Abstract
We have previously reported that the serum of many children with the Hemolytic Uremic Syndrome (HUS) is unable to stimulate cultured endothelial cells to generate normal amounts of Prostacyclin (PGI2), a potent inhibitor of platelet aggregation and thrombus formation.
Small, uncontrolled, non-randomized case studies suggest that the intravenous infusion of normal plasma, or the use of plasma exchange, is beneficial in treating HUS by virtue of replacing a “missing” factor needed for normal PGI2 production.
We therefore measured the ability of normal serum to enhance the ability of HUS sera to stimulate cultured endothelial cells to produce PGI2, as assessed by the radioimmunoassay measurement of its stable metabolite, 6-keto PGF1α. The results (mean±SD) of the paired (normal sera:HUS sera) mixing experiments (n=7) are as follows:
The in vitro addition of normal sera to HUS sera in a 1:3 volume ratio resulted in a significant increase (p=0.01) in PGI2 production. The 1:6 mixture values did not achieve significance, however (p>0.1, paired t test). These mixing experiments support the “missing factor” hypothesis.
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Sieqler, R., Smith, J., Lynch, M. et al. 1634 IN VITRO PROSTACYCLIN PRODUCTION IN THE HEMOLYTIC UREMIC SYNDROME FOLLOWING THE ADDITION OF NORMAL SERUM. Pediatr Res 19, 383 (1985). https://doi.org/10.1203/00006450-198504000-01658
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DOI: https://doi.org/10.1203/00006450-198504000-01658