al. Voltage-sensor sodium channel mutation cause hypokalemic periodic paralysis type 2 enhanced inactivation and reduced current [ J ]. Proc Natl Acad Sci, 2000, 97 : 9549.
  • 9Sugiura Y, Makita N, Li L, et al. Cold induces shifts of voltage dependence in mutant SCN4A, causing hypokalemic periodic paralysis [J]. Neurology, 2003, 61 : 914.
  • 10Kung AW, Lau KS, Fong GC, et al. Association of novel single nucleotide polymorphisms in the calcium channel alpha 1 subunit gene (Car1. 1 ) and thyrotoxic periodic paralysis [ J ]. J Clin Endocrinol Metab, 2004, 89 : 1340.

共引文献3

同被引文献77

引证文献16

二级引证文献25

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部