吉非替尼致严重腹泻和低钾血症

1例83岁女性患者因右肺腺癌左肺转移和可疑肝转移口服吉非替尼0.25 g、1次/d。用药27 d后患者出现严重腹泻伴恶心呕吐,实验室检查示血钾2.1 mmol/L,粪培养结果为阴性,排除感染性腹泻。未停用吉非替尼,给予补钾、止泻等治疗4 d,患者痊愈。4 d后患者再次出现上述症状,实验室检查示血钾2.96 mmol/L...     

青壮年低钾血症心电图改变与临床病因关系

目的 探讨青壮年低钾血症患者心电图改变与临床病因关系.方法 将104例青壮年患者的心电图改变与临床病因及血清钾浓度作对比分析.结果 青壮年低钾血症患者心电图异常改变80例(76.92%),其中以U波增高80例(76.92%)、ST段改变64例(61.54%)、T波改变62例(59.62%);心电图异常发生率随血清钾浓度的降低而呈递增.结论 青壮年低钾血症患者的病因以原发疾病造成的钾摄入不足为主,随着血钾浓度的降低,心电图异常发生率增加,改变随之加重.     

术前无症状低钾血症干预结果分析

目的：探讨术前无症状低钾血症的干预方法。方法：择期手术患者5278例，诊断为低钾血症453例，其中无症状低钾血症58例，按干预方法不同分为：观察组2658例，低钾血症1984例，其中无症状低钾血症20例；对照组2620例，低钾血症255例。其中无症状低钾血症38例，比较不同的干预后两组患者低钾血症与无症状低钾血症的发生率、平均发现时间、平均择期手术时间。结果：观察组低钾血症的发生率7．44％，明显低于对照组9．73％（x2=-5．89，P〈0．05）；观察组无症状低钾血症的发生率0．75％，明显低于对照组1．45％（x2=5．78，P〈O．05）；观察组术前无症状低钾血症平均发现时间、平均择期手术时间明显短于对照组（t=3．52，t=3．33，P均〈0．01）。结论：术前无症状低钾血症干预，可以降低了术后低血钾症的发生。     

低剂量棉酚男性避孕效果和副作用的临床观察

棉酚的男性避孕作用和副作用（如：不可逆性不育和低血钾症）均为男性学学者所熟悉，其副作用使棉酚至今不能成为广泛应用的男性避孕药。本文试图通过减低棉酚的起效量和维持量以减少或避免副作用的发生。结果发现：每天服用１０ｍｇ或１２．５ｍｇ，待精子密度降为≤４００万／ｍｌ时，改服维持量（隔天１０ｍｇ，或１２．５ｍｇ）均有避孕效果，但起效期较长。服药期间血清ＦＳＨ、ＬＨ和睾酮水平无明显变化，尿β－２ＭＧ和ＮＡＧ以及血钾也无明显异常，服药者更无低血钾症状出现。服药对象的女方无妊娠。     

三甲基氯化锡引起低血钾症的肾脏机制探讨

目的探讨三甲基氯化锡(trim ethyltin ch loride,TMT)引起低血钾症的肾脏机制。方法将SD大鼠随机分成3组,每组10只,分别经腹腔注射TMT 0、10.0、21.5 m g/kg,测定0.5 h、1 d、3 d、6 d和11 d血浆的钾。将大鼠随机分成2组,每组10只,分别经腹腔注射TMT 0、10.0 m g/kg,测定1 d、6 d和11 d的24 h尿量和尿钾浓度。将大鼠随机分成6组,每组10只,分别经腹腔注射TMT 0、10.0 m g/kg,测定1 d、6 d和11 d的肾小管上皮细胞膜钠钾ATP酶的活力。结果大鼠腹腔注射TMT 10.0、21.5 m g/kg后0.5 h,血钾显著下降(P<0.05),6 d和11 d血钾仍低于正常水平(P<0.05);给予TMT 10.0 m g/kg后1 d、6 d和11 d,尿量先增后减、尿排总钾均显著增加(P<0.05);1 d、6 d和11 d肾小管上皮细胞膜钠钾ATP酶活力均显著低于对照组(P<0.01)。结论TMT引起低血钾症的主要原因是肾脏排钾持续增多,其机制与TMT引起肾小管细胞膜钠钾ATP酶活力下降,进而引起K 的重吸收下降有关。     

沙丁胺醇雾化吸入致低钾血症的临床分析

目的研究雾化吸入沙丁胺醇对血清钾的影响。方法将支气管哮喘急性发作收住院患者48例分成沙丁胺醇和氨茶碱两组进行治疗。观察3 d,用药前后沙丁胺醇组与氨茶碱组血清钾浓度的变化。结果发现两组患者治疗后血清钾浓度均较治疗前有一定程度的降低,沙丁胺醇组降低程度显著,治疗前后比较差异有统计学意义(P＜0．01);但氨茶碱组治疗前后比较差异无统计学意义(P＞0．05)。结论沙丁胺醇雾化吸入后明显使血钾降低,因此,在临床使用中要注意这一副作用,以免发生不良后果。     

慢性心衰并低钾血症QT离散度与室性心律失常的关系

目的：了解心衰并低血钾时校正QT离散度（QTcd)与室性心律失常的关系。方法：分别测量健康对照组。单纯心衰组、心衰并低血钾组及其血钾纠正后的QTcd，并进行比较，同时对各组室性心律失常发生率进行比较。结果：心衰并低血钾组QTcd及室性心律失常发生率明显高于血钾纠正后及单纯心衰组的（P＜0．05－0．01）。结论：QTcd可作为监测心衰并低血钾时室性心律失常危险性的指标。     

低钾血症34例诊治体会

目的探讨低钾血症的临床表现、诊治措施预后情况。方法对34例低钾血症患者资料进行回顾性分析，并按缺钾程度分为轻度组、中度组、重度组，观察患者的诊治、疗效及转归情况。结果低钾血症如得到积极诊治，预后较好。结论低钾血症是临床上常见的电解质紊乱疾病，及时治疗，疗效好。     

Hypokalemic rhabdomyolysis in a child with Bartter’s syndrome

Hypokalemia represents a rare cause of rhabdomyolysis. Some reports have described a few adult patients affected by Bartters syndrome and Gitelmans syndrome with rhabdomyolysis due to severe hypokalemia. We report the first pediatric patient with Bartters syndrome in whom rhabdomyolysis developed when her plasma potassium level was less than 2 mEq/l. Prompt intravenous fluid and potassium prevented tubular damage and acute renal failure. We recommend determining serum creatine phosphokinase in all patients affected by Bartters syndrome and profound hypokalemia.     

A founder mutation in the CLCNKB gene causes Bartter syndrome type III in Spain

The term Bartter syndrome encompasses a group of closely related inherited tubulopathies characterized by markedly reduced NaCl transport by the distal nephron. At present, five different genetic variants have been demonstrated. The majority of patients with so-called classic Bartter syndrome carry inactivating mutations of the CLCNKB gene encoding the basolateral ClC-Kb chloride channel (Bartter syndrome type III). The purpose of this study was to investigate the underlying mutation in cases of classic Bartter syndrome followed at our center.Ten patients, including two sisters, with clinical and biochemical features of classic Bartter syndrome were included in the mutational analysis. They originated from different regions of Spain with either Basque or Spanish ancestry. There was no history of consanguineous marriage in any of the kindreds. The parents and siblings of each patient, as well as a population of 300 healthy control adult subjects, were also analyzed. All ten patients were found to be homozygous for an identical missense mutation in the CLCNKB gene, substituting a threonine for an alanine at codon 204 (A204T) in the putative fifth transmembrane domain of the protein. None of the 300 control subjects were homozygous for the A204T allele. Overall, the A204T mutation was detected on 2/600 control chromosomes. Despite sharing a common mutation, the clinical manifestations of the syndrome in the patients varied from lack of symptoms to severe growth retardation.Demonstration of a point mutation within the CLCNKB gene as the apparently unique cause of Bartter syndrome type III in Spain is highly suggestive of a founder effect. Our results also support the lack of correlation between genotype and phenotype in this disease.