Errors in plasma creatine kinase estimations on fetal blood samples resulting from contamination with amniotic fluid and maternal blood: Relevance for the prenatal diagnosis of duchenne muscular dystrophy

1984 ◽  
Vol 4 (2) ◽  
pp. 119-134 ◽  
Author(s):  
R. J. Edwards ◽  
C. H. Rodeck ◽  
D. C. Watts
2008 ◽  
Vol 21 (5) ◽  
pp. 354-355 ◽  
Author(s):  
O. Török ◽  
K. Norregaard-Hansen ◽  
M. Szokol ◽  
K. Csécsei ◽  
A. Harsányi ◽  
...  

1977 ◽  
Vol 23 (12) ◽  
pp. 2341-2343 ◽  
Author(s):  
H L Verrill ◽  
N A Pickard ◽  
H D Gruemer

Abstract Currently, the most useful clinical laboratory aid in establishing the carrier state of Duchenne muscular dystrophy is to determine creatine kinase (EC 2.7.3.2) activity in the plasma. The considerable overlap between plasma creatine kinase activities of controls and of carriers at the childbearing age contributes appreciable difficulty to genetic counseling of potential carriers. The consistent failure of lymphocyte cap formation in Duchenne muscular dystrophy patients and carriers in this study suggests a valuable tool for the confirmation of the carrier state.


1992 ◽  
Vol 134 (2) ◽  
pp. 313-317 ◽  
Author(s):  
M. R. Johnson ◽  
A. Abbas ◽  
K. H. Nicolaides ◽  
S. L. Lightman

ABSTRACT Relaxin was measured in maternal blood and amniotic fluid samples at 9–40 weeks and in fetal blood samples at 19–41 weeks of pregnancy. In amniotic fluid, concentrations of relaxin rose from 58 ng/1 (geometric mean) at 10 weeks to 142 ng/l at 14 weeks and declined subsequently to 55 ng/l at 22 weeks. In maternal blood, mean relaxin concentrations were ten times greater than in amniotic fluid, and concentrations decreased with gestation. Since there was no significant association between the relaxin concentrations in the two compartments, relaxin in the amniotic fluid may be derived from the decidualized endometrium rather than the maternal circulation, alternatively its metabolism may be different in the two compartments. The absence of detectable concentrations of relaxin in any of the fetal blood samples demonstrates that there is no significant placental transfer or fetal synthesis of this peptide. Journal of Endocrinology (1992) 134, 313–317


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