Iron Homeostasis at High Altitude in Patients With Pulmonary Hypertension.

Abstract

Iron deficiency aggravates hypoxic pulmonary vasoconstriction, exacerbating the increase of pulmonary arterial pressure at high altitude (HA). This may be especially relevant for patients with pulmonary hypertension (PH) travelling to HA, who moreover have a high prevalence of iron deficiency. Currently, no data is available on iron parameters and their influence on HA adaptation in PH-patients. In a randomized cross-over trial, 27 patients (44% female, mean age 61.7 ± 13.6 y) with pulmonary arterial hypertension (67%) or chronic thromboembolic PH (33%) were assessed at baseline (Zurich, 470 m) and during a stay at 2500 m. Blood samples were taken at baseline and after 20 h at 2500 m. A significant increase in ferritin (131 ± 68 to 140 ± 75, p = 0.002), transferrin (28.0 ± 4.7 to 30.3 ± 4.4, p = 0.012) and soluble transferrin receptor (sTfR) levels (2.7 ± 0.7 to 2.9 ± 0.6, p = 0.014) was observed at HA, all of which correlated with decreasing hepcidin levels. Arterial partial pressure of carbon dioxide (PaCO₂) was inversely correlated with transferrin levels (Pearson's r = -0.57, p < 0.001), and baseline transferrin concentration was an independent predictor of PaCO₂ at baseline and HA (p = 0.037). Furthermore, transferrin levels < 30 µmol/L were an independent predictor of mean nocturnal oxygen saturation (SpO₂) at baseline and HA. The need for oxygen supplementation at HA could be predicted using a model including baseline transferrin, achieving a positive predictive value of 84%, suggesting that transferrin may serve as a useful clinical marker to identify PH patients at risk of oxygen desaturation at HA.