A 46-year-old male patient was diagnosed as suffering from acute myocardial infarction, but his serum creatine kinase (CK) level was extremely low and no CK isozymes were detected in the serum. The total CK activities in the skeletal muscle amounted to only 2% of that of the control. Electrophoresis of the CK isozymes in the skeletal muscle showed that CK-MM was absent but the CK-BB and abnormal isozyme bands were present. There was no evidence of myocardial ischemia, although the exercise treadmill test revealed ST segment depression in the chest leads. One of the patient's sisters had an extremely low serum CK level suggesting inheritance of this abnormality. This is the first report of a case showing familial deficiency of CK.

We describe the influence of autoantibodies that bind creatine kinase BB (CK-BB) on the methods for MB isoenzyme. If these autoantibodies are present in patients' sera, they cause the formation of macro CK type 1 (immunoglobulin-linked CK-BB). In some of these cases they can bind not only endogenous CK-BB but also CK-MB without significantly affecting enzyme activity. Although these antibodies show distinctly less affinity for CK-MB than for CK-BB, they nevertheless bind CK-MB in these particular sera, because their concentration exceeds that of CK-BB isoenzyme. If a person with such autoantibodies has an acute myocardial infarction, the immunoinhibition method for CK-MB, which does not discriminate between CK-MB and CK-BB, will recognize the increase and peak of CK-MB with time, although persistent macro CK activity will be superimposed on the typical isoenzyme pattern. However, isoenzyme electrophoresis and recently introduced immunoenzymometric assays for CK-MB in these cases may be less sensitive for detecting myocardial infarctions, because the typical increase in CK-MB activity may be identified later in the progression of symptoms, or even be missed.

With the objective of evaluating the clinical usefulness of a new immunologic method (Merck-1-Test CK-MB), in the determination of the CK-MB activity, 48 patients admitted to the Coronary Unit for angina pectoris were studied. Samples of blood were gathered upon admission and every 4 hours for 48-72 hours, determining in each one of them the total CPK, SGOT, LDH, and CK-MB; electrocardiograms (ECG) were taken and all possible causes for the increase in the enzymatic activity were recorded. Results were analyzed in order to study the following aspects: in the patients in which an acute myocardial infarction was diagnosed the CK-MB activity was studied, also the relation of CK-MB to the remaining parameters, each parameter's sensitivity and specificity and the relationship of the CK-MB to the prognosis of the patients. The usefulness of CF-MB in the differential diagnosis of myocardial necrosis and variations in the total CKP curve in the clinical course of acute myocardial infarction unrelated to myocardial necrosis were evaluated too. The following conclusions were drawn from the analysis of the data. The immunological method has the advantages of its sensitivity and easily and quickly performance (15 minutes), but it has the disadvantage that it detects CK-BB (elevated in cebrovascular disorders). Twenty-four hours after the onset of symptoms, the negativity of CK-MB does not exclude the diagnosis of a myocardial necrosis. CK-MB is more sensitive than total CPK in diagnosing the extent of the area of necrosis. CK-MB is very specific for myocardial necrosis but less sensitive than other parameters. A positive CK-MB upon the patient's admission confirmed the diagnosis of necrosis in 60 percent of the cases, but in 18 percent error was induced because of false positives. CK-MB permitted confirmations of the diagnosis of myocardial infarction in 33 percent of cases in which there was only a suggestion of necrosis by the ECG. The variation in the curve of total CPK in the course of an acute myocardial infarction is subjected to such a great number of factors intercurrent with time, that caution should be exercised in trying to relate a specific elevation of total CPK to an unsuccessful maneuver or to a possible extension of the area of necrosis.

Malignant hyperthermia developed in the 94th minute of anesthesia undergone by a nearly 5-year-old girl. Two minutes after re-filling the halothane vaporizer, muscle rigor and tachyarrhythmia occurred. Massive myoglobinuria setting in on the day of operation reached its peak on the 1st postoperative day. Only following this were the highest CK activities to be recorded. CK-BB could not be detected at any time.

OBJECTIVE

To compare the effects of three traditional Chinese medicinal compounds on energy metabolism related enzymes in cerebral tissue of rats after focal cerebral ischemia and reperfusion (I/R).

METHODS

The local cerebral I/R model was established by ligation of the middle cerebral arteries (MCA). The animals were divided into the sham-operative group, the model group, the Yiqi Huoxue Recipe (YHR) group, the Zhengan Xifeng Decoction (ZXD) group and the Xinglou Chengqi Decoction (XCD) group. The mitochondria in brain tissue was obtained by density-centrifugation and differential centrifugation, then the activities of succinate dehydrogenase (SDH), Na+ -K+ -ATPase, creatine kinase-BB (CK-BB) in homogenate of brain tissue were measured by chemical chromometry.

RESULTS

Activities of SDH and Na+-K+ -ATPase were lower and that of CK-BB was higher in the model group than those in the sham -operative group at all time points after I/R (P< 0.01). Compared with those in the model group, activity of Na+ -K+ -ATPase was higher only in the ZXD group at 24 h after I/R, while at 48 h and 72 h after I/R, activities of both SDH and Na+ -K+ -ATPase were higher in all the treatment groups. As for the activity of CK-BB, it was lower in all the treatment groups (P < 0.05). The optimal effect was shown in the ZXD group at 24 h, in the XCD group at 48 h, and in the YHR group at 72 h after I/R.

CONCLUSIONS

The three traditional Chinese medicinal compounds could reduce pathologic injury after focal cerebral I/R in rats by promoting activity of SDH and Na+ -K+ -ATPase and inhibiting that of CK-BB, the optimal effect of ZXD was shown at 24 h after I/R, that of XCD at 48 h after I/R and of YHR at 72 h after I/R.

Background" Autism spectrum disorder (ASD) is a serious neurodevelopmental disorder that impairs a child's ability to communicate with others. It also includes restricted repetitive behaviors, interests and activities. Symptoms manifest before the age of 3. In the previous studies, we found structural abnormalities of the temporal lobe cortex. High spine densities were most commonly found in ASD subjects with lower levels of cognitive functioning. In the present study, we retrospectively analyzed medical records in relation to the neonatal levels of total serum bilirubin (TSB), neuron-specific enolase (NSE), creatine kinase brain band isoenzyme (CK-BB), and neonatal behavior in ASD patients from Southern China.

METHODS

A total of 80 patients with ASD (ASD group) were screened for this retrospective study. Among them, 34 were low-functioning ASD (L-ASD group) and 46 were high-functioning ASD (H-ASD group). Identification of the ASD cases was confirmed with a Revised Autism Diagnostic Inventory. For comparison with ASD cases, 80 normal neonates (control group) were selected from the same period. Biochemical parameters, including TSB, NSE and CK-BB in the neonatal period and medical records on neonatal behavior were collected.

RESULTS

The levels of serum TSB, NSE and CK-BB in the ASD group were significantly higher when compared with those from the control group (P < 0.01, or P < 0.05). The amounts of serum TSB, NSE and CK-BB in the L-ASD group were significantly higher when compared with those in the H-ASD group (P < 0.01, or P < 0.05). The Neonatal Behavioral Assessment Scale (NBAS) scores in the ASD group were significantly lower than that in the control group (P < 0.05). Likewise, the NBAS scores in the L-ASD group were significantly lower than that in the H-ASD group (P < 0.05). There was no association between serum TSB, NSE, CK-BB and NBAS scores (P>> 0.05) in the ASD group.

CONCLUSIONS

The neonatal levels of TSB, NSE and CK-BB in ASD from Southern China were significantly higher than those of healthy controls. These findings need to be investigated thoroughly by future studies with large sample.

OBJECTIVE

This study was carried out on cerebrospinal fluid (CSF) to investigate the perioperative course of certain ischaemic markers, namely neurone-specific enolase (NSE), creatine kinase (CK-BB), hypoxanthine, and lactate in order to identify a disturbed cerebral energy utilisation which could be responsible for the development of temporary mental dysfunctions. Those dysfunctions are characterised by preserved memory content and perception, but the coordination and association of these functions are disturbed. Typical clinical signs are motor restlessness, disordered emotions, and symptoms of dementia. Little is known about the aetiology of those symptoms, but they are most likely due to various events, such as direct drug effects, the extent of surgical trauma, sensorial deprivation, and disturbed perfusion.

METHODS

Eight orthopaedic patients (ASA III or IV) scheduled for removal of their total hip replacement were anaesthetised by catheter-spinal anaesthesia (CSA) for pain relief in combination with standardised, modified neuroleptanalgesia (NLA). At six defined times (15 hours preoperatively, immediately before and after surgery and 6, 24, and 36 hours postoperatively) CSF samples were drawn and the ischaemic markers were determined by means of radioimmunoassay (NSE), electrophoresis (CK-BB), photometry (lactate), and high-pressure liquid chromatography (hypoxanthine). The release of ischaemic markers into CSF correlates linear with the extent of ischaemic brain damage.

RESULTS

Mean concentrations of the following ischaemic markers increased in all patients intraoperatively: NSE from 12.3 ng/ml to 13.4 ng/ml, hypoxanthine from 1.86 mumol/l to 3.73 mumol/l, and lactate from 1.4 mmol/l to 2.0 mmol/l respectively, all of which returned to normal within 36 hours. The CK-BB concentrations were all within normal values and not affected by the operation during this investigation.

CONCLUSIONS

Although no clinical signs of temporary mental dysfunction have been observed, the results indicate that in CSF ischaemic markers temporarily undergo certain changes in their concentrations during the removal of total hip replacements in elderly patients. These changes are reason for assuming that risk patients may suffer a temporary disturbed cerebral energy utilisation intraoperatively, even if stable clinical and cardiovascular conditions prevail under anaesthesia. Such a temporary ischaemic penumbra might be responsible for the postoperative development of temporary mental dysfunctions.

BACKGROUND

In a prospective study, we measured plasma markers of myocardial damage induced by radiofrequency catheter ablation (RFA) with the protein biochip microarray system.

METHODS

A total of 32 consecutive patients undergoing RFA for atrioventricular nodal re-entry tachycardia (AVNRT), right atrial flutter (AFL) and atrial fibrillation (AF) were included in the study. Cardiac troponin I (cTnI), creatine kinase isoenzyme MB (CK-MB), heart-type fatty acid binding protein (hFABP) and glycogen phosphorylase BB (GPBB) were measured using biochip array technology at baseline and 24 h after the procedure.

RESULTS

Values for all markers increased 24 h after RFA (cTnI: 0.92+/-0.49 microg/L vs. 0.33+/-0.06 microg/L, p<0.001; CK-MB: 3.79+/-2.04 microg/L vs. 1.85+/-0.55 microg/L, p<0.001; hFABP: 2.82+/-0.95 microg/L vs. 2.00+/-0.95 microg/L, p<0.001; GPBB: 9.07+/-5.83 microg/L vs. 4.70+/-2.50 microg/L, p<0.001). The correlations between plasma marker levels and RFA time were cTnI: r=0.63, p<0.01; CK-MB: r=0.75, p<0.01; hFABP: r=0.55, p<0.05, GPBB: r=0.51, p<0.05; the correlation between RFA time and number of RF applications was significant (r=0.81, p<0.001). Patients with RFA due to AF or flutter had elevated cTnI, CK-MB and hFABP levels compared to patients with AVNRT (cTnI: 1.14+/- 0.49 microg/L vs. 0.59+/-0.25 microg/L, p<0.05; CK-MB: 4.46+/- 2.07 microg/L vs. 2.81+/-1.54 mug/L, p<0.05; hFABP: 3.21+/- 0.98 microg/L vs. 2.25+/-0.54 microg/L, p<0.01).

CONCLUSIONS

Myocardial injury induced by RFA can be detected by cTnI, CK-MB, hFABP and GPBB. Plasma cTnI, CK-MB and hFABP levels significantly increased in patients with AFL and AF compared to patients with AVNRT. The increase of cTnI, CK-MB and GPBB levels correlates with the total duration of RFA.

Although central nervous system (CNS) involvement, such as intellectual impairment simulating dementia, in myotonic dystrophy (MyD) has been well documented, the cause of this condition remains unclear. In has been reported that the progressive cases of MyD are often accompanied with respiratory disturbance and sleep apnea syndrome (SAS). We studied the relation between CNS involvement and respiratory disorders in 15 MyD patients. They consisted of 10 males and 5 females with ages ranging from 21 to 58 years (average 46 +/- 8.4 years old). Arterial blood gas (ABG) analysis, respiratory function test, and monitoring of arterial oxygen saturation (SaO2) during sleep were carried out. In some cases abnormal respiration during sleep was analyzed with polysomnography. For an assessment of CNS involvement the following examinations were performed; intelligence quotient (WAIS-IQ); electroencephalography (EEG); brain computed tomography (CT); and cerebrospinal fluid (CSF) levels of neuron-specific enolase (NSE), S-100b and creatine kinase BB isoenzyme (CK-BB) which were estimated by using enzyme immunoassay. ABG analysis demonstrated the presence of hypercapnia (PaCO2>> 45 torr) during wakefulness in MyD patients. During sleep 14 of the 15 patients showed frequent desaturation phenomenon (SaO2 < 90%), indicating the episodic hypoxemia. Polysomnographic study revealed the occurrence of SAS of both obstructive and central types in all the cases examined. IQ test disclosed intellectual impairment in 80% of the 15 patients, and EEG showed slowing of basic rhythm in the majority of the cases. On brain CT both enlarged ventricles and dilated sulci were commonly observed.(ABSTRACT TRUNCATED AT 250 WORDS)

High CK BB isoenzyme activity has been demonstrated in the CSF of many patients with various neurologic disorders and is considered to reflect brain tissue damage [1, 2]. Increased CK BB activity in the CSF has been described in a patient with fatal pneumonococcal meningitis [3] and also in two patients with viral encephalitis [1]. Since routine laboratory tests are of limited value for assessing the prognosis of patients with CNS infections, the present investigation was undertaken to study the possibility of early detection of brain tissue damage in such patients by determining the CK BB activity in the CSF. The CK BB activity in the control subjects was less than or equal to 10 nkat/liter, which is in accordance with a previous study based on bioluminescence assay [2]. Six of the seven patients with neurologic complications in the present study had marked increases of the CK BB activity. In the patient with brain death due to HSV infection, serial measurements of the CK BB activity in the CSF have shown a maximal fourfold increase from the value of 45 nkat/liter found on admission. In one of the patients with purulent meningitis who developed a slight hydrocephalus, the CK BB activity was normal, but no focal brain damage was found by computed tomography in this case. The results indicate that increased CK BB activity in the CSF is related to the clinical outcome of patients with infections of the CNS. Thus, the determination of the CK BB activity seems to be useful for assessing the prognosis of patients with bacterial and viral meningitis and encephalitis.

The serum concentrations of both CK-BB and NSE in patients with various lung carcinoma have been determined by the enzyme immunoassay. Serum CK-BB levels were found to be significantly increased (less than 1.0 ng/ml) in patients with a small cell carcinoma (51 cases, 74.5%), adenocarcinoma (77 cases, 36.5%), and a squamous cell carcinoma (68 cases, 39.7%). The serum NSE levels also were increased (less than 6.0 ng/ml) in cases of small cell carcinoma (72.5%), adenocarcinoma (27.3%), and squamous cell carcinoma (26.5%). Since the serum concentrations of bos CK-BB and NSE changed in parallel with the clinical course, they may be useful biomarkers for monitoring the clinical course of patients with lung cancer, especially in cases of small cell carcinoma.

We evaluated the effectiveness of 5-day antibacterial therapy for bacterial meningitis in children. The study group included 26 children from 2 months to 15 years of age, admitted with microbiologically confirmed bacterial meningitis in 1990-1993 and treated for 5 days. A historical comparison group of 49 patients treated for 8 to 15 days was used. Penicillin monotherapy (300 mg/kg body weight) was used for meningococcal and pneumococcal meningitis and ampicillin (300 mg/kg body weight) for Haemophilus influenzae b meningitis. On day 5 of therapy the activity of aspartate aminotransferase (AST), lactic dehydrogenase (LDH), creatine phosphokinase (CPK) and gamma-glutamyl-transpeptidase (gamma GT) in the CSF was determined by photocolorimetric assay and the concentration of creatine kinase BB (CK-BB) by ELISA. IL-6 was analysed using EIA technique and a cerebral ultrasound was performed at the time of the termination of the antibacterial therapy. The mean follow-up time was 1.3 years for children in the study group and 3.2 in the control group. The time of hospitalisation was shorter in children treated for 5 days (p < 0.005). Complete clinical recovery was 81% in the study group and 66% in the comparison group at the time of the termination of antibacterial therapy. No relapses occurred. The activity of AST, CPK, LDH, and gamma GT in the CSF had returned to normal by the 5th day of therapy, but almost a 7-fold higher concentration of CK-BB was registered. The concentration of IL-6 in the CSF decreased with the therapy from 1,800 pg/ml to 685 pg/ml but still remained high.(ABSTRACT TRUNCATED AT 250 WORDS)

In a group of 3000 hospital patients the prevalence of immunoglobulin bound creatine kinase (macro CK type 1) was 4.3%. The relative frequency was greater in the older age categories. The highest prevalence was found in patients with rheumatic and cardiac diseases. In a group of 556 cardiac patients selected for coronary angiography a prevalence of 13.8% was observed. No significant correlation was obtained between the findings of the coronary angiography and the activity of macro CK type 1. CK MB results determined by ion-exchange or immuno-inhibition techniques in macro CK type 1 positive patients are falsely positive. Macro CK type 1 may be seen as an antigen-antibody complex against CK BB, which originates at least partly from the vascular wall.

Surfactant replacement therapy in patients with neonatal respiratory distress syndrome (RDS) is a new therapeutic approach. There is now convincing evidence that the incidence and severity of RDS can be reduced. Surfactant (CUROSURF) was intratracheally applied to a group of fifteen intubated preterm infants with severe RDS (29 +/- 2.1 weeks of gestation and 1204 +/- 301 g birth weight) at 9.1 +/- 2.5 hours of life. For detection of potential neurological risk we performed serial ultrasound examinations (US), serial measurements of Creatine-Kinase Isoenzyme levels (CK-BB) looking for the presence of human antibodies to different brain antigens (BSA) as markers for neonatal cerebral injury. Using these diagnostic methods, there was no evidence of any negative influence of surfactant therapy on cerebral function of treated preterm infants.

A 58-year-old Chinese male presented with precordial distress and was found to have elevated creatine kinase (CK)-myocardial bound (MB) (determined by the Kodak Ektachem Clinical Chemistry Slide method) activity and an abnormal electrocardiogram. Eventually, the patient was diagnosed with an annular ulcerative tumor 10 cm above the anal orifice. The tumor was an adenocarcinoma of the rectum and was immunoreactive for CK-BB (brain type). CK isoenzyme electrophoresis disclosed both BB and MM (muscle type) bands. We concluded that the level of CK-MB determined using the Kodak Ektachem Clinical Chemistry Slide method was spuriously elevated in our patient with adenocarcinoma of the rectum, without evidence of myocardial injury. Institutions using the Kodak Ektachem Clinical Chemistry Slide system for CK should be aware of this possibility.

A case of a spurious rise in cardiac troponin-T in an 85 year old Caucasian man with myelodysplastic syndrome and multiple malignancies but with intact cardiac and renal function is reported. The patient presented to the accident and emergency department with fever and chest pain. Inconsistent laboratory findings in biochemical markers diagnostic of myocardial infarction were observed. Discrepant findings included a rise in the concentration of the cardiac specific marker troponin-T in the absence of an increase in creatine kinase (CK) isoenzyme MB activity. Somewhat surprisingly, there was a significant and consistent increase in CK isoenzyme BB activity. Awareness of the increase in troponin-T concentrations in patients with multiple clinical non-cardiac problems may prevent an erroneous diagnosis of myocardial infarction and avert institution of unduly aggressive treatment.

The significance of creatine kinase (CK) in the diagnosis of acute myocardial infarction was evaluated. The serum level of CK-MB, a CK isozyme was determined by the immunoinhibition method. The CK-MB activity could be determined by the immunoinhibition method in a short time with an autoanalyzer, suggesting that the immunoinhibition technique is adequate as a method of emergency examination. The immunoinhibition method has the disadvantage of error induction because of contamination with CK-BB, CKm and macro-CK by this method. Thus, CK-MB activity should be determined in parallel with total CK activity. When a significant contribution from CK-BB is suspected, its presence should be confirmed by other methods. The present results suggest that the efficiency of coronary artery reperfusion therapy can be evaluated earlier by determination of CK-MB activity than by that of total CK activity.

Small cell lung carcinoma (SCLC) is histologically simple, and shows a characteristic ultrastructure and very complex functions. Recently, a large amount of information has been accumulated by fundamental research, largely involving studies on many cultured cell lines. Now their potential application to the therapy of SCLC is being sought. A characteristic ultrastructural feature is the presence of dense-cored neurosecretory-type granules 100-200 nm in diameter. In addition, epithelial cell characteristics are noted. Predominance of either a neurosecretory or epithelial nature may affect the responsiveness of tumors to therapy. Many kinds of brain-gut hormones are produced by SCLC. Gastrin-releasing peptide (GRP) has attracted much attention as an autocrine growth factor for SCLC. Aromatic L-amino acid decarboxylase (AADC), neuron-specific enolase (NSE) and creatine kinase BB (CK-BB) are rather specific to SCLC. NSE and CK-BB together with GRP are good monitoring markers during treatment. Amplification of c-myc, N-myc and L-myc is seen in SCLCs. Areas both with and without N-myc amplification are found in both the primary site and metastatic sites in a single case. Del 3p(14-23) is characteristic for SCLC but SCLCs without such deletion are also present. A cytologically "variant" type is composed of cells simulating "large cells", in which the doubling time is short, AADC and GRP are undetectable, granules are rare, and the cells are resistant to radiation. However, one cell line of the classic type has revealed reversible squamous cell change in the absence of retinoic acid, becoming radioresistant without showing any remarkable changes in AADC, NSE or CK-BB. Since SCLC mixed with "large cells" or "small cell carcinoma of undifferentiated type" is resistant to therapy and possesses a more epithelial nature, small cell carcinoma with a large cell component has been proposed as a subtype. The question of whether this subclassification is practical should be confirmed by prospective study.

The primary aims of this study were to investigate mitochondrial metabolism during experimental allergic encephalomyelitis (EAE) animal model axonal injury and to determine the correlation among neurological function scores, pathological changes, and the activities of the BB isoenzyme of creatine kinase (CK-BB), catalase (CAT), and calpain in the brain tissues of EAE rats. Another goal was to preliminarily define the mechanism of mitochondrial metabolism resulting from the effect of beta 2 adrenergic agonists in the process of EAE animal model axonal damage. EAE was induced in specific pathogen free Wistar rats by guinea pig spinal cord homogenate, complete Freund's adjuvant, and pertussis vaccine. We recorded the behavioral change in EAE rats, detected pathological changes in central nervous tissue, and observed the changes of the CK-BB, CAT, and calpain in the EAE rat brain and spinal cord. The results indicated that the average neurologic function score increased in the EAE group compared to that of the controls (P < 0.01). In addition, CAT and CK-BB activities significantly decreased and the calpain activity significantly increased compared with those of the control group (P < 0.05). The decrease of the activity of central nervous CK-BB and CAT content, as well as the increase of calpain activity at the highest time point were considered to be the consequences of EAE. Furthermore, the results revealed that use of salbutamol could alleviate disease symptoms and reduce the recurrence of the EAE disease.

We compared the usefulness of four serum assays for classifying patients originally suspected of having an acute myocardial infarction. One of these is the long-used measurement of total creatine kinase (CK) activity. The other three are relatively new immunoassays: myoglobin by RIA, CK-BB by RIA, and CK-MB by immunoinhibition. When we evaluated test effectiveness with use of conventionally derived reference ranges, the results were misleading. However, by using receiver operating characteristic curves, we were able to effectively compare the four tests at all possible decision levels, rather than at only one. Multiple closely sequential serum specimens were obtained during the first four days after the onset of chest pain. Total CK, CK-MB, and CK-BB all behaved similarly, reaching peak diagnostic effectiveness at 18-20 h, when all three correctly classified 95% of the infarct patients, with a zero false-positive rate. However, total CK was more useful in identifying infarcts later in their courses than were the two CK isoenzyme tests. Myoglobin assay was most effective earlier in the course, at about 7 to 8 h. Our results indicate (a) that the tests for myoglobin and for CK or its isoenzymes are complementary and (b) that of the three CK tests, measurement of total CK activity provides the most information over the broadest segment of a patient's course.

BACKGROUND

Macro CK (creatine kinase) as a reason for high CK values has been known since 1979. Even in the era of troponin determination for the diagnosis of myocardial infarction, an elevated CK value can still cause confusion, especially as CK-MB rises earlier than troponin. The case report should remind us of this often forgotten differential diagnosis of elevated CK.

METHODS

A 73-year-old patient was treated with leuprorelin hormone therapy for prostate cancer (stage pT1c G2). In addition, he received percutaneous radiation therapy of the prostate and high-dose-rate brachytherapy twice with 10 Gy each. Close to 1 year later, he complained for the first time of dyspnea on exertion and thoracic tightness. Serum CK was 232 U/l, and CK-MB 62 U/l, which was confirmed by several controls. Troponin T test was negative, and GOT, GPT, LDH, and PSA were all within the normal range. Acute myocardial infarction was ruled out on clinical grounds and by six sequential ECGs. Subsequently, the patient remained without further cardiac complaints and in good condition. Isoenzyme electrophoresis finally solved the problem and revealed CK-BB-IgG complex type 1 (macro CK-1).

CONCLUSIONS

High CK-MB values in cardially healthy patients should remind us of the possibility of macro CK which is seen in approximately 0.5% of cases and should be included in the differential diagnosis.

Creatine kinase (CK)-MB subunit has been recognized as a useful marker for acute myocardial infarction (AMI). However, we recently experienced one case of osteopetrosis with moderately high CK-MB and an abnormal (more than 100%) CK-MB/total (T)-CK ratio without evidence of AMI in a medical examination. We have already experienced 17 cases with an abnormal CK-MB/T-CK ratios in addition to the present case. Those cases were patients with malignant tumor with metastasis (n = 13), leukemia (2), liver cirrhosis (1), and cerebral death (1), and thereby the band of macro-CK was found in the electrophoresis. However, we detected neither the band of macro-CK nor the abnormal levels of tumor markers such as CEA, alpha-fetoprotein, CA-19-9 in the present case. Instead of the macro CK, the high level of CK-BB was detected in electrophoresis. In the medical examination, especially in screening tests, the CK-MB was generally assayed with use of the immunoinhibition method in automated analyzers. The method principle was based on the absence of CK-BB in the patient serum. Since the patient had the past history of pathological fracture in his boyhood, this patient was diagnosed as osteopetrosis. These results suggest that we must consider the possibility of osteopetrosis when an abnormal CK-MB and CK-MB/T-CK ratio without evidence of serious diseases were found. This is simply because of the assay method of immunoinhibition for CK-MB activity.

The authors report on a profound increase in creatine kinase isoenzyme MB (CK-MB) activity in three patients following uneventful cryoablation of the prostate under general anaesthesia: Just after the arrival at the recovery room CK-MB levels were 321 U/l, 245 U/l and 433 U/l, respectively. Other clinical investigations as well as additional laboratory tests ruled out myocardial infarction in all three patients. Electrophoresis of the CK-isoenzymes revealed an increase in CK-BB activity and an increase in atypical CK-BB as a cause of these findings. The presence of these isoenzymes leading to interferences with the antibody commonly used in CK-MB assays could explain the determination of a false positive CK-MB elevation in the three patients. Moreover, it is shown that this method of CK-MB activity determination may result in CK-MB levels higher than 100% of the whole CK activity. In addition, it is discussed that in patients suffering from prostatic carcinoma or other malignoma, "non-CK-M elevations" may occur. Therefore, the authors conclude that after cryoablation of the prostate additional tests like troponin T test and 12 channel ECG are required to rule out suspected myocardial infarction.