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Decreased exhaled nitric oxide in sickle cell disease: Relationship with chronic lung involvement
Author(s) -
Girgis Reda E.,
Qureshi Mohammed A.,
Abrams Judith,
Swerdlow Paul
Publication year - 2003
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.10284
Subject(s) - medicine , acute chest syndrome , exhaled nitric oxide , gastroenterology , nitric oxide , sickle cell anemia , pathogenesis , dlco , cardiology , respiratory disease , lung , asthma , disease , diffusing capacity , spirometry , lung function
A deficiency in airway nitric oxide (NO) could contribute to pulmonary vaso‐occlusion in sickle cell disease (SCD). We measured the fractional expired concentration of NO (FE NO ) by chemiluminescence during a slow vital capacity maneuver against a positive pressure of 16 cm H 2 O at an expiratory flow rate of 50 mL/sec in 44 stable ambulatory adults with SCD and 30 healthy controls. A history of acute chest syndrome was present in 29 patients, and 22 complained of dyspnea. Mean ± SD FE NO was significantly reduced in the SCD group compared with controls (14.8 ± 8.4 vs. 24.9 ± 13.5 ppb, P < 0.001). SCD patients with dyspnea had lower FE NO than those without dyspnea (10.1 ± 5.7 vs. 19.6 ± 8 ppb, P < 0.001) and those with a history of ACS had lower values than those no episodes of ACS (13.0 ± 8.3 vs. 18.4 ± 7.6 ppb, P < 0.05). There was a weak correlation between FE NO and percent‐predicted DLCO ( r = 0.4, P = 0.02) among the SCD patients. We conclude that exhaled NO is reduced in adults with SCD, and this may play a role in the pathogenesis of acute chest syndrome and chronic sickle cell lung disease. Am. J. Hematol. 72:177–184, 2003. © 2003 Wiley‐Liss, Inc.