Clinical significance of measuring inflammatory markers in patients with pulmonary arterial hypertension.

215 interleukin 6, the expression of which is also modulated by BMPR2.5 The currently enrolling clinical trials in PAH with molecules such as FK506, rituximab, and anakinra selectively targeting the immune system are promising. In the study by Jasiewicz et al.,3 10 patients were incident cases who received PAH-targeted therapy at entry to the study. It would be interesting to see whether the levels of OPG and sRANKL changed in this group during the 6-month follow-up. Finally, different subtypes of PAH are characterized by different mechanisms and inflammatory profiles. The development of PAH associated with congenital heart disease is triggered by mechanical overload of the pulmonary vessels resulting from an increased flow through the pulmonary circulation, while some molecular mechanisms are thought to be involved in the initiation and progression of idiopathic PAH. Jasiewicz et al.3 did not report any significant differences in serum OPG and sRANKL concentrations between patients with idiopathic PAH, PAH associated with congenital heart disease, and PAH associated with connective tissue disease. Does it mean that their results can be generalized to the whole PAH population or maybe the numbers of study groups were too small to prove heterogeneity of OPG and RANKL levels in different PAH etiologies?