Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Anschutz School of Medicine, 12700 East 19th Avenue, 9C03, Aurora, CO, 80045, USA.
Department of Medicine, University of Colorado Anschutz School of Medicine, Aurora, CO, USA.
Respir Res. 2022 Sep 5;23(1):230. doi: 10.1186/s12931-022-02157-9.
Imbalance in L-arginine and nitric oxide (NO) metabolism has been implicated in the pathophysiology of asthma and obstructive sleep apnea (OSA), and both diseases impact the other's morbidity. We sought to determine whether L-arginine/NO metabolism differs between adults with asthma with or without comorbid OSA, and its association with asthma morbidity.
This is a cross-sectional study of 322 adults with asthma recruited in Denver, CO and New York City, NY. Data were collected on OSA status, spirometry, and metrics of asthma control and morbidity. L-Arginine metabolites were quantified in patient serum. Bivariate analyses and multiple regression were performed to determine differences between L-arginine metabolism, OSA and association with asthma morbidity.
Among the 322 participants, 92 (28.5%) had OSA. The cohort was 81.6% female, 23.4% identified as Black and 30.6% as Latino. Patients with asthma and OSA had significantly higher serum concentrations of NO synthase inhibitor asymmetric dimethylarginine (ADMA) (p-value = 0.019), lower L-arginine to ornithine ratios (p-value = 0.003), and increased ornithine (p-value = 0.001) and proline levels (p-value < 0.001) compared to those without OSA. In adjusted models, OSA was associated with worse asthma control, adjusted mean difference in asthma control questionnaire of 0.36 (95% confidence interval [CI]: 0.06 to 0.65), and asthma quality of life questionnaire, adjusted mean difference: - 0.53 (95% CI: - 0.85 to - 0.21), after adjusting for relevant covariates including body mass index and L-arginine metabolites.
Adults with asthma and OSA had increased ADMA, an inhibitor of nitric oxide synthase, and greater metabolism of L-arginine via the arginase pathway compared to those with asthma alone, indicating a possible shared pathophysiological mechanism of these diseases.
精氨酸和一氧化氮（NO）代谢失衡与哮喘和阻塞性睡眠呼吸暂停（OSA）的病理生理学有关，这两种疾病也会相互影响发病率。我们旨在确定哮喘合并或不合并 OSA 的成年人之间的精氨酸/NO 代谢是否存在差异，及其与哮喘发病率的关系。
这是一项在科罗拉多州丹佛和纽约市招募的 322 名哮喘成年人的横断面研究。收集 OSA 状态、肺功能和哮喘控制及发病的指标。在患者血清中定量测定 L-精氨酸代谢物。进行了双变量分析和多元回归，以确定 L-精氨酸代谢、OSA 之间的差异及其与哮喘发病率的关系。
在 322 名参与者中，92 名（28.5%）患有 OSA。该队列中 81.6%为女性，23.4%为黑人，30.6%为拉丁裔。与无 OSA 患者相比，哮喘合并 OSA 患者的血清一氧化氮合酶抑制剂不对称二甲基精氨酸（ADMA）浓度明显更高（p 值=0.019），L-精氨酸/鸟氨酸比值更低（p 值=0.003），且精氨酸（p 值=0.001）和脯氨酸水平更高（p 值<0.001）。在调整模型中，与无 OSA 患者相比，OSA 与哮喘控制更差相关，哮喘控制问卷的调整平均差异为 0.36（95%置信区间[CI]：0.06 至 0.65），哮喘生活质量问卷的调整平均差异为-0.53（95%CI：-0.85 至-0.21），在调整了包括体重指数和 L-精氨酸代谢物在内的相关协变量后。
与单纯哮喘患者相比，哮喘合并 OSA 的成年人的 ADMA（一氧化氮合酶抑制剂）增加，L-精氨酸通过精氨酸酶途径代谢增加，这表明这些疾病可能存在共同的病理生理机制。
