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酸中毒,乳酸性

酸中毒,乳酸性的相关文献在1997年到2020年内共计53篇,主要集中在内科学、神经病学与精神病学、药学 等领域,其中期刊论文53篇、专利文献31105篇;相关期刊33种,包括中国临床保健杂志、国际输血及血液学杂志、传染病信息等; 酸中毒,乳酸性的相关文献由203位作者贡献,包括于华众、吴朝明、李章平等。

酸中毒,乳酸性—发文量

期刊论文>

论文:53 占比:0.17%

专利文献>

论文:31105 占比:99.83%

总计:31158篇

酸中毒,乳酸性—发文趋势图

酸中毒,乳酸性

-研究学者

  • 于华众
  • 吴朝明
  • 李章平
  • 杨艳玲
  • 王朝霞
  • 程俊彦
  • 陈寿权
  • 丁冬生
  • 乔娜娜
  • 乔红刚
  • 期刊论文
  • 专利文献

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    • 王之舟; 程红勤; 白向荣; 金颖; 姜德春; 张嵊鹏
    • 摘要: 1例45岁男性患者因颅内病变行开颅活检术,术后为预防癫痫先给予丙戊酸钠800 mg溶于0.9%氯化钠注射液8 ml静脉推注,继之用该浓度丙戊酸钠溶液以0.6 ml/h的速度持续静脉泵入.给药1h后,患者血清乳酸水平逐渐升高,最高达到14.7 mmol/L,伴代谢性酸中毒和代偿性呼吸性碱中毒,酸碱度最低7.09,剩余碱最低-26.3,导致患者昏迷.考虑患者的高乳酸血症及代谢性酸中毒可能与丙戊酸钠有关,停用丙戊酸钠,给予5%碳酸氢钠注射液静脉滴注和血液净化治疗.3d后,患者的乳酸水平恢复正常,代谢性酸中毒基本纠正,神志转清.
    • 张晶卉; 乔娜娜; 李文
    • 摘要: 本文报道SUCLG1基因复合杂合突变所致的以轻度甲基丙二酸尿症获诊的新生儿琥珀酰辅酶A连接酶缺乏症1例.患儿生后2d发病,以“呕吐、拒奶”就诊于山东大学齐鲁医院,血气分析提示代谢性酸中毒及高乳酸血症.实验室检查提示血氨轻度升高、血清转氨酶轻度升高、同型半胱氨酸正常.影像学检查提示脑发育不良及心脏多发畸形.血液氨基酸及酰基肉碱谱、尿有机酸谱分析提示甲基丙二酸尿症.行全外显子组测序,结果显示,SUCLG1基因有2个新突变,即c.40A>G(p.M14V)突变和6~9号外显子的杂合缺失,分别来自于患儿母亲和父亲.患儿经扩容、纠酸等治疗,代谢性酸中毒好转,但乳酸持续偏高,出现水肿及呼吸衰竭,家长放弃治疗,出院后死亡.SUCLG1基因突变可导致琥珀酰辅酶A连接酶缺乏症、线粒体DNA耗竭综合征.该病无特效治疗,对于喂养困难、乳酸酸中毒、多脏器受累的新生儿,应行遗传代谢病筛查,基因检测为确诊手段.
    • 肖妍; 王鹏; 李如兵; 田俊英; 付忠华; 毛远桂; 张红艳
    • 摘要: 患者男,27岁,2017年10月3日因热液烫伤躯干、臀部及四肢等多处6h后收入笔者单位,烧伤总面积约60%体表总面积,深度为深Ⅱ~Ⅲ度.入院后立即给予抗休克、补液及抗感染等对症支持治疗,行2次清创植异种(猪)皮手术后,创面愈合良好.入院第12天根据血微生物培养及药物敏感试验结果使用利奈唑胺抗感染,患者血乳酸水平持续升高,8d后停用利奈唑胺,口服维生素B1 1周后,乳酸水平逐渐降至正常.该病例主要分析利奈唑胺是否直接导致高乳酸血症及其重要机制,目的在于提示临床医师在使用利奈唑胺时应警惕高乳酸血症的风险,如出现此风险,应立即停用利奈唑胺并口服维生素B1纠正高乳酸值,必要时调整治疗计划.%On October 3rd,2017,one male patient,aged 27 years,was admitted to our hospital 6 hours after hydrothermal scald of torso,buttocks,and limbs.The total area of burn was about 60% total body surface area,and the depth was from deep partial-thickness burn to full-thickness burn.Immediately after admission,the patient was given symptomatic support treatments,such as anti-shock,fluid replacement,and anti-infection,etc.After being treated by debridement and xenogenic (porcine) skin grafting for 2 times,the wounds were healed well.On the 12th day of admission,linezolid was used to prevent infection according to the results of microbial culture and drug sensitivity test,since when the level of his blood lactate continued to increase.After 8 days,linezolid was discontinued and vitamin B1 was given orally for 1 week,and the level of lactic acid gradually decreased to normal in result.This case was used mainly to analyze whether linezolid could directly cause hyperlacticemia and its important mechanism,aiming at reminding clinicians of being alert to the risk of hyperlacticemia when using linezolid.If hyperlacticemia occurs,linezolid should be discontinued immediately and vitamin B1 should be taken orally to correct the high lactic acid value,and the treatment plan should be adjusted if necessary.
    • 肖艰; 焦一伟; 彭薇; 刘晓冬
    • 摘要: 目的 探讨弥漫大B细胞淋巴瘤(DLBCL)合并乳酸酸中毒的临床特点、发病机制、治疗方法及其疗效.方法 选择2012年9月30日和2013年1月8日收治的,经淋巴结活检及免疫组织化学检查确诊为DLBCL,并在治疗过程中并发乳酸酸中毒导致死亡的2例患者为研究对象.对其临床特点、发病机制、治疗方法及其疗效进行分析,并进行相关文献复习.结果 2例患者均接受积极抗感染、溶解淋巴瘤细胞、纠正电解质及酸碱平衡紊乱等对症治疗,但疗效均不佳.2例患者均于确诊后7d内,出现血清乳酸水平明显升高,分别达到15.0 mmol/L和5.2 rnmol/L,并最终由于严重酸碱平衡紊乱导致死亡.国内外文献检索结果显示,超过70% DLBCL合并乳酸酸中毒患者在起病后1个月内死亡,该病具体病理生理机制尚未完全明确.血液净化治疗可为该类患者的化疗赢取时间,而其最终病情缓解,则有赖于对原发病的控制.结论 乳酸酸中毒是DLBCL的一种罕见的临床并发症,病情进展迅速,导致患者病死率极高.对于该类患者的成功诊治,主要依赖于早期诊断及积极化疗.%Objective To explore the clinical characteristics,pathophysiology,treatments and effects of diffuse large B cell lymphoma (DLBCL) combined with lactic acidosis.Methods On 30th September 2012 and 8th January 2013,a total of 2 death cases of DLBCL combine with lactic acidosis were included in the study.These 2 cases were dingnosed DLBCL by lymph node biopsy and immunohistochemical examination.Their clinical charcteristions,pathophysiology,treatments and effects were observed.And domestic and foreign related literature were reviewed.Results These 2 cases were treated with active antiinfection,dissolving lymphoma cells,correcting electrolyte and acid-base disorders.But their treatment effects were bad.Their serum level of lactic acid was increased significantly in a week after diagnosis,which were 15.0 mmol/L and 5.2 mmol/L,respectively.These 2 cases finally died of severe acid-base disorder.The retrieval of literature presented the poor prognosis of DLBCL combine with lactic acidosis,more than 70% of patients died within 1 month.The pathogenesis of malignancy-induced lactic acidosis is not well understood,the blood purify can earn enough time for chemical therapy treatment.To alleviate the disease depends on the control of the primary disease.Conclusions DLBCL combine with lactic acidosis is extremely rare in clinical,but it has rapid progress and high mortality.Prompt diagnosis and treatment of underlying lymphoma or leukemia remains the only way to achieve complete resolution of lactic acidosis in these patients.
    • 庄耀宁; 林秋英; 魏碧蓉
    • 摘要: 总结1例糖尿病患者双胍类药物相关乳酸酸中毒突发心搏骤停的护理经验.通过对患者实施心搏骤停的抢救、胸痛的护理、降低乳酸浓度的护理、肝功能不全的护理、出院指导等一系列护理措施,最终患者明显好转出院.
    • 周方强; 刘锐
    • 摘要: 众多动物实验论证了丙酮酸根离子具有临床常用输液中阴离子所没有的优异生物学特性,包括提高细胞缺氧耐受性、抗氧化与抗炎作用,纠正缺氧型乳酸性酸中毒及保护线粒体功能等.因此,适用于危重病的液体治疗:既避免常规液体的“复苏损伤”毒性,如0.9%氯化钠溶液导致的高氯性酸中毒和乳酸钠溶液所致的糖酵解抑制,以及二者的炎症反应等,又在扩容同时防治多器官功能衰竭,特别是保护肠道屏障功能,表明其优越性.反复动物体内实验和初步的临床试验已显示其保护器官功能和改善氧化代谢的作用,尤其是有效纠正缺氧型乳酸性酸中毒.它能在无氧或缺氧下经乳酸脱氢酶还原反应和刺激缺氧诱导因子-1α活性,保护糖酵解代谢;在缺氧下逆转受抑制的丙酮酸脱氢酶活性,促进糖的氧化代谢,加速堆积的乳酸氧化清除.无论经静脉、腹腔和口服液体复苏,丙酮酸钠溶液都能在致死性休克动物的液体治疗中发挥以上功能.本文重点讨论以上给药途径的作用.此外,它还有防治糖尿病器官并发症,如视网膜病变和一定条件下的抗肿瘤活性,显示其重大的潜在的临床应用价值和良好前景,值得深入关注.%Numerous animal studies have demonstrated that pyruvate holds superior biological properties relative to anions in traditional solutions in fluid therapy for critical illness.The beneficial characteristics include increase of hypoxia tolerance,anti-oxidative and inflammatory effects,correction of hypoxic lactic acidosis and protection of mitochondrial function.Therefore,pyruvate-enriched solutions are potentially suitable for fluids resuscitation in critical care patients to prevent "resuscitation injury" induced by traditional fluid.For example,0.9% sodium chloride solution commonly induces hyperchloremic acidosis,sodium lactate solution may inhibit glycolysis and both can lead to systemic inflammatory reactions in clinical fluid therapy.Pyruvate in fluid therapy is not only a volume expander,but also a therapeutic agent in prevention of multi-organ,particularly intestinal barrier,dysfunction.Thus,pyruvate appears its superiority in fluid therapy.Many animal experiments in vivo and preliminary clinical trials have demonstrated that pyruvate protects organ function and improves oxidative metabolism,specially corrects hypoxic lactic acidosis.It protects glycolytic metabolism under hypoxia,even anoxia,through lactate dehydrogenase reaction and stimulation of hypoxia inducible factor-1α;it also promotes glucose oxidative metabolism under hypoxia due to its restoration of inhibited activity of pyruvate dehydrogenase,resulting in improvement of lactic clearance.The pyruvate favorable function can be achieved by intravenous,peritoneal or oral administrations in fluid therapy of fatal shock animals.These aspects were mainly reviewed in this paper.In addition,pyruvate prevents organ complications associated with diabetes,such as retinopathy,and shows anti-cancer property under some conditions.Current findings strongly demonstrate its huge potential values and promising prospects in clinical application.Further concerns and investigations are warranted.
    • 周茜; 邱峰; 龙锐
    • 摘要: 1例61岁男性2型糖尿病患者空腹饮52度白酒约400 ml后约30 min服用二甲双胍850 mg,约4 h后出现剑突下闷痛不适、心悸,约7 h后出现恶心及呕吐.实验室检查示血pH 7.16,乳酸15.0 mmol/L,剩余碱-12.6 mmol/L,碳酸氢盐 15 mmol/L,诊断为糖尿病乳酸酸中毒.给予吸氧、纠正酸中毒、补液等综合对症支持治疗,并停用二甲双胍,改为罗格列酮4 mg口服、1次/d.18 h后患者剑突下闷痛明显减轻,未再出现恶心、呕吐,复查示血pH 7.41,乳酸1.8 mmol/L,剩余碱2.3 mmol/L,碳酸氢盐27 mmol/L.%A 61-year-old male patient with type 2 diabetes received an oral metformin 850 mg about 30 minutes after drinking about 400 ml liquor containing 52% of alcohol into an empty stomach.About 4 hours later, the patient developed stuffy pain below xiphoid process and palpitation, and about 7 hous later, he developed nausea and vomiting.The laboratory examination showed that the blood pH 7.16, lactic acid 15.0 mmol/L, base excess-12.6 mmol/L, bicarbonate 15 mmol/L.He was diagnosed as diabetic lactic acidosis.Comprehensive treatments such as oxygen inhalation, acidosis correction, fluid infusion were given and metformin was changed to oral rosiglitazone 4 mg once daily.Eighteen hours later, the discomfort below xiphoid process was markedly improved, nausea and vomiting did not recur, his laboratory examination results showed the blood pH 7.41, lactic acid 1.8 mmol/L, base excess 2.3 mmol/L, and bicarbonate 27 mmol/L.
    • 贾爱华; 李艳艳; 乔红刚; 高志飞; 张剑; 韩建伦; 井长信
    • 摘要: 目的 总结乳酸酸中毒合并低血糖昏迷、糖尿病酮症酸中毒和高钾血症患者的临床特点,提高临床医师对乳酸酸中毒合并低血糖昏迷、糖尿病酮症酸中毒患者的救治能力.方法 对乳酸酸中毒合并低血糖昏迷、糖尿病酮症酸中毒和高钾血症患者1例的临床特点、病情演变结合文献进行分析.结果 该患者由于同时使用苯乙双胍和格列本脲导致低血糖和酸中毒同时发生,通过补液、积极纠酸、降低血钾和控制血糖治疗2d后病情稳定,乳酸降至正常,生命体征平稳.结论 由苯乙双胍导致的乳酸酸中毒致细胞内血钾转移至细胞外,造成高钾血症;治疗时可加大碳酸氢钠的使用量,积极纠酸,以免错过治疗时机.%Objective To ummarized the clinical characteristics of lactic acidosis combined with hypoglycemic coma,diabetic ketoacidosis and hyperkalemia,so to improve the physician's treatment ability by summary the clinical feature of lactic acidosis combined with hypoglycemic coma,diabetic ketosis and hyperkalemia.Methods Analyzed the clinical characteristics and disease development of one case with lactic acidosis combined with hypoglycemic coma,diabetic ketoacidosis and hyperkalemia,and reviewed literature.Results The patient had hypoglycemia and acidosis at the same time due to taking phenformin and glibenclamide.After 2 days,the patient was better through correcting acidosis,intravenous fluid therapy,lowering blood potassium and controlling blood glucose.Conclusion Because acidosis caused the potassium transfer from intracellular to extracellular,the latter leads to hyperpotassemia,lactic acidosis caused by phenformin should be treated with intravenous fluid therapy,correcting acidosis.
    • 倪芬; 姜焕玲; 曹钰
    • 摘要: 病人,男,47岁,因"腹痛、腹泻和反复呕吐4d,意识模糊1d"就诊于我院急诊科。病人发病前有持续每日服用大剂量二甲双胍和苯乙双胍(剂量不祥)病史,既往有高血压、肾结石并肾盂积水病史。
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