Creatine kinase variant type I in children with anoxic insult.
We evaluated 31 consecutive patients, including 11 children, with creatine kinase variants (CKV) in our laboratory during a year. All had a clinical history of central hypotonia with myocardial damage resulting in severe central hypoxia. Seven of the 11 were neonates and had Apgar scores of 2.8 (SD 2.3) at 1 min and 4.8 (SD 2.4) at 5 min, which reflected their severe birth hypoxia. For the seven neonates, the mean value for total serum creatine kinase (EC 2.7.3.2; CK) was 773 (SD 553) U/L. The mean percentage CKV was 20.7% (SD 12.5%). The other four children were being evaluated for failure to thrive; all had birth asphyxia with residual cerebral palsy and seizure activity. These older children had a lower percentage of CKV (7.3%, SD 1.01%) than did the neonates, but the total CK (725, SD 1335 U/L) was not significantly different. In four neonates there was a three- to 20-day delay in the appearance of CK variant, which followed a marked increase in total CK activity. Tissue necrosis is apparently an important factor in the pathogenesis of Type I CK variant.
D001238:Asphyxia Neonatorum / Q000201:enzymology; D002648:Child; D002675:Child, Preschool; D003402:Creatine Kinase / Q000097:blood*; D004587:Electrophoresis, Agar Gel; D006801:Humans; D000860:Hypoxia / Q000201:enzymology*; D007223:Infant; D007231:Infant, Newborn; D007527:Isoenzymes
D007527:Isoenzymes; D003402:Creatine Kinase