血清CK-MB活力假性增高原因分析及临床意义

目的 探讨某些非心源性疾病患者血清肌酸激酶同工酶（CK-MB）活性升高的原因及与疾病的关系。方法 采用日立7180型全自动生化分析仪测试CK及CK-MB,检出CK-MB异常升高者,且CK-MB/CK超过30%者,进一步用CK同工酶琼脂糖凝胶电泳鉴定,并结合病情进行分析。结果 42例非心肌梗死患者血清标本中（包括3例溶血标本）,总CK活力相对较低,癌症患者CK-MB假阳性比例较大,其中CK-MB占CK总活力在30%-49%有24例,大于50%的有18例。42例经CK同工酶电泳证实,CK-MB活性实际为正常,但出现脑型肌酸激酶同工酶（CK-BB）或异常CK同工酶带。结论 应用酶免疫抑制法测定非心肌梗死患者CK-MB时,如果CK-MB超过CK30%以上,可能是血清中CK-BB、巨CK、腺苷酸激酶的存在,影响CK-MB的假性升高。     

免疫抑制法检测血清肌酸激酶同工酶活性高于肌酸激酶总活性的原因探讨

目的探讨肌酸激酶同工酶(CK-MB)活性高于肌酸激酶(CK)总活性的原因。方法用免疫抑制法测定出现CK-MB活性高于总活性的20例患者血清、20例心肌梗死患者血清、20例健康体检者血清。对这三组标本同时用免疫抑制法测CK-MB、酶法测总CK;用电泳法分离各个组分,由扫描仪对各条酶谱进行扫描。结果CK-MB活性高于总活性的患者血清中在CK-MM、CK-MB中间多出一条区带,为巨CK;或在CK-MM后面靠阴极端出现一条CK-MT区带。结论对于CK-MB活性高于CK总活性的患者血清,建议用其他方法进行复查,避免假阳性对实验结果的影响。     

9例CK-MB活性高于CK总活性的原因探讨

目的分析血清肌酸激酶同工酶(CK-MB)活性高于肌酸激酶(CK)总活性的原因。方法使用VITROS350干式化学仪器及其配套试剂,回顾性分析9例免疫抑制法检测CK-MB活性高于CK活性的患者,分析心肌酶谱检测结果,比较心电图及脑部CT检查结果。结果由于免疫抑制法的方法学原因导致CK-MB活性高于CK总活性。9例患者中6例为脑梗死,3例为恶性肿瘤。当总CK活性200U/L,CK-MB/CK25%,表明肌酸激酶脑型同工酶或巨型肌酸激酶存在,与6例脑梗死患者病情相符。恶性肿瘤患者CK-MB活性高于CK总活性时,需做测定空白,以扣除血清中残留的腺苷酸激酶活力的影响。结论当CK-MB活性高于总CK活性时,要针对疾病的不同情况,及时与临床联系,避免误诊及漏诊。     

血清CK-MB活性大于总CK活性的原因初探及处理

目的 对血清CK-MB活性大于总CK活性的现象进行原因初探及处理.方法 在HITACHI 7600-020全自动生化仪上采用免疫抑制法测定样本CK和CK-MB活性,依据CK-MB活性测定值分为恶性肿瘤患者组、心肌梗死组和正常组.同时利用热失活(将血清置于45℃水浴20 min后)再次测定其CK和CK-MB活性:在MINIVIDAS全自动荧光酶标仪上采用荧光免疫法测定CK-MB质量.结果 20例恶性肿瘤患者血清免疫抑制法测定CK-MB＞CK,热失活处理后CK-MB常规方法测定活性保存率在43.4%～78.1%,均数为59.2%;而心肌梗死组和健康体检者组的活性保存率均＜1%.结论 恶性肿瘤中的异常CK同工酶被认为是造成CK-MB假性增高的重要原因之一,利用热失活方法可以有效鉴别.CK-MB质量测定法因其方法学特性,可以排除上述干扰,是鉴别CK-MB假性增高的最佳方法.     

肌酸激酶同工酶MB活性大于总肌酸激酶活性的原因分析

目的分析血清生化指标肌酸激酶同工酶MB(CK-MB)活性大于总肌酸激酶(CK)的原因。方法对该院2015年1~9月同时检测血清CK和CK-MB的16 262例门诊标本结果进行分析。结果共发现CK-MB活性大于总CK的标本24例,其中心血管神经系统疾病患者14例、肿瘤患者4例、风湿病患者1例、妊娠期妇女3例、儿科患者2例。结论当体内出现大量CK-BB和巨CK时,会影响免疫抑制法检测CK-MB的活性,从而造成CK-MB的假性增高。虽然免疫抑制法检测简单迅速,但存在局限性,临床需结合检测原理和患者病情加以鉴别,避免误诊。     

血清肌酸激酶同工酶活性大于肌酸激酶活性常见原因分析

目的 探讨肌酸激酶同工酶(CK-MB)活性大于肌酸激酶(CK)活性的常见原因.方法 选取2009年1月至2010年1月住院患者中CK-MB活性大于或等于CK活性,临床已排除心肌梗死的患者26例,CK测定采用速率法,CK-MB测定采用免疫抑制法.结果 26例患者中脑损伤21例(包括急性颅脑损伤、自发性脑出血及头晕待查的患者),肿瘤患者3例,其他不明原因者2例.结论免疫抑制法测定CK-MB是建立在忽略CK-BB基础上的,易受到巨CK或CK-BB异常增高的干扰,这种方法学上的缺陷是造成CK-MB活性大于或等于CK活性的主要原因.可通过琼脂糖电泳法,最终确定有无CK-BB或巨CK的干扰,也可用此法直接测定CK-MB.     

免疫抑制法检测患者血清CK-MB假性升高原因分析

目的：评价免疫抑制法测定CK-MB在临床上的应用意义。方法在罗氏MODULAR全自动生化分析仪检测系统上,分别用免疫抑制法和速率法检测血清CK-MB和CK,计算CK-MB/CK比值;对CK-MB/CK比值大于30%的样本结果进行统计分析。结果血清CK-MB/CK比值大于30%的114例患者血清中,恶性肿瘤患者51例,占44.7%;心脑血管疾病26例,占22.8%;2型糖尿病13例,占11.4%;类风湿性疾病4例,小儿支气管炎3例,其余17例。结论免疫抑制法测定CK-MB存在假性升高,当CK-MB/CK比值大于30%,应警惕CK-BB或巨肌酸激酶（巨CK）的存在,结合临床症状可排除心肌梗死,以免造成误诊和漏诊。     

免疫抑制法测定CK-MB活性假性升高40例分析

肌酸激酶同工酶（CK-MB）是肌酸激酶（CK）的同工酶之一,是临床诊断心肌梗死的主要酶学指标,其测定方法很多,目前临床检验工作中广泛采用免疫抑制法。但由于免疫抑制法测定CK-MB存在一定检测方法学方面的误差,对某些不存在心肌损害的人群,受其血清中巨CK或含量较高的CK-BB的影响,应用免疫抑制法测出的CK-MB会假性增高,常会误导临床诊断。     

免疫抑制法检测肌酸激酶同工酶活性高于肌酸激酶的临床价值分析

目的探讨免疫抑制法检测肌酸激酶同工酶(CK-MB)结果高于肌酸激酶(CK)活性的临床价值。方法回顾分析4例免疫抑制法检测CK-MB结果高于CK活性的病例,并比较心内科与脑外科心肌酶谱检测结果CK-MB/CK比值。结果结果4例病例中3例为颅脑损伤,1例为结肠癌术后,4例病例均无心肌损伤;脑外科CK-MB/CK比值明显高于心内科(P<0.05)。结论免疫抑制法检测CK-MB活性假性高于CK活性,或CK-MB/CK比值上高有重要的脑损伤警示价值。     

血清CK-MB/CK大于45.9%在肿瘤筛查中的应用

目的：评价血清肌酸激酶同工酶（CK-MB）活性与肌酸激酶（CK）活性的比值在健康体检人员中进行恶性肿瘤筛查的价值。方法：回顾性研究。收集2009年8月至2013年9月间的住院患者,经组织病理学检查确诊为恶性肿瘤的患者120例,健康对照组120例为来我院健康体检者,排除恶性肿瘤及任何心源性及其它疾病。用BECKMAN COULTER AU680生化系统进行血清肌酸激酶同工酶和肌酸激酶活性的检测,计算二者的比值,并采用t检验进行统计学分析。结果：健康对照组120例,CK-MB/CK平均值为25.2%,肿瘤组CK-MB/CK的平均值为45.9%,经统计学分析,二者有显著区别。结论：健康查体人员若CK-MB/CK升高,应该做进一步的检查,以便排除是否有恶性肿瘤的发生。     

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.     

Apparent elevation of serum CK-MB not due to acute myocardial infarction.

An increased serum level of the MB isoenzyme of creatine kinase (CK-MB) is a useful marker for acute myocardial infarction. Although described extensively in clinical chemistry literature, there is little information in standard medical references about false positives for this test. We report two cases where high levels of measured CK-MB activity were in fact due to another form of CK, associated with internal malignancy.     

APPARENT ELEVATION OF SERUM CK-MB NOT DUE TO ACUTE MYOCARDIAL INFARCTION

An increased serum level of the MB isoenzyme of creatine kinase (CK-MB) is a useful marker for acute myocardial infarction. Although described extensively in clinical chemistry literature, there is little information in standard medical references about false positives for this test. We report two cases where high levels of measured CK-MB activity were in fact due to another form of CK, associated with internal malignancy.     

Release patterns of CK-MB and mitochondrial CK following myocardial ischaemia

Following myocardial damage as in acute myocardial infarction (AMI) or open heart surgery, the tissue damage might result in a release of mitochondrial CK (CK-MIT). The presence of this CK isoenzyme in serum may be detected after chromatographic separation of CK-activity on Sephacryl S-200. By combining chromatographic separation of CK-MB with immunologic inhibition of CK-M, both CK-MB and CK-MIT can be estimated in serum. Using this procedure changes in enzyme activities were studied in ten patients with AMI and twelve patients subjected to open heart surgery using cardioplegia. Following AMI CK-MB peaked about 24 h after onset of ischaemic symptoms. CK-MIT increased similarly and reached a plateau after 24 h where it remained during an additional 24-36 h. At peak CK-MB concentration, the corresponding CK-MIT activity was about 22% of the CK-MB activity. Following cardiac surgery there was a rapid release of CK-MB with a peak about 5 h after release of aortic cross-clamping, and with a simultaneous CK-MIT activity amounting to 19% of the CK-MB activity. In conclusion, CK-MIT is released into serum following myocardial ischaemia. Its appearance has time characteristics similar to that of other mitochondrial enzymes. The CK-B method does not specifically determine CK-B, but non-CK-M, which in cardiac ischaemia at peak serum CK-MB concentrations includes about 20% CK-MIT.     

影响肌酸激酶同工酶活性检测结果的因素探讨

目的探讨应用酶免疫抑制法检测血清肌酸激酶（CK）同工酶——CK—MB酶活力单位时,引起临床假阳性的因素,以科学合理地解释每一检测结果及解决方法。方法采用回顾性研究,分析125例非心肌梗死患者,应用酶免疫抑制法检测血清标本中CK、CK—MB酶活力单位,分析可能引起检测值CK—MB酶活力单位假性升高的影响因素。结果86例成人非心肌梗死患者中,总CK活力相对较低,癌症患者、脑梗死患者、变态反应疾病患者CK—MB假阳性比例较大,其中CK—MB占CK总活力大于5％有59例,其中53例在6％～21％,6例大于38％;38例新生儿中CK活性范围为145～1974U／L,其中1例新生儿呼吸窘迫综合征患儿CKMB占CK总活力达90％;另1例溶血标本也引起假阳性。结论应用酶免疫抑制法检测非心肌梗死患者CK—MB酶活力单位假性升高的影响因素,可能是血清中存在巨CK、CK—BB、AK等,影响试剂单克隆抗体与肌酸激酶中的M亚基结合,存在未被抑制的CK—M、M亚基同时与B亚基参加酶促反应,而且因计算时结果乘以2,更加扩大误差,是该方法学缺点造成的错误结果,不能作为诊断依据。     

The value of serum CK-MB and myoglobin measurements for assessing perioperative myocardial infarction after cardiac surgery

In 41 patients who underwent coronary bypass surgery, creatine kinase (CK)-MB mass concentration was repeatedly measured in serum during and after the intervention using a new two-site immunoenzymetric assay (IEMA). Serum CK-MB activity was determined with the use of four different techniques: immunoinhibition, immunoinhibition-immunoprecipitation, column chromatography and electrophoresis. Myoglobin (Mb) was also measured in each specimen by radioimmunoassay. In the 33 patients who followed a completely uneventful postoperative course, the cumulated CK-MB release was, on the average, 12.2-fold less than after acute myocardial infarction. The CK-MB peak concentrations using the IEMA were 33 +/- 3 micrograms/l (X +/- SEM) and occurred 6.4 +/- 0.5 h after the intervention was started; CK-MB levels had decreased to 2.9 +/- 0.4 micrograms/l at the end of the first postoperative day. The evolution of the CK-MB concentration was parallel to that of the enzyme activity. The serum Mb maximum concentrations (518 +/- 39 micrograms/l) were reached after 3.3 +/- 0.1 h. The other eight patients developed perioperative myocardial infarction (PMI); in this group, the cumulated CK-MB release was higher, and the serum CK-MB postoperative curves were of three different types. The patients with delayed CK-MB peaks (type I pattern) or sustained elevations (type III) of this isoenzyme also showed increased serum Mb levels at the end of the first postoperative day. The PMI patients with early (10 h) CK-MB elevations (type II) did not demonstrate abnormal serum Mb levels.(ABSTRACT TRUNCATED AT 250 WORDS)     

Serum CK-MB isoenzyme after aortic and mitral valve replacements

A release of the MB fraction of creatine kinase (CK) enzyme into the serum due to myocardial manipulation and trauma occurs in patients undergoing cardiac surgery. Thus, the appearance of CK-MB activity as such is not sufficient to indicate of perioperative myocardial infarction. The mean (+/- SD) serum CK-MB isoenzyme level was 95 +/- 103 U/l 18 hours after aortic or mitral valve replacement in 76 patients. Thirteen patients undergoing closure of an atrial septal defect served as controls. They had a significantly lower (p less than 0.01) isoenzyme level postoperatively: 45 +/- 39 U/l. Two patients had the ECG changes of definite myocardial infarction after valve replacement and they also showed high CK-MB values, while the other patients with high enzyme level had no ECG signs suggesting acute infarction. CK-MB values correlated with the aortic cross-clamping time (r = 0.39, p less than 0.001) and weakly with the precordial ECG voltage of SV1 + RV5 (r = 0.25, p less than 0.01). While these findings may reflect the sensitivity of a thick myocardial wall to ischaemia during surgery, the postoperative recovery was not related to the serum CK-MB level.     

Diagnostic use of CK-MM and CK-MB isoforms for detecting myocardial infarction

Following acute myocardial infarction, total CK and CK-MB levels begin to rise 5 to 6 hours after the onset of chest pain. The serial profile of the rise and fall of both activities is nearly always indicative of AMI. The recent increase in the use of thrombolytic agents in an attempt to attain reperfusion of occluded coronary arteries alters the enzyme profiles observed in blood after AMI. After successful reperfusion a washout phenomenon occurs in which early restoration of blood flow to damaged myocardium causes an early rise in total CK and MB levels above the normal range 2 to 4 hours after AMI, with earlier and higher peak enzyme values. Recently reports have appeared describing numerous serum and plasma CK-MM and CK-MB isoform patterns after AMI. Following release from injured myocardium CK-MM3 and CK-MB2 (designated the tissue isoforms) are converted in the circulation to post-translation products (MM2, MM1, MB1, respectively). Studies have now shown that CK-MM isoform patterns provide a unique means of assessing the time of onset of necrosis and a monitor of the duration of enzyme release from the site of injury. Following AMI, MM3, the MM3/MM1 ratio, or both rises and peaks earlier than either total CK or CK-MB levels. During successful reperfusion, the rate of rise of CK-MM3 is more rapid and the MM3/MM1 ratio peaks earlier than without reperfusion. However, any concomitant release of CK-MM3 from skeletal muscle would decrease the clinical utility of MM isoforms in detecting myocardial damage. Recent advances in technology have shown that CK-MB2 rise parallels the CK-MM increase and also rises earlier than total CK and total MB levels and provides increased specificity for the myocardium. The full potential of the diagnostic utility of MM and MB isoforms will not be realized until a reliable, sensitive, simple, and rapid quantitative assay becomes available.     

Effect of creatine kinase-MM subtype composition on a CK-MB immunoinhibition assay

Immunoinhibition (INH) by use of polyclonal anti-human CK-M antibody may be used to measure CK-MB in serum. Previous studies have shown that inhibiting antibodies prepared against purified muscle extracts may inhibit CK-MM by greater than 99%. Using patients' sera and muscle homogenates incubated with human serum, we studied the effect of CK-MM subtype composition on an INH assay. We found that with increasing time from the CK-releasing event, e.g., myocardial infarction, or with longer in vitro incubation, the proportion of CK-MM1 increased and the proportion of uninhibited CK-MM increased from 0.2% to 0.7-0.8%. As a consequence, CK-MB activity may be overestimated by as much as 1.6% of total CK when uncorrected INH results are used. Inhibition was maximal in samples containing 100% CK-MM3, the tissue subtype. Because of the time-dependent change in CK-MM subtypes, published results for INH from studies in which CK-MM purified from muscle was used may not be directly applicable to clinical specimens.