心肌肌钙蛋白Ⅰ快速检测在急性心肌梗死诊断中的价值

比较心肌肌钙蛋白Ⅰ(CTnI)与几种常用的急性心肌梗死(AMI)诊断标记物的临床应用价值。方法对36例AMI和70 例非心肌梗死患者同时检测血清CTnI、肌酸激酶(CK)、肌酸激酶同功酶(CK-MB)、乳酸脱氢酶(LDH)、天冬氨酸转氨酶(AST)和α-羟丁 酸脱氢酶(α-HBD)等6项指标,并进行2组间比较,分别对AMI和非心肌梗死组各指标间的差异作对比分析。结果CTnI诊断AMI的敏 感性(91.7％)高于CK(75.0％)、CK-MB(63.9％)、AST(66.3％)、LDH(75.0％)、α-HBD(69.4％),P<0.05～0.01;CTnI诊断AMI的特异 性(95.7％)与CK-MB(92.6％)相近(P>0.05),高于CK(84.3％)、ASr(81.4％)、LDH(72.9％)及α-HBD(80.0％),P<0.05～0.01。结论 CTnI对AMI的诊断具有较高的敏感性和特异性,作为一种心肌损伤的特异标记物,具有较好的临床应用价值。     

血清谷氨酸脱氢酶对肝移植患者的预后评价

目的探讨血清谷氨酸脱氢酶（glutamate dehydrogenase，GLD）与肝移植患者预后的关系。方法应用德国临床化学学会推荐的速率法测定30例肝移植患者血清GLD活性并动态观察其变化的规律。结果对30例肝移植术中及术后早期患者血清GLD、ALT、AST、LDH活性进行连续监测。在术中供肝血流再灌注后，患者血清中此4种肝酶的活性开始明显上升。患者的预后与GLD升高的幅度及恢复至正常的时间的长短有关。预后不良的患者术后GLD峰值（均值5898．52U／L）明显高于预后良好的患者（均值285．08U／L）。分别以肝移植术后GLD、ALT的峰值800U／L、1400U／L为临界值预测肝移植术后预后。肝移植术后GLD峰、ALT峰预测准确率分别为86．7％、90％。将肝移植术后GLD恢复正常值天数以14天为界预测肝移植预后。其动态变化对预后的预测准确率为100％。结论肝移植术后早期血清GLD水平与预后有密切关系，GLD是预测肝移植预后的一个有价值的酶学指标。     

精神病病人血清酶测定的临床价值

目的 探讨精神病病人血清中肌酸激酶（CK）、肌酸激酶同工酶（CK-MB）、乳酸脱氢酶（LD）和天门冬氨酸氨基转移酶（AST）检测的临床意义.方法 采集85例精神病病人和90例健康人空腹静脉血,在全自动生化分析仪上测定CK、CK-MB、LD和AST 水平.结果 精神病组血清CK、CK-MB、LD和 AST水平均高于正常对照组,差异有显著性（t=2.101～8.557,P〈0.05）.结论 精神病病人血清中CK、CK-MB、 LD和AST显著增加.     

急性运动对小鼠心肌线粒体功能的影响

目的：探讨不同强度运动对心肌线粒体功能的影响。方法：40只小鼠随机分为安静对照组（A组）、90min运动组（B组）、力竭组（C组）及力竭后恢复24h组（D组）各10只，以游泳为运动方式，观察各组血清肌酸激酶（CK）、乳酸脱氢酶（LDH）、ATP合成活性及脂质过氧化水平丙二醛（MDA）的变化，并在光镜和电镜下观察心肌超微结构。结果：与A组比较，C组血清CK、LDH水平及心肌MDA水平显著增高（P〈0．05）．ATP合成能力显著下降（P〈0．05），电镜下心肌超微结构损伤明显。结论：急性力竭运动可造成线粒体损伤和心肌损伤，力竭运动后24h各项指标基本恢复。     

中枢神经系统感染血清心肌酶的变化及其临床意义

目的研究成年人中枢神经系统感染时血清心肌酶的变化及其临床意义。方法收集病毒性脑炎（病脑组）45例和结核性脑膜炎（结脑组）22例,另有体检正常者40例为对照组。采用东芝全自动生化分析仪,以酶速率法测定所有患者的血清天冬氨酸转氨酶（AST）、乳酸脱氢酶（LDH）、肌酸激酶（CK）、肌酸激酶心肌型同工酶（CK-MB）、α-羟丁酸脱氢酶（α-HBDH）水平。结果62.2％（28／45）病脑组血清心肌酶出现异常,与对照组比较差异有统计学意义（P〈0.01）;18.2％（4／22）结脑组血清心肌酶出现异常,与对照组比较,差异无统计学意义（P〉0.05）。病脑组患者血清中AST、LDH、CK水平及结脑组血清中AST、CK水平均明显高于对照组（P〈0.05或〈0.01）,病脑组CK-MB、α-HBDH水平及结脑组LDH、CK-MB和α-HBDH水平与对照组比较,差异无统计学意义（P〉0.05）;结脑组CK水平明显低于病脑组（P〈0.05）。障碍组血清心肌酶水平均明显高于无障碍组（P〈0.05）。结论中枢神经系统感染常伴随心肌细胞损伤,血清心肌酶水平升高,对该类患者应常规行血清心肌酶测定。     

齐拉西酮对精神分裂症患者心肌酶表达水平的影响

目的：探讨抗精神病药物齐拉西酮对精神分裂症患者心肌酶表达水平的影响。方法对63例精神分裂症患者进行齐拉西酮治疗,检测并比较治疗前后进行血清肌酸激酶（CK）、肌酸激酶同工酶MB（CK-MB）、乳酸脱氢酶（LD H ）水平。结果精神分裂症患者齐拉西酮治疗后1周末、4周末、24周末上述血清心肌酶水平与治疗前比较差异有统计学意义（P＜0．05）。结论长时间服用抗精神病药齐拉西酮可导致精神分裂症患者血清心肌酶代谢的异常。     

肌酸激酶同工酶检测在急性心肌梗死中的临床价值

目的 探讨肌酸激酶（CK）MB和MM同工酶（CK-MB和CK-MM）亚型在急性心肌梗死（AMI）患者中的变化规律与其预后的关系,评价CK同工酶的亚型检测在AMI心肌早期再灌注、梗死延迟或再梗死诊断中的临床价值。方法 采用琼脂糖凝胶电泳系统将血清CK同工酶亚型分离为CK-MM3、CK-MM2、CK-MM1、CK-MB2和CK-MB1,并分析比较21例AMI患者血清CK同工酶亚型在发病后0～6小时、24小时和72小时的动态变化。结果 AMI患者血清CK-MB和CK-MM在发病后6h开始升高,其中以CK-MB2和CK-MM3升高为主,MB2／MB1〉1．36,MM3／MM1〉0．7;12-24小时达峰值,CK-MB／CK〉30％。15例早期再灌注的AMI患者血清CK、CK-MB和CK-MM在72小时下降至正常,但6例无早期再灌注患者仍处于较高水平,其中MB2／MB1〉1．29,MM3／MM1〉0．65。结论 CK同工酶的亚型检测能反映AMI患者心肌组织损伤的动态过程,可作为一项较灵敏的生化指标,有助于诊断AMI心肌早期再灌注、梗死延迟或再梗死。     

Hereditary deficiency of lactate dehydrogenase M-subunit

A family with a complete deficiency of lactate dehydrogenase M-subunit was investigated. The propositus was an 18-year-old male who complained of exertional pigmenturia and easy fatigue. Marked discrepancy was observed in the ratio between creatine kinase and lactate dehydrogenase (CK/LDH). Electrophoretic analysis of serum LDH isoenzymes of the propositus demonstrated only one activity band of LDH H₄. A complete lack of the LDH M-subunit was similarly demonstrated in erythrocytes, leukocytes and in the intermediate vastus muscle. LDH levels in the muscle specimen were markedly decreased in the patient, whereas CK and aspartate aminotransferase were almost the same as in a control subject. LDH isoenzymes of erythrocytes were analyzed in 5 siblings and in the parents. This demonstrated a complete lack of LDH M-subunit in 3 siblings. The ratio between H-subunit and M-subunit (H/M) in erythrocyte LDH suggested a partial absence of the M-subunit in two siblings and in the parents.An abortive increase of blood lactate and a marked increase in blood pyruvate were observed immediately after ischémie work of the forearm, accompanied by an increase in serum creatine kinase and myoglobinuria. The present case represents a newly described form of genetically determined myopathy.     

血清肌钙蛋白Ⅰ在急性心肌梗死诊断中的临床价值

目的 急性心肌梗死(AMI)是威胁人类生命的主要疾病之一,及时诊治是挽救生命的关键.初步研究表明,肌钙蛋白Ⅰ (cTnI)作为心肌细胞内特有的结构蛋白成分释放入血循环是心肌细胞损伤的高度敏感和特异的标志.本研究通过定性和定量测定比较心肌cTnI与几种常用的AMI诊断标记物的临床应用价值.方法 对40例AMI和65例非心肌梗死患者同时检测血清cTnI、肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)、乳酸脱氢酶(LDH)、天门冬氨酸氨基转移醇(AST)和α-羟丁酸脱氢酶(α-HBD)等6项指标,并进行两组间比较,分别对AMI和非心肌梗死组各指标间的差异作对比分析.结果 cTnI诊断AMI的敏感性(92.5％)高于CK(72.5％)、CK-MB(65.0％)、AST(62.5％)、LDH(60.0％)、α-HBD(62.5％),P＜0.05;cTnI诊断AMI的特异性(96.3％)与CK-MB(93.8％)相近(P＞0.05),高于CK(87.8％)、AST(76.9％)、LDH(84.6％)及α-HBD(81.5％),P＜0.05.结论 cTnI对AMI的诊断具有较高的敏感性和特异性,作为一种心肌损伤的特异标记物,具有较好的临床应用价值.     

An improved spectrophotometric assay of pyruvate dehydrogenase in lactate dehydrogenase contaminated mitochondrial preparations from human skeletal muscle

In mitochondria-enriched preparations of human skeletal muscle, the measurement of pyruvate dehydrogenase activity, as determined by conventional spectrophotometric assay of NADH accumulation, is underestimated due to the oxidizing activity of the contaminating lactate dehydrogenase. Using a model reaction system consisting of varying mixtures of purified lactate and pyruvate dehydrogenases, we found that the presence of oxamate, a competitive inhibitor of the lactate dehydrogenase, allowed the measurement of a linear rate of pyruvate dehydrogenase activity without interference from lactate dehydrogenase. In the presence of 25 mM oxamate, this holds true up to a ratio of 30:1 for lactate to pyruvate dehydrogenases, respectively. A similar result was obtained when using human skeletal muscle mitochondria contaminated by lactate dehydrogenase. Rates of pyruvate dehydrogenase activity ranging from 50 to 120 nmol/min/mg protein could be routinely measured in such mitochondrial fractions. We concluded that the use of oxamate allows a spectrophotometric assay for pyruvate dehydrogenase activity to be utilized when screening for pyruvate dehydrogenase deficiency in mitochondria-enriched preparations of human skeletal muscle.     

慢性肾脏病患者若干血清酶的变化及临床意义

目的探讨慢性肾脏病（CKD）3～5期患者血清酶的变化及其临床意义。方法273例CKD患者根据肾小球滤过率分为三组,检测其血清酶指标,包括天门冬氨酸氨基转移酶（aspartate aminotransferase,AST）、丙氨酸氨基转移酶（alanine aminotransferase,ALT）、肌酸激酶（creatinekinase,CK）、乳酸脱氢酶（lactate dehydrogenase,LDH）、碱性磷酸酶（alkaline phosphatase,ALP）,各组间进行比较,并分别与70例健康体检者（健康对照组）进行比较。结果CKD5期患者的CK、LDH水平高于健康对照组及CKD3、4期;CKD3～5期患者血清ALP水平高于健康对照组,AST水平低于健康对照组;ALT在本研究中各组间差异无统计学意义。结论CKD患者部分血清酶水平不同于健康对照组,这种变化可能与慢性肾脏病患者肾性骨病、贫血、感染等有关,可对疾病临床诊断产生一定的影响。     

Mulligan手法治疗腰椎小关节紊乱的临床疗效

目的：观察运用Mulligan手法治疗腰椎小关节紊乱的临床疗效。方法：82例腰椎小关节紊乱患者随机分为观察组(n = 41)和对照组(n = 41),观察组采用Mulligan手法治疗,对照组采用腰部斜扳法治疗。隔天治疗一次,共治疗三次。2组患者分别在治疗前、治疗后进行视觉模拟评分法和JOA腰背痛疗效评价系统评定,并进行肌酸激酶(CK)和乳酸脱氢酶(LDH)检验。结果：治疗后,观察组VAS评分较治疗前及对照组治疗后有明显下降(P<0.05);观察组血清CK检验数值较治疗前有明显下降(P<0.05);对照组血清CK检验数值较治疗前,观察组与对照组血清LDH检验数值较治疗前均无统计学差异(P>0.05);观察组显效率(含痊愈)及总有效率较对照组有明显升高(P<0.05)。结论：Mulligan手法对腰椎小关节紊乱的疗效明显,可以有效的减轻疼痛,调整腰椎关节,调节腰部周围肌群平衡,从而恢复腰部运动功能。     

注射用灯盏花素对临床生化检验项目的干扰研究

目的研究注射用灯盏花素对常用临床生化检验项目检测结果的干扰。方法将注射用灯盏花素加入体检健康者混合血清标本中作为实验标本,以注射用水加入体检健康者混合血清标本中作为对照标本,采用日立公司7600-010全自动生化分析仪及配套试剂进行总胆红素(TBIL)、直接胆红素(DBIL)、总蛋白(TP)、清蛋白(ALB)、丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)、乳酸脱氢酶(LDH)、尿素(UREA)、肌酐(CREA)、尿酸(UA)、总胆固醇(TCHO)、三酰甘油(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、a-羟丁酸脱氢酶(α-HBDH)、肌酸激酶(CK)、肌酸激酶同工酶MB(CKMB)、钾(K)、钠(Na)、氯(CL)、钙(Ca)检测,并进行统计学分析。结果注射用灯盏花素对CREA、UA、TG、TCHO、HDL-C及LDL-C检测存在干扰可能。结论注射用灯盏花素可干扰部分生化检验项目的检测。对于可能存在药物干扰的检验项目,应在用药前或药物经半衰期代谢后进行检测。     

An increase in creatine kinase secondary to acute pancreatitis: a case report

Creatine kinase (CK) activity is found in high concentrations in skeletal muscle, cardiac muscle and brain. Here, we describe a 64-year-old woman with acute pancreatitis and elevated serum CK activity. This association is extraordinarily rare. In particular, laboratory findings which were found to be abnormal were serum CK 4.150 U/l (peaked 1 day after admission) with the CK-MB fraction being less than 5%, lactate dehydrogenase (LDH) 424 U/l, serum lipase 1.265 U/I and serum amylase 1.105 U/l. Some data regarding the phenomenon of acute pancreatitis and elevated serum CK activity are given.     

Change in concentrations of myogenic components of serum during 93 h of strenuous physical exercise

Effects of 93 h of long, strenuous ranger training on activities of creatine kinase (CK) and lactate dehydrogenase (LD), along with their isoenzymes, and on concentration of myosin light chain were examined in sera of young soldiers. Total CK activity in serum was measured before, during, and after the training. Throughout, total CK activity in serum increased steadily. At the end of the training, activity of CK-MB was increased but its activity ratio to total CK remained unchanged; the activity ratio of LD1/LD2 also was not increased, although total LD activity was increased. Myosin light chain was increased by about fourfold at the end of the training and remained high for three days thereafter. However, its concentration was much lower than in myopathies such as polymyositis and Duchenne muscle dystrophy. The increased activities in serum of total CK and CK-MB isoenzyme on strenuous physical exercise evidently were of noncardiac origin. Although CK activity was comparable with that seen in myopathies accompanied by disintegration of skeletal muscle, the relatively low concentration of myosin light chain in serum suggests minimal skeletal muscle damage.     

IgA-CK-BB complex with CK-MB electrophoretic mobility can lead to erroneous diagnosis of acute myocardial infarction

This patient, on admission, presented with a tentative diagnosis of myocardial infarction: the electrocardiogram showed a nonspecific ST-segment and T-wave abnormalities, and total creatine kinase (CK; EC 2.7.3.2) activity was slightly increased (238 U/L). However, a high electrophoretic value for CK-MB (50% of total CK activity) and the electrophoretic pattern of lactate dehydrogenase (EC 1.1.1.27) isoenzymes ruled out myocardial infarction. The isoenzyme migrating as CK-MB was found later to contain no immunologically normal CK-M subunits, and it was bound to IgA. A mixture of the patient's serum and a human serum control containing all CK isoenzymes showed altered electrophoretic mobility only for CK-BB, indicating that the patient's serum contained antibodies to the B unit of CK. Elution from a Sephadex G-200 column showed that the peak at which most of the anodic CK was eluted corresponded to a molecular mass of approximately 200 kDa. Evidently this atypical isoenzyme was an IgA-CK-BB complex. Because this macro CK type 1 can mimic CK-MB, it may therefore be a source of confusion.     

SARS与其他病毒性肺炎发病不同时期血液生化指标变化特点的比较

目的　通过比较分析严重急性呼吸综合征 (SARS)与其他病毒性肺炎患者血清中各项生化指标的变化特点 ,探讨 SARS发病机制。方法　采用 Roche诊断公司的试剂盒和日立 76 0 0全自动生化分析仪 ,检测 SARS患者和 4 0例其他病毒性肺炎患者发病急性期及恢复后血液中总蛋白 (TP)、血清白蛋白 (Alb)、总胆固醇 (TC)、甘油三酯 (TG)、钙 (Ca)、铁 (Fe)、乳酸脱氢酶 (L DH)、肌酸激酶 (CK)、丙氨酸转氨酶 (AL T)和天冬氨酸转氨酶 (AST)的变化 ,并将 4 0例健康体检者的血指标作为正常对照 ,比较两种病毒性肺炎患者上述各指标的变化和差异。结果　与正常人比较 ,SARS患者急性期血液中 TC、Fe、Ca、Alb明显降低 (P<0 .0 5或P<0 .0 1) ,而血清 L DH、CK、AL T和 AST活性则均升高 ,以 CK的增高和 Fe的下降最为明显 (P<0 .0 5或P<0 .0 1) ;TP和 TG变化不明显。其他病毒性肺炎组 AL T、AST、L DH较正常人稍增高 ,Fe、Ca、Alb、TC、CK稍降低 ,但均无统计学意义 ,TP、TG变化不大。SARS患者恢复期除 AL T、AST仍高于正常 (P均 >0 .0 5 )外 ,其余各指标均恢复到正常范围内。结论　 SARS患者急性期上述血液生化指标的异常变化与其他病毒性肺炎患者相比 ,变化幅度更大 ,大剂量抗病毒药引起 Fe下降和肝脏损害造成 TC合成障碍有重     

Pyruvate dehydrogenase subcomplex with lipoamide dehydrogenase deficiency in a patient with lactic acidosis and branched chain ketoaciduria

The overall and three component activities of pyruvate dehydrogenase complex were measured in the liver and muscle from a patient who died at 1.9 years with increased concentrations of serum lactate, α-ketoglutarate and branched chain amino acids. The component activities of both lipoate acetyltransferase and pyruvate dehydrogenase were similar to those of normal controls, but the overall pyruvate dehydrogenase complex activity was 11 to 30% of controls and lipoamide dehydrogenase activity was not detected. The overall activity was significantly increased by the addition of lipoamide dehydrogenase purified from human liver.Immunochemical studies carried out with antibody prepared against lipoamide dehydrogenase from rat liver, could detect no immunoreactive material in liver and muscle homogenates from the patient, suggesting that the deficiency of lipoamide dehydrogenase activity was due to the lack of enzyme protein.     

Technique and Practical Problems: Determination of Respiratory Gases by Paramagnetic Oxygen Analyser and Carbon Dioxide Catharometer

We report a marked shift in whole-blood glucose measurements when a widely available glucose analyser is used. We compared a conventional glucose dehydrogenase (GDHG) method after protein precipitation and a direct polarographic method in conjunction with immobilized glucose oxidase. The polarographic method gave mean whole blood glucose levels from 79% to 95% of those measured by the GDHG method. No such difference was found in either plasma or serum samples or in water-based control samples.

The stability of glucose in fluoride oxalate tubes appears to be poorer than is usually assumed. We observed a 5-10% decrease in whole-blood glucose concentrations during the first hour after sampling under routine conditions.     

Activity of alcohol dehydrogenase (ADH) isoenzymes and aldehyde dehydrogenase (ALDH) in the sera of patients with breast cancer

Numerous experiments have shown that alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) play a significant role in the metabolism of many biological substances. Some metabolic disorders that can lead to breast carcinogenesis may be the cause of changes in ADH and ALDH activity. In previous experiments we found a changed level of class I ADH activity in breast cancer tissues. The changed level of this enzyme in cancer cells may be reflected by the enzyme's activity in the serum. Therefore, in this study we measured the activity of ADH isoenzymes and ALDH in the sera of patients with breast cancer. Serum samples were taken for routine biochemical investigation from 45 women with breast cancer before treatment. Among all tested classes of ADH isoenzymes, only class I had higher activity in the serum of patients with breast cancer in stage IV. The total ADH and ALDH activities were not significantly higher in patients with breast cancer than in healthy controls. The changes in activity, especially in class I ADH, appear to be caused by isoenzymes being released from the organ damaged by metastatic disease.