Plasma homocysteine is elevated in COPD patients and is related to COPD severity

Abstract

Background

Although recent studies have found that total plasma homocysteine (tHCY) and chronic obstructive pulmonary disease (COPD) are both risk factors for cardiac disease, there have been few studies of plasma homocysteine levels in COPD patients. We tested the hypothesis that total plasma homocysteine (tHCY) would be elevated in patients diagnosed with COPD compared with controls.

Methods

We studied 29 COPD outpatients and 25 asymptomatic subjects (controls) over age 55 years with measurement of forced expiratory volume in one second (FEV₁), forced vital capacity (FVC), St. Georges Respiratory Questionnaire (SGRQ) score, tHCY and serum C-reactive protein (sCRP).

Results

There was no difference between controls vs. COPD patients in mean age or gender but mean (SD) FEV₁ was 2.25 (0.77) vs 1.43 (0.60) L; FEV₁% predicted 76.1 (17.2) vs 49.1 (16.3) p < 0.001 in both cases. Median (IQR) tHCY was 8.22 (6.63, 9.55) in controls vs 10.96 (7.56, 13.60) micromol/l for COPD, p = 0.006 and sCRP 0.89 (0.47, 2.55) vs 2.05 (0.86, 6.19) mg/l, p = 0.023. tHCY(log) was also higher in (r, p) smokers (0.448, 0.001), patients with low FEV₁% (−0.397, 0.003), males (0.475, <0.001), but high SGRQ Total score (0.289, 0.034), and high sCRP (0.316, 0.038). tHCY(log) was independently related to (regression coefficient, p) sCRP(log) (0.087, 0.024), male gender (0.345, <0.001) and presence of COPD (0.194, 0.031). Median (IQR) tHCY GOLD Stage I and II 8.05 (7.28, 11.04), GOLD Stage III and IV: 11.83(9.30, 18.30); p = 0.023.

Conclusions

Plasma homocysteine is significantly elevated in COPD patients relative to age and sex-matched controls and is related to serum CRP and COPD severity.

Keywords:

• COPD
• Homocysteine
• CRP
• SGRQ
• FEV₁

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Corrigendum

Acknowledgements

We would like to acknowledge helpful advice from Dr. F. Ramlakhansingh, Prof. D. Ramdath, Prof. M. Omer, Dr. S Pooran, Mr. Desmond Parker, the staff at The Port of Spain General Hospital (POSGH), Biochemistry laboratory at POSGH, and Immunology and Pathology laboratories at Eric Williams Medical Sciences Complex (EWMSC), Faculty of Medical Sciences, University of the West Indies. We are especially grateful to the patients and volunteers who took the time to participate in our study. Funding was departmental. Portions of this manuscript have been presented in abstract form at the 2006 American Thoracic Society Meeting, May 2006 in San Diego, USA.

Conflict of interest

Dr. Seemungal has received speaking honoraria from GlaxoSmithKline, ASTRA Zeneca, Pfizer, and Boehringer Ingelheim. Dr. Wedzicha has received research grant funding and/or honoraria for lectures and advisory boards from GlaxoSmithKline, Astra Zeneca, and Boehringer Ingelheim. The other authors admit to no conflicts of interest.