Key result
Continuous prostacyclin is linked to higher thrombomodulin and lower P-selectin levels in PAH.
Why the study?
Thrombosis in situ related to endothelial cell injury may contribute to pulmonary hypertension, but the role of P-selectin and thrombomodulin in this process was unclear.
Does continuous prostacyclin therapy improve plasma levels of P-selectin and thrombomodulin in patients with pulmonary arterial hypertension?
Observational (n=105)
Does continuous prostacyclin therapy improve plasma levels of P-selectin and thrombomodulin in patients with pulmonary arterial hypertension?
p-value: p=<0.05
Continuous prostacyclin therapy improves biomarkers of endothelial injury and altered hemostasis (P-selectin and thrombomodulin) in patients with pulmonary arterial hypertension.
No takes yet. Share an insight, caveat, or question.
Coagulation marker shifts after prostacyclin in PH are hypothesis-generating; leaves open clinical relevance and need for larger outcome trials.
Sakamaki et al. (2000) conducted an observational in Pulmonary hypertension (n=105). Continuous prostacyclin therapy vs. Baseline (pre-therapy) was evaluated on Plasma levels of soluble P-selectin and thrombomodulin (p=<0.05). Continuous prostacyclin therapy significantly increased thrombomodulin levels and decreased P-selectin levels in patients with primary and secondary pulmonary arterial hypertension (P<0.05).
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