Iron metabolism in patients with pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension

BACKGROUND: Many patients with pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension experience iron deficiency, which is associated with decreased exercise capacity and higher mortality.

AIM: To examine iron metabolism and the prevalence of iron deficiency in patients with pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension based on various laboratory criteria.

MATERIALS AND METHODS: The study included 20 patients with pulmonary arterial hypertension and 51 with chronic thromboembolic pulmonary hypertension. All patients underwent blood tests, C-reactive protein, NT-proBNP, and iron metabolism indicators, namely, serum iron, transferrin, serum ferritin, and soluble transferrin receptors. Transferrin saturation and soluble transferrin receptors to the logarithm of ferritin ratio were calculated.

RESULTS: The prevalence of iron deficiency based on various criteria was higher in the pulmonary arterial hypertension group. In the chronic thromboembolic pulmonary hypertension group, the following differences were observed: female patients had higher serum ferritin levels (p=0.04) and transferrin saturation (p=0.024), whereas serum ferritin levels were higher in both groups (p <0.001) and among women (p=0.001). The levels of soluble transferrin receptors to the logarithm of ferritin ratio in the chronic thromboembolic pulmonary hypertension group were lower (p=0.018); however, when compared with the female subgroup, the differences disappeared. In the pulmonary arterial hypertension group, serum ferritin level of <30 μg/L and transferrin saturation <20% helped identify 70–75% of patients with iron deficiency. In the chronic thromboembolic pulmonary hypertension group, in which aseptic inflammation plays a major role in its pathogenesis, only the use of parameters such as soluble transferrin receptors to the logarithm of ferritin ratio of >2 and transferrin saturation of <20% allowed identifying a comparable number of patients with iron deficiency (50–53%).

CONCLUSION: The results of the study of iron metabolism indicate that pathogenetic variants of iron deficiency vary among patients with pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension. In the pulmonary arterial hypertension group, absolute iron deficiency is much more common, whereas in the chronic thromboembolic pulmonary hypertension group, inflammation probably makes a more significant contribution, which in most cases leads to the development of functional iron deficiency and requires the use of diagnostic criteria recommended for patients with chronic diseases.