重型肝炎并发低血钾症——附60例分析

本组重型肝炎60例并发低血钾者22例,并发低血钾的原因有:(1)饮食量减少,钾的摄入量不足。(2)药源性低血钾如激素、高渗糖和利尿剂的使用。本文分析了低血钾的危害,提出了防治低血钾的措施。     

体外循环术后低钾血症的高浓度静脉补钾治疗

目的 探讨高浓度静脉补钾治疗体外循环术后低钾血症的临床经验。方法 回顾性分析我院1998-2000年重症监护室体外循环术后连续100例心脏病人的临床资料。浓度为112.4-206mmol/L的氯化钾溶液以6．7-16．8mmol/hr的速度，经中心静脉输注共219次，以纠正低钾血症。结果 分析显示，采用此种方法能安全有效提高血钾水平，未发现致命性心律失常；血钾浓度与手术前病人缺钾程度、体外循环持续时间、术后尿量等密切相关。但血钾浓度增高值与补钾剂量间无显著直线相关关系。结论 这种高浓度静脉补钾方法能快速、有效、相对安全的纠治体外循环术后低钾血症，有一定的临床应用价值。     

糖尿病合并低钾血症30例分析

目的分析糖尿病并发低钾血症的原因。方法选择因糖尿病于笔者所在医院内科住院治疗的患者30例,所有患者于门诊或住院时检测血钾浓度为〈3.5mmol/L,记录患者的临床资料,总结分析可能引起糖尿病低钾血症的原因。结果导致低钾血症的主要原因中,9例为利尿剂（30%）,9例为酮症酸中毒（30%）,5例为使用胰岛素（16.7%）,其他因素占23.3%;年龄超过60岁因为酮症酸中毒而发生低钾血症的患者较其他两个年龄段明显减少,利尿剂导致的低钾血症较其他两组为高。结论糖尿病合并低钾血症临床症状特异性较低,应引起临床医生的足够重视。     

Side Effects of Diuretics

Diuretics are amongst the most widely used drugs. Fortunately enough, there are rather few clinically relevant side effects. The following side effects are discussed in this paper: disturbances of electrolyte, acid-base- and water balance, metabolic changes (uric-acid, carbohydrate-metabolism, lipid metabolism), unspecific side effects and drug interactions. Finally the prevention of side reactions of diuretics is briefly mentioned.     

Hypothalamic regulation of sodium-potassium pump activity in skeletal muscle

The suppression of active Na+-K+ transport in rat skeletal muscle during hypokalemia was counteracted by bilateral electrolytic lesion of the ventromedial hypothalamic nucleus. This reversal effect was unaffected even after pancreatectomy or adrenalectomy. The anomalous electrolyte content in hypokalemic rat muscles was aggravated by lesion of the dorsomedial hypothalamic nucleus and of the anterior hypothalamus. The results indicate that the hypothalamus is involved in the regulation of the Na+-K+ transport system in skeletal muscle during hypokalemia.     

高浓度静脉补钾治疗危重患者低钾血症33例疗效观察与监测

目的:探讨中心静脉微量泵入高浓度钾治疗危重患者低钾血症的疗效与监测.方法:将66例合并低钾血症的危重患者随机分为治疗组和对照组各33例,治疗组补钾速度为6.66～13.32 mmol/h,对照组为4 mmol/h,两组均进行严密监护与血钾浓度监测,血钾正常时停止补钾. 结果:补钾24 h后,血钾浓度治疗组(4.73±0.40)mmol/L、对照组(3.76±0.35)mmol/L,补钾液体量治疗组(240.00±49.77)ml/d,对照组(2400.00±834.39) ml/d,两组比较差异有统计学意义(P<0.01).结论:微量泵入高浓度钾治疗危重患者低钾血症可以在短时间内纠正低钾血症,是安全有效的.     

Paraneoplastic hypokalemia in acute myeloid leukemia: a case of renin activity in AML blast cells

 Hypokalemia due to renal potassium loss has frequently been observed in patients with acute myeloid leukemia (AML). The pathogenic mechanism for this hyperkaluresis is unclear. In this report we describe a patient with AML FAB M4, in whom the clinical course, the electrolyte disturbances, the serum aldosterone levels, and the diffuse hyperplasia of the adrenal cortex documented a typical case of marked secondary hyperaldosteronism. On analysis of the leukemic cells of this patient compared with normal bone marrow cells, a significant increase of renin-like activity in the cytosol of the blast cells was noted. Activation of the renin-angiotensin-aldosterone system by paraneoplastic production of renin-like activity in AML blast cells might contribute to the hypokalemia often observed in patients with acute myeloid leukemia. Received: 19 March 1996 / Accepted: 30 April 1996     

外伤性脊髓损伤后的低钾症（附31例报告）

对我院１９８２年以来救治的脊柱骨折脱位台并截瘫（包括不全瘫）２９６例中出现低钾症的３１例进行了分析。此症发生率约１０．４％，其特点是①外伤性脊髓损伤后出现低钾；②大部分由禁食、使用激素、脱水剂引起；③多在伤后２￣５ｄ出现；④颈椎脊髓损伤后多见。治疗本症的原则是及时发现，及时诊断，及时补充钾。低钾不纠正，必将影响脊髓损伤的康复，且易 并发褥疮和肺部感染等，甚至加重呼吸肌的麻痹或心力衰竭而死亡。     

复方甘草酸单铵S治疗抗结核药肝损害疗效及不良反应分析

目的探讨注射用复方甘草酸单铵S治疗抗结核药肝损害的疗效及其不良反应。方法选取原肝功能正常、无肝病基础,在强化抗结核过程中出现肝功能损害的结核病患者78例,停用吡嗪酰胺后随机分成两组,每组39例。对照组给予还原型谷胱甘肽,治疗150 mg/d;观察组给予复方甘草酸单铵S治疗,120 mg/d,并分别在第1、2、3周后比较肝功能丙氨酸氨基转移酶(ALT)及监测血钾水平,观察有无水肿和高血压不良反应。结果两组强化抗结核后发现,肝功能损害的时间差异无统计学意义(P>0.05);两组保肝治疗前,肝功能指标ALT差异无统计学意义(P>0.05),但治疗后第1、2、3周,两组间差异有统计学意义(P<0.05)。除第2～3周ALT下降,速率差异无统计学意义外(P>0.05),余各时间段两组间ALT下降速度的差异均有统计学意义(P<0.05)。两组出现低血钾情况差异有统计学意义(P<0.05),而出现水肿、高血压或原有高血压加重情况差异无统计学意义(P>0.05)。结论注射用复方甘草酸单铵S对抗结核药肝功能损害疗效确切,在与还原型谷胱甘肽比较中显出一定的优势,但易出现低血钾、水钠潴留或高血压及原高血压加重等不良反应。     

A novel mutation in <Emphasis Type="Italic">KCNJ1</Emphasis> in a Bartter syndrome case diagnosed as pseudohypoaldosteronism

Bartter syndrome (BS) is a genetic disorder with hypokalemic metabolic alkalosis and is classified into five types. One of these, type II BS (OMIM 241200), is classified as neonatal Bartter syndrome, which is caused by mutations in the KCNJ1 gene. Transient hyperkalemia and hyponatremia are usually noted in the early postnatal period, but as type II BS is a relatively rare disease, its exact clinical course and genetic background have not yet been thoroughly characterized. This report concerns a male type II BS patient with a novel mutation in the KCNJ1 gene. The unique clinical findings of this case are that hyperkalemia (8.9 mEq/l), hyponatremia, and metabolic acidosis detected in the early postnatal period led to a diagnosis of pseudohypoaldosteronism (PHA). As an adolescent, however, the patient currently shows normal potassium levels and normal renal function, although with hypercalciuria and nephrocalcinosis, without having received any treatment. In such cases, KCNJ1 mutations should be suspected. In our case, genetic analysis of the KCNJ1 gene identified a novel homozygous 1-bp deletion mutation (c.607 del. C in exon 5).