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FRI0279 Anemic hypoxia is associated with pulmonary arterial hypertension in patients with systemic lupus erythematosus
  1. K.-J. Kim1,
  2. I.-W. Baek1,
  3. C.-H. Yoon1,
  4. J.-J. Choi2,
  5. W.-U. Kim1,
  6. C.-S. Cho1
  1. 1Internal Medicine, The Catholic University Of Korea, College Of Medicine, Seoul
  2. 2Internal Medicine, CHA University, Bundang CHA General Hospital, Sungnam, Korea, Republic Of

Abstract

Background Pulmonary arterial hypertension (PAH) is a serious and often fatal complication of systemic lupus erythematosus (SLE), but its pathogenesis is still unclear. Hypoxia-induced pulmonary vascular remodelling has been suggested to be a crucial mechanism for PAH.

Objectives To investigate the association between anemic hypoxia and PAH in patients with SLE.

Methods A post hoc analysis was performed of the prospective cross-sectional study to determine the PAH in 116 patients with SLE. PAH was defined as resting pulmonary artery systolic pressure (PASP) ≥ 40 mmHg by echocardiography. Duration of anemia was calculated as cumulative months of anemia (defined by hemoglobin [Hb]<10 g/dL) during the preceding years. Oxygen delivery (DO2) was estimated by the product of cardiac output (CO) and arterial oxygen content (CO x %Saturation x 1.39 x Hb). Serum IL-6 level and plasma N terminal-pro B-type natriuretic peptide (NT-proBNP) were also quantified.

Results Among 116 SLE patients, PAH was detected in 11 patients (9.5%). The range of PAH was 40.4-90 mmHg. Twenty-one patients (18.1%) showed PASP of 30-40 mmHg. Compared to patients without PAH, patients with PAH had lower Hb levels (9.8±0.5 versus 11.9±0.2 g/dL, P=0.001), but longer duration of anemia during the preceding 1, 2, and 3 years, respectively (all P<0.05). Importantly, DO2 value of patients with PAH were significantly lower than those of patients without PAH (7.9±0.8 versus 10.0±0.2 ml/min/kg, P=0.006). Moreover, DO2 value inversely correlated with PASP and serum NT-proBNP levels (Y=-0.241, P=0.013 and Y=-0.292, P=0.001, respectively). In multivariate regression analysis, duration of anemia was independently associated with the presence of PAH in SLE patients (P=0.006). When patients were divided into three groups according to tertiles of Hb well as PASP, serum IL-6 significantly increased across the tertiles of PASP (P for trend=0.038), but decreased across the tertiles of Hb (P for trend=0.001).

Conclusions Our study suggests that prolonged exposure to anemic hypoxia, which is associated with increased serum IL-6, might be a component of pathogenesis of PAH in SLE patients.

Acknowledgements Nothing specified.

Disclosure of Interest: None Declared

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