Serum Uric Acid Levels Correlate with the Severity and the Mortality of Primary Pulmonary Hypertension

Nagaya, Noritoshi; Uematsu, Masaaki; Satoh, Tsuyoshi; Kyotani, Shingo; Sakamaki, Fumio; Nakanishi, Norifumi; Yamagishi, Masakazu; Kunieda, Takeyoshi; Miyatake, Kunio

doi:10.1164/ajrccm.160.2.9812078

Cited by 237 publications

(189 citation statements)

References 29 publications

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“…Elevated uric acid levels have long been known to be a poor prognostic sign in acute illness [51]. Several studies have demonstrated that an elevated urate level in PH correlates with severity of disease [52][53][54][55][56]. In one study, 90 patients with IPAH underwent right heart catheterisation and serum uric acid estimation, and were then followed for a mean of 31 months [54].…”

Section: Uric Acidmentioning

confidence: 99%

“…A number of studies have sought to define the prognostic value of biomarkers in PH. Several markers have been shown to be independent predictors of mortality in PAH, including serum uric acid [54], BNP [10] and NT-proBNP [28]. Cardiac troponin T is an independent predictor of mortality in patients with PH of various classes [58], and in sickle cell disease elevated NT-proBNP is a major risk factor for death [34].…”

Section: Prognosismentioning

confidence: 99%

“…Biomarkers can potentially offer additional information to the clinician for monitoring the efficacy of treatment and the patient's clinical course. Serum uric acid levels decrease with successful treatment with prostacyclin of patients with IPAH [54]. Exhaled NO may be useful in the long-term monitoring of patients on prostacyclin [89] and bosentan [62].…”

Section: Response To Therapymentioning

confidence: 99%

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Biomarkers in pulmonary hypertension

Warwick

Thomas²,

Yates³

2008

European Respiratory Journal

137

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There have been significant recent advances in the understanding of the pathophysiology of pulmonary hypertension, and a growing number of therapeutic agents have become available to the treating physician. Traditional methods of diagnosing and monitoring this condition have comprised echocardiography and right heart catheterisation, in addition to functional measures, such as estimation of functional class and the 6-min walk test. An increasing number of biomarkers have been described that are elevated in pulmonary hypertension and which may assist the clinician in diagnosis and in the assessment of disease severity and response to treatment.The present article details the more important biomarkers, their potential applications and the evidence supporting their use.

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Section: Uric Acidmentioning

confidence: 99%

Section: Prognosismentioning

confidence: 99%

Section: Response To Therapymentioning

confidence: 99%

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Biomarkers in pulmonary hypertension

Warwick

Thomas²,

Yates³

2008

European Respiratory Journal

137

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show abstract

“…Higher vWF levels at baseline and despite therapy are independently associated with an increased risk of death in PAH [60]. Similarly, a variety of biomarkers tied to cardiac function have been investigated in PAH [38,50,63,64]. The best studied, natriuretic peptides are produced by the cardiac atria and ventricles in response to myocyte stretch and may serve as endocrinologic indicators of heart function.…”

Section: Plasma Biomarkersmentioning

confidence: 99%

Surrogate End Points in Pulmonary Arterial Hypertension: Assessing the Response to Therapy

Snow¹,

Kawut²

2007

Clinics in Chest Medicine

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Pulmonary arterial hypertension (PAH) is a rare disease which is characterized by increased pulmonary vascular resistance and right heart failure. Recent discoveries in disease pathophysiology have been translated into effective therapies tested in clinical trials. The studies which have led to the regulatory board approval of therapies for PAH have focused on surrogate and intermediate end points, thought to reflect quantity and quality of life, respectively. However, validation of many of these surrogates is incomplete. It is also unknown which indicators of function or long-term survival should be used to formulate decisions regarding addition, discontinuation, or combination of therapies. Identification of suitable end points would therefore not only help investigators design appropriate clinical trials, but also assist clinicians in caring for patients with PAH. Hemodynamic, cardiac imaging, plasma biomarkers, and exercise testing hold some promise as potential surrogate end points for PAH. Functional status and quality of life assessments may also have important roles. Future studies should validate the most promising surrogate markers, so that patients, clinicians, subjects, and investigators may benefit from the advantages they confer on clinical care and on clinical trials.The past several years have yielded an explosion of randomized clinical trials (RCTs) of several new medical therapies for pulmonary arterial hypertension (PAH). The hopes for these and all treatments for potentially fatal diseases are 1) to improve how a patient feels or functions and/ or 2) to prolong survival. While simply stated, the assessment of progress towards these goals may be quite complex [1][2][3][4][5][6].New PAH therapies have gained regulatory board approval based on studies with intermediate and surrogate end points as primary outcomes, believed to reflect the impact of these drugs on quality of life (QOL) and survival, respectively. While hemodynamic, plasma, cardiac imaging, exercise, functional, and QOL parameters are promising candidates, the reliability and validity of these measures are not clearly established. In addition, there are no RCTs addressing the use of such end points in guiding management decisions in PAH, such as changing, intensifying, escalating, or combining therapies. Despite this lack of evidence, clinicians who

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“…In recent years, it has become of growing importance to have precise early and convenient method to diagnose PAH in SCD [7]. Several biomarkers such as brain natriuretic peptide [8], endothelin-1 9 (ET1) and UA [10][11][12] were found to have good correlations in patients with PAH. However, the association between UA and PAH in SCD is unknown.…”

Section: Introductionmentioning

confidence: 99%

Uric Acid as a Potential Biomarker of Pulmonary Arterial Hypertension in Patients with Sickle Cell Disease

Joshi

Anjum

Gowda

et al. 2011

Indian J Hematol Blood Transfus

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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) C30 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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Serum Uric Acid Levels Correlate with the Severity and the Mortality of Primary Pulmonary Hypertension

Cited by 237 publications

References 29 publications

Biomarkers in pulmonary hypertension

Biomarkers in pulmonary hypertension

Surrogate End Points in Pulmonary Arterial Hypertension: Assessing the Response to Therapy

Uric Acid as a Potential Biomarker of Pulmonary Arterial Hypertension in Patients with Sickle Cell Disease

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