Clinical Chemistry
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Clinical Chemistry 32: 689-691, 1986;
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ludvigsen, C. W.
Right arrow Articles by Haven, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ludvigsen, C. W.
Right arrow Articles by Haven, M.

Clinical Chemistry, Vol 32, 689-691, Copyright © 1986 by American Association for Clinical Chemistry

Creatine kinase variant type I in children with anoxic insult

CW Ludvigsen, C Muus, I Meyer and M Haven

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.




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1986 by the American Association for Clinical Chemistry.