Macro-creatine kinase type 1 possibly induced by intravenous hyperalimentation

109

Clinicu Chimicu Actu, 178 (1988) 109,110 Elsevier

CCA 04300

Letter to the Editor

Macro-creatine kinase type 1 possibly induced by intravenous hyperalimentation

Dear Editor,

We observed @-macro creatine kinase (CK) type 1 in an adolescent girl following intravenous hyperalimentation. She was admitted for evaluation of loss of appetite and anorexia. She showed no clinical manifestations except for low body weight (38 kg, height 165 cm) and had no suspected autoimmune disease [l]. She was treated with intravenous hyperalimentation catheterized through an infraclavicular vein puncture into the superior vena cava. Infusion of 1500 ml of solution containing 5% dextrose, 10% fructose and 3% WHO formulation amino acids was performed daily. Laboratory data after catheterization revealed increased aspartate and alanine transaminase and total CK activity. Electrophoretic separation of the CK isoenzymes (Titan III ISO-FLUOR, Helena Laboratories) revealed two bands of CK activity. One band corresponded in mobility to that of CK-MM in the marker; the second band migrated anodically with a mobility between that of CK-MM and CK-MB. Measurement of CK activity in the presence of anti-M antibody indicated that the major isoenzyme was CK-MM. The immunoprecipitin reaction [2] showed &A-lambda bound to the enzyme. Calculated activation energy [3] was 55.9 kJ/mol, indicating that mitochondrial CK was not present. Thus, the cathodal band observed in the serum was confirmed to be macro-CK type 1. Total CK activity increased to 1667 U/l (RR: 18-86 U/l) and macro-CK type 1 to 850 U/l (56% of the total) at their peak. When the catheter was removed, total CK began to decrease, and macro-CK disappeared on electrophoresis 14 days later (Fig. 1). The half-life in serum was 2 days for both total CK and macro-CK type 1. Mixing sera from a normal subject with the infusion solution used for alimentation did not result in activation of total CK or the appearance of macro-CK in the sera. Based on these observations, the cause of elevated macro-CK type 1 was suspected to be: (a) mechanical stimulation during catheterization releasing CK-MM from tissue; and (b) secondarily, immunoglobulin binding to form macro-CK type 1. We did not believe that macroCK type 1 formed initially and then accumulated

0009-8981/88/%03.50

0 1988 Elsevier Science Publishers

B.V. (Biomedical

Division)

110 I.V.

therapy

----I

I .V. therapy -I

100 U/l

50

0 DAYS

Fig. 1. Changes of AST activity (A), total CK activity (0) and the activity of macro-CK type 1 (0) in relation to intravenous hyperalimentation (I.V. therapy). The activity of macro-CK type 1 was quantified from the electrophoretic fraction and total CK activity.

serum. If the latter had been the case, the increased total CK would not have decreased as rapidly.

in

a Hiroshi Ihara, a Yutaka Aoki, b Yoko Saito and b Tsugutoshi Aoki a Department

of Laboratory

Medicine and b Department of Pediatrics, Ohashi Hospital, School of Medicine, Toho University, Tokyo, Japan

References 1 Schifferli JA, Despont JP, Cruchaud A, Carpentier N, Jearmet M, Schmidt M. Macro-creatine kinase type 1: immunological studies in 14 patients with comments on clinical significance. Arch Path01 Lab Med 1986;110:425-429. 2 Hayashi K, Tozawa T. Determination of creatine kinase (CK) linked immunoglobulins by immunoprecipitin reaction in free liquid media. Physico-Chem Biol (Seibutsu-butsuri-kagaku) 1986;30:457-460. 3 Stein W, Bohner J, Steinhart R, Eggstein M. Macro creatine kinase: determination and differentiation of two types by their activation energies. Clin Chem 1982;28:19-24.

Correspondence to: Dr. H. Ihara, Meguro-ku, Tokyo 153, Japan.

Ohashi

Hospital,

School of Medicine,

Toho University,

2-17-6 Ohashi,