ELEVATED CREATINE PHOSPWKINASE AND CREATINE F’HDBHMNASE-MB IN

Elevated creatine phosphokinase (CPK) levels, sometimes including the creatine phosphokinase- myocardial band (CPK-MB), have been reported in several clinical conditions other than acute myocar- dial infarction, as well as in normal subjects [l-9].

Clinical observations of patients admitted to our emergency room for evaluation of shortness of breath and chest discomfort, accompanied by ele- vated CPK values but normal electrocardiograms, raised the possibility that hyperventilation per se may cause hyper-CPK-emia.

Few small studies have dealt with the subject of CPK elevation during an asthmatic attack [5-g]. While most of them attributed the phenomenon to steroid myopathy, isoproterenol and theophylline cardiotoxicity, and hypereosinophilia syndrome, Burki and Diamond [9] clarified that the increase in serum CPK in asthma is probably derived from respiratory muscles, owing to the work of breathing.

A preliminary prospective study demonstrated that after hyperventilation, three of eight healthy subjects showed elevated CPK values.

Eight healthy volunteers were chosen to partici- pate in this study on the basis of their medical his- tory and the results of physical examinations and routine laboratory tests. These included erythro- cyte sedimentation rate, complete blood count, electrolytes, glucose, and kidney and liver function tests @MAC), as well as electrocardiograms (ECG), chest radiographs, and spirometry. The number of men and women was equal, and the mean age was 31.6 years (range: 25 to 39 years).

Spirometry was conducted in the early morning, prior to physical activity. The volunteers were in- structed to breathe rapidly into a modified spirom- eter until dizziness or fatigue occurred. ECG, SMAC, and tests for specific muscle enzymes (CPK, CPK-MB, serum glutamic oxaloacetic trans- aminase, lactic dehydrogenase, and aldolase) were performed 1 hour before, and 6 and 24 hours after spirometry.

Elevated CPK values were recorded in three of the eight subjects (p <0.05); the MB fraction was higher than normal in one of the three. The results of the remainder of the tests, including ECG and muscle enzyme profiles, were all within the normal range.

Comments. Testing the correlation between hy- perventilation and high CPK values revealed that three of eight (37% p <0.05) healthy volunteers demonstrated a rise in CPK following a short period of intense hyperventilation. It is likely that rapid diaphragm movement in the course of hyperventi- lation leads to the release of CPK from this muscle. Although in one of the three subjects, the increase in CPK from 13 to 60 units was within the normal limits of 0 to 100, the elevation was considered pathologic by definition, since it was three times the basic value [5]. The CPK-MB fraction was higher than normal in another of the three subjects.

To date, clinicians have associated dyspnea in the presence of high CPK values with ischemia. Despite the small number of patients in our experiment, and the need for a wider prospective study, our preliminary work as well as the reports concerning CPK elevation in asthma [5-91 seems to indicate that elevations in CPK can be caused by hyperven- tilation per se and need not suggest a myocardial insult. This finding could result in less importance being attached to high CPK levels in the differen- tial diagnosis of myocardial ischemia, and prevent unnecessary investigation and hospitalization of patients who present with atypical chest pain.

RAN OREN, M.D. IZIDORE S. Lossos, M.D.

Hadassah University Hospital Jerusalem, Israel

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Submitted May 12, 1992, and accepted in revised form September 21. 1992

(ACKNOWLEDGMENT: We are indebted to Professor A. Gutman, Head of the

Clinical Biochemistry Department, Hadassah University Hospital, Ein Karem, for

her cooperation.)

January 1993 The American Journal of Medicine Volume 94 113