低钾性周期性麻痹41例临床分析

目的提高对低钾性周期性麻痹临床表现的认识,提出治疗及预防措施以及护理建议。方法分析41例周期性麻痹病例的临床表现及辅助检查结果。结果男29例,女12例,年龄17～55岁,平均32.1岁,其中40岁以下30例,占73.2%。发病季节为5～9月份者32例,占78.0%。均表现为不同程度的骨骼肌驰缓性瘫痪,合并感觉障碍8例,伴有甲状腺功能亢进者9例（22.0%）。16例肌酶学指标均有不同程度的升高,有低钾性心电图改变者35例,占85.4%。结论低钾性周期性麻痹的发病以青壮年男性为主。多发于夏秋季节,可有多种诱因存在。急性肌无力为其临床特点,低钾血症、特征性心电图改变有利于确立诊断。部分不典型病例合并有甲亢,血清肌酶升高,以及感觉异常,临床注意与急性脊髓病变,以及格林巴利综合征、肌炎等相鉴别。治疗上主要是快速补钾,以口服为主。注意适当的心理疏导。     

伴肌酸磷酸激酶增高的低钾性周期性麻痹26例分析

目的：探讨低钾型周期性麻痹的患者血清肌酸激酶、电解质等各项检查的结果,并分析它们之间的关系。方法：对26例低钾型周期性麻痹患者的临床表现及血清肌酸激酶、电解质等各项检查的结果进行回顾性分析。结果：26例低血钾麻痹患者均伴有肌酶学改变,为血清肌酸磷酸激酶（CPK）及同工酶的升高,补钾后,临床症状完全改变,CPK基本恢复正常。结论：血清肌酸激酶的增高在一定程度上反映了骨骼肌的的受损程度,是低钾型周期性麻痹重要临床特征之一。     

低钾型周期性瘫痪46例血清肌酶检测观察

目的:探讨低钾型周期性瘫痪(hypokalemic periodic paralysis,HOPP)患者血清肌酶改变的临床意义.方法:复习46例HOPP患者临床资料,观察其血清肌酶改变情况.结果:46例中肌酸激酶升高28例,天冬氨酸转氨酶升高20例,肌酸肌酶同工酶升高14例,且升高程度与血钾降低程度呈负相关.结论:血清肌酶升高可作为HOPP的观察指标之一,血钾与血清肌酶的检测有助于HOPP的诊断.     

甲状腺功能亢进性低钾麻痹补钾致高钾血症10例分析

甲状腺功能亢进(甲亢)性周期性麻痹临床可分为低钾型、高钾型和正常血钾型,其中以低钾型麻痹最为常见。低钾型麻痹发作时,经补钾治疗纠正低钾血症后,肌肉麻痹可终止。有报道甲亢低钾型周期性麻痹经补钾治疗导致高钾血症的发生[1],我们在临床工作中也有类似发现。本文将补钾治疗     

低钾型周期性麻痹36例临床分析

目的:探讨低钾型周期性麻痹的临床特点,进一步认识低钾型周期性麻痹的诊断及治疗。方法:对36例低钾型周期性麻痹患者的临床表现及辅助检查结果进行回顾性分析。结果:男女比例8∶1,青年男性为高发,散发多见。36例患者中继发于甲亢者15例。四肢腱反射变化显著,36例患者中反射消失6例、减退18例、正常8例、活跃4例。有心电图资料者36例,有典型心电图低血钾改变者30例。有血清CPK资料者18例,升高者6例。结论:低钾型周期性麻痹的正确诊断是关键,治疗及时与否与预后密切相关。     

低血钾麻痹血清肌酶学变化分析

目的探讨低血钾麻痹患者血清肌酶的变化及临床意义。方法用速率法测定36例低血钾麻痹患者的血清肌酶,观察血清肌酶含量与临床的关系。结果低血钾麻痹患者各项肌酶含量与对照组比较均有不同程度的升高,其中肌酸磷酸激酶(CK)、天门冬氨酸转氨酶(AST)、乳酸脱氢酶(LDH)升高的患者分别为27例(75%)、21(58.3%)、11例(30.6%)。血钾越低肌酶升高越显著,且与临床表现越明显。结论血清肌酶增高是低血钾麻痹患者的重要特征之一,并且可以作为判断病情及估计预后的指标。     

甲亢伴周期性麻痹发作的临床特点与代谢特征

目的　探讨甲亢伴周期性麻痹的临床与代谢特点。方法　分析 38例甲亢并周期性麻痹发作的临床特征 ,同时检测患者的血钾、血糖、血磷、血镁、醛固酮及胰岛素水平。结果　本病多发于青壮年男性 ,部分患者甲亢的临床症状与体征基本缺如 ,瘫痪下肢比上肢重 ,多有瘫痪肢体肌肉胀痛感 ,瘫痪肢体腱反射亢进或正常 ,出现低钾血症、低磷酸盐血症、低镁血症、血浆醛固酮升高、血糖及胰岛素水平升高。结论　周期性麻痹继发于甲亢的高比例应引起重视 ,治疗的关键在于补钾和甲亢的控制     

周期性麻痹发作期患者一氧化氮表达的临床意义

目的了解一氧化氮(NO)对周期性麻痹患者发病的影响.方法低钾型周期性麻痹患者,在弛缓性瘫痪发作期及肌力恢复后,同时检测血钾、NO、一氧化氮合酶(NOS).观察不同病期患者血NO、NOS的变化与疾病的关系.结果42例患者在瘫痪发作期血NO、NOS均明显降低;经治疗后,NO、NOS随血钾和肌力的恢复而趋于正常.瘫痪期NO的变化与血钾降低的程度呈正相关(r=0.3511,P＜0.05);与肌无力程度无明显相关.结论NO参与了周期性麻痹患者弛缓性瘫痪的发病.其作用机理可能与操纵钾离子通道而使血钾降低有关.     

PA低钾型患者血清CK、CK-MB及ARR与血钾的相关性分析

目的探讨原发性醛固酮增多症(PA)低血钾型患者血清肌酸激酶(CK)、肌酸激酶同工酶(CK-MB),醛固酮/肾素比值(ARR)与血钾的相关性。方法选取2016年1月至2018年1月在我院治疗的102例PA患者,根据血钾水平将他们分为血钾正常组(血K~+≥3.5mmol/L)和低血钾组(血K+3.5mmol/L),检测两组患者血脂、血糖,血清肌酐(Cr)、CK、CK-MB、立位ARR、卧位ARR等指标。结果 (1)两组患者血清总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、Cr、葡萄糖(GLU)比较差异无统计学意义(P0.05);低血钾组血清CK、CK-MB、立位ARR、卧位ARR明显高于血钾正常组,差异有统计学意义(P0.05)。(2)血钾正常组患者血清CK、CK-MB,立位ARR、卧位ARR与血钾无显著相关性(P0.05)。低血钾组患者CK、CK-MB,立位ARR、卧位ARR与血钾水平呈显著负相关(r=-0.433、-0.428、-0.389和-0.400,P0.05)。结论PA低钾型患者血清CK、CK-MB,立位、卧位ARR明显升高,且这些指标与患者血钾水平有一定相关性。     

43例低钾血症患者血清肌酶学分析

目的探讨低钾血症患者的血清肌酶学的改变。方法回顾性分析43例低钾血症患者血清肌酶学水平。结果67％的低钾血症患者可出现不同程度的血清肌酶学的升高，低钾水平越严重，肌酶学升高比例越明显，但及时纠正低钾状态后肌酶学亦迅速纠正。结论低钾血症为内科急症，可导致肌酶学不同程度的升高，及时处理可很快逆转肌酶学的升高。     

低钾型周期性瘫痪临床特点分析

目的总结分析低钾型周期性瘫痪(HOPP)的临床特点。方法回顾分析38例HOPP患者的临床表现及主要辅助检查。结果 38例HOPP患者中有18例由多种诱因诱发,8例为甲状腺功能亢进症,其症状与甲状腺功能无平行关系。HOPP表现为肢体瘫痪,呈对称性,近端重于远端,从下肢发展到上肢。血清钾均降低,22例出现白细胞、中性粒细胞增高,22例有肌酶学变化,以肌酸磷酸激酶(CK)增高为主。口服补钾治疗为主要措施,甲亢性低钾型周期瘫痪须合用抗甲状腺药物及β受体阻滞剂。结论 HOPP发作由多种诱因诱发,部分与甲状腺功能亢进症有关。多数有肌酶学变化,以CK增高明显。     

对甲亢性周期性瘫痪18例患者的临床治疗体会

目的探讨以周期性瘫痪（periodic parchysis）为主要临床表现的TPP患者的治疗及相关发病因素，并加以分析。方法对18例TPP患者的临床治疗进行回顾分析，检测血中甲状腺游离激素Fr4、F33、TSH，血清钾和血清肌酶的变化情况。结果18例患者均有FT4↑、FT3↑，TSH↓，血钾偏低，有14例患者肌酸激酶、肌酸激酶同工酶升高，12例患者天门冬氨酸转氨酶升高。结论对TPP患者的重要临床观察指标为血中游离甲状腺激素FT4、FT3、TSH，血清钾和血清肌酶的检测，及时控制甲亢和维持血钾正常是治疗关键。     

Impairment of skeletal muscle adenosine triphosphate-sensitive K+ channels in patients with hypokalemic periodic paralysis

The adenosine triphosphate (ATP)-sensitive K+ (KATP) channel is the most abundant K+ channel active in the skeletal muscle fibers of humans and animals. In the present work, we demonstrate the involvement of the muscular KATP channel in a skeletal muscle disorder known as hypokalemic periodic paralysis (HOPP), which is caused by mutations of the dihydropyridine receptor of the Ca2+ channel. Muscle biopsies excised from three patients with HOPP carrying the R528H mutation of the dihydropyridine receptor showed a reduced sarcolemma KATP current that was not stimulated by magnesium adenosine diphosphate (MgADP; 50-100 microM) and was partially restored by cromakalim. In contrast, large KATP currents stimulated by MgADP were recorded in the healthy subjects. At channel level, an abnormal KATP channel showing several subconductance states was detected in the patients with HOPP. None of these were surveyed in the healthy subjects. Transitions of the KATP channel between subconductance states were also observed after in vitro incubation of the rat muscle with low-K+ solution. The lack of the sarcolemma KATP current observed in these patients explains the symptoms of the disease, i.e., hypokalemia, depolarization of the fibers, and possibly the paralysis following insulin administration.     

Thyrotoxic periodic paralysis: a case report and review of the literature

Hypokalemic periodic paralysis occurring in thyrotoxicosis is rare in Caucasians and is not often highlighted as an endocrine emergency. Periodic paralysis, without familial background, manifests only in the thyrotoxic patient. Thyrotoxic periodic paralysis is a self-limiting disorder that is cured by the treatment of the underlying hyperthyroidism. We report an unusual case of acute onset weakness from thyrotoxic periodic paralysis in a young Chinese migrant who had a normal serum potassium level at the time of initial presentation, though on subsequent presentation one week later, he had the typically associated hypokalemia. We also review the literature on thyrotoxic periodic paralysis.     

Potential Usefulness of Early Potassium Supplementation for Preventing Severe Hypokalemia Induced by Liposomal Amphotericin B in Hematologic Patients: A Retrospective Study

Purpose

Liposomal amphotericin B (L-AMB) is an essential antifungal agent for patients with hematologic diseases; however, the drug causes severe hypokalemia at a high frequency. Meanwhile, there is little evidence regarding the risk factors for L-AMB–induced severe hypokalemia, and the prevention protocol has not been established. The goal of this study was to identify the risk factors related to severe hypokalemia induced by L-AMB in hematologic patients.

A Patient Suffering from Hypokalemic Periodic Paralysis Is Deficient in Skeletal Muscle ATP‐sensitive K+ channels

Hypokalemic periodic paralysis (HOPP) is a rare disease associated with attacks of muscle weakness and hypokalemia. In the present study, immunoprecipitation/Western blotting has shown that a HOPP patient was deficient in sarcolemmal K_ATP channels. Real‐time RT‐PCR has revealed that HOPP has decreased mRNA levels of Kir6.2, a pore‐forming K_ATP channel subunit, without affecting the expression of other K_ATP channel‐forming proteins. Based on these findings, we conclude that HOPP could be associated with impaired expression of Kir6.2 which leads to deficiency in skeletal muscle K_ATP channels, which may explain the symptoms and clinical signs of this disease.     

Thyrotoxic hypokalemic periodic paralysis triggered by high carbohydrate diet

Thyrotoxic hypokalemic periodic paralysis is an uncommon disorder characterized by elevated thyroid hormone, muscle weakness or paralysis, and intracellular shifts of potassium leading to hypokalemia. This article presents a case of thyrotoxic hypokalemic periodic paralysis in a 22-year old Hispanic man with nonfamilial thyrotoxic hypokalemic periodic paralysis triggered by a high carbohydrate diet. Laboratory studies showed elevated thyroid hormone, decreased thyroid-stimulating hormone, and hypokalemia. Rapid reduction in thyroid hormone levels by giving antithyroid drugs such as propylthiouracil and prompt potassium therapy with frequent measurements of serum potassium levels during therapy to avoid catastrophic hyperkalemia when potassium starts to shift back from intracellular to extracellular compartments can lead to successful outcome.     

急性心肌梗死早期低血钾与心衰的关系

目的 探讨急性心肌梗死（AMI）患者早期低钾血症的变化以及与心力衰竭的关系。方法收集200例急性心肌梗死的患者,发病时间小于24小时,所有患者均为首次入院。根据血钾浓度分为低钾血症组和正常血钾组,其中低钾血症组又分为重度低钾组（〈2．50mmol／L）、中度低钾组（2．51mmol／L-3．0mmool／L）和轻度低钾组（3．01-3．50mmol／L）。所有患者予以常规积极治疗,观察心力衰竭发生情况。结果AMI患者低钾血症的发生率为73．5％,低钾血症组心力衰竭的发生率为51．7％,明显高于正常组（22．6％）,其中重度低钾组心衰的发生率78．2％,中度低钾组为58．3％,轻度低钾组为38．9％。结论急性心肌梗死早期易出现低钾血症,并且随着血钾浓度的降低,心力衰竭的发生率也明显增高。     

老年腹膜透析患者低钾血症的危险因素分析

目的调查老年腹膜透析患者出现低钾血症的状况,并分析其可能的危险因素。方法采用横断面研究。184例腹膜透析患者,其中老年组患者100例。调查患者的一般资料、透析状况、血清钾水平、饮食钾摄入量、经尿和腹膜透析液钾丢失量及合并症发生情况。结果老年组腹膜透析患者低钾血症的发生率为27.0%,血钾水平与腹膜透析剂量呈负相关（r=-0.257,P=0.021）,腹膜透析剂量是该组患者出现低钾血症唯一独立性影响因素（P=0.009）。结论腹膜透析剂量与老年腹膜透析患者发生低钾血症有关。