The apolipoprotein(a) size polymorphism is associated with XXXX .

@entity1 @entity8 @entity3208 @entity3452 @entity1985 @entity214
BACKGROUND: The atherogenic serum lipoprotein(a) [ @entity3452 ] is significantly elevated in @entity1 with @entity1985 . The underlying mechanism for this elevation is poorly understood. METHODS: We investigated in 207 @entity1 with @entity1985 and 274 controls whether the apolipoprotein(a) [apo(a)] kringle-IV repeat polymorphism explains the elevated @entity3452 levels in these @entity1 . RESULTS: @entity1 showed a tremendous elevation of @entity3452 concentrations when compared to controls (mean 60.4 vs. 20.0 mg/dL and median 29.8 vs. 6.4 mg/dL, P < 0.0001). Primary and secondary causes contributed to this elevation. The primary causes became apparent by a markedly elevated number of low-molecular-weight apo(a) phenotypes which are usually associated with high @entity3452 levels. This frequency was 35.7% in @entity1 compared to only 24.8% in controls (P= 0.009). In addition, secondary causes by the pathogenetic mechanisms of the @entity1985 itself resulted in a different increase of @entity3452 in the various apo(a) isoform groups. Based on the measured @entity3452 concentrations in each subject, we calculated separately the @entity3452 concentrations arising from the two expressed isoforms by estimating the relative proportion of the two serum isoforms in the @entity3208 ( @entity214 ) agarose gel electrophoresis. Low-molecular-weight isoforms were associated with 40% to 75% elevated @entity3452 concentrations when compared to matched isoforms from controls. High-molecular-weight apo(a) isoforms showed 100% to 500% elevated @entity3452 levels compared to matched isoforms from controls. The severity of the @entity1985 as well as the degree of @entity8 did not influence the @entity3452 concentrations. CONCLUSION: The tremendously increased @entity3452 levels in @entity1985 ar caused by primary genetic as well as disease-related mechanisms.
