Asymmetric Dimethylarginine and the Effect of Folate Substitution in Children with Familial Hypercholesterolemia and Diabetes Mellitus Type1

  • MUDr Petr Jehlicka, Charles University Faculty Hospital, FN Plzen, Czech Republic
  • MUDr Frantisek Stozicky, Charles University Faculty Hospital, FN Plzen, Czech Republic
  • MUDr Otto Mayer, Charles University Faculty Hospital, FN Plzen, Czech Republic
  • MUDr Jaroslav Racek, Charles University Faculty Hospital, FN Plzen, Czech Republic
  • MUDr Jana Varvarovska, Charles University Faculty Hospital, FN Plzen, Czech Republic
  • MUDr Konrad Siala, Charles University Faculty Hospital, FN Plzen, Czech Republic
  • Objective: a recently discussed cardiovascular risk factor is asymmetric dimethylarginine (ADMA), which is known to act as an endogenous inhibitor of endothelial nitric oxide synthase.
    The aim of the study: to establish the relationship between ADMA and ultrasonographically or biochemically determined endothelial dysfunction in children, and furthermore to ascertain the effect of folate supplementation on this parameter. The study cohort included 32 children with familial hypercholesterolemia (FH), 30 with diabetes mellitus type 1 (DM1) and 30 age matched healthy children as a control group. Furthermore, twenty eight randomly selected FH and DM1 children were re-examined after 3-months supplementation with folic acid.
    Results: baseline levels of ADMA (0.94±0.18, 0.84±0.18, 0.77±0.14, in μmol/L, respectively) and oxidized low density lipoproteins oxLDL (73.69±24.9, 51.71±23, 55.7±30, in mU/L, respectively) were significantly higher in FH group than in DM1 and healthy children. Children in the DM1 group had significantly lower homocysteine concentrations, nevertheless ADMA levels were normal. Folic acid supplementation significantly lowered homocysteine and hsCRP levels in both FH and DM1 groups; however, ADMA and oxLDL concentrations remained unchanged.
    Conclusions: ADMA and oxLDL appear to be associated with ED in children with FH and thus may support early diagnosis of preclinical atherosclerosis in these children. Administration of folic acid does not appear to influence these markers in both FH and DM1 children.