ArticleIndian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion2011
Uric Acid as a potential biomarker of pulmonary arterial hypertension in patients with sickle cell disease.
Article in Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 9 citations in OpenAlex.
- Targeted Proteomic Analysis of Sickle Cell Disease Patients With Elevated Tricuspid Regurgitation Velocity.Proteomics. Clinical applications · 2025Article
- Nontargeted Plasma Proteomic Analysis of Renal Disease and Pulmonary Hypertension in Patients with Sickle Cell Disease.Journal of proteome research · 2024Article
- Focus on Early Events: Pathogenesis of Pulmonary Arterial Hypertension Development.Antioxidants & redox signaling · 2019Review
- Relative abundance of 'Candidatus Tenderia electrophaga' is linked to cathodic current in an aerobic biocathode community.Microbial biotechnology · 2018Article
- Evaluating risk factors for chronic kidney disease in pediatric patients with sickle cell anemia.Pediatric nephrology (Berlin, Germany) · 2017Observational
- Effect of iloprost on biomarkers in patients with congenital heart disease-pulmonary arterial hypertension.Clinical and experimental pharmacology & physiology · 2017Article
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10 authors at 1 institution in 1 country.
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Abstract
Serum uric acid (UA) is emerging as a strong and independent marker for pulmonary arterial hypertension (PAH). PAH is well recognized as a life threatening complication of sickle cell disease (SCD). However, the association between UA and PAH in SCD is unknown. We reviewed electronic medical records (EMR) of 559 consecutive adult SCD patients from Kings County Hospital Center (KCHC) between January 2005 and February 2010. Patients (n = 96) with measurement of UA in close temporal proximity to the transthoracic echocardiography (TTE) were identified. PAH was defined as pulmonary artery systolic pressure (PASP) ≥30 mm Hg. Patients (n = 16) with other risk factors which may cause PAH and chronic renal insufficiency were excluded. In 18 patients, TTE could not measure PASP. Finally, 62 patients were selected. Statistical analysis was performed using Student t tests, Pearson correlation coefficient and multivariate regression analysis. Out of 62 patients, 30 had PAH. Patients with PAH had a higher UA level (8.67 ± 4.8 vs. 5.35 ± 2.1, P = 0.001). We found strong positive correlation between the UA level and PASP (r = 0.71; P < 0.0001). This correlation was independent of diuretic use. UA could be a potential marker for PAH in SCD. However, its' prognostic and pathophysiologic role in SCD patients with PAH needs to be further investigated.
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