哮喘患者吸入特异性变应原对血清脂肪连接素（Adiponectin）的影响
2009/05/18
脂肪结合素与哮喘有关，但在人类这种关联的方向性仍不是很清楚。在大鼠中，已证实这种关联是双向的，即吸入变应原能影响血清脂肪结合素，给予外源性脂肪结合素也会影响哮喘。为试图证实在哮喘患者中吸入特异性变应原是否可影响血清脂肪结合素的水平，Akshay Sood等人进行了一项临床研究。
研究对象为8个致敏的轻度哮喘患者和6个健康对照者。哮喘患者通过吸入特异性变应原（皮肤试验阳性的变应原）、乙酰甲胆碱及其他不相关的变应原（皮肤试验阴性的变应原）激发。对照组用不相关的变应原激发。连续10次留取血清标本：激发前1次，激发后9次，检测血清脂肪结合素、脂肪素、脂肪结合素/脂肪素比值、嗜酸细胞活化趋化因子、肿瘤坏死因子α，并将这些检测结果做成曲线，评价基线和峰值，计算图线下面积，并将反复检测的结果进行了方差分析和配对T检验等统计学分析。
结果表明，无论是哮喘组还是对照组，各自激发试验前后的血清检测数据均无明显差异。II类错误不太好解释这些结果，因为这项研究在检测血清脂肪结合素差异方面有足够的能力，正如文章中报道的那样。
另外，总体的数据显示出哮喘患者的血清脂肪结合素昼夜变异曲线较健康人群要低。哮喘患者的血清脂肪结合素浓度较健康人低。哮喘患者吸入特异性变应原后并未强烈引起血清脂肪结合素浓度的改变。这种逆向相关性（如，脂肪结合素对哮喘的作用）有待进一步的研究。如果未来的研究证实血清脂肪结合素对哮喘是一种保护性因子，那么，调节脂肪结合素可能成为治疗哮喘的新方法。
（于娜 中国医科大学附属第一医院呼吸科 110001 摘译）
（Chest February 2009 135:287-294; doi:10.1378/chest.08-1705）
（Chest February 2009 135:287-294; doi:10.1378/chest.08-1705）
Effect of Specific Allergen Inhalation on Serum Adiponectin in Human Asthma
Keywords: adipokine 、adiponectin 、allergen inhalation challenge 、asthma 、leptin
Keywords: adipokine 、adiponectin 、allergen inhalation challenge 、asthma 、leptin
Akshay Sood, MD, MPH, FCCP*,
Clifford Qualls, PhD,
JeanClare Seagrave, PhD,
Christine Stidley, PhD,
Tereassa Archibeque, RRT,
Marianne Berwick, PhD and
Mark Schuyler, MD, FCCP
Abstract
Background: Adiponectin is associated with asthma. The direction of this association is not known in humans. In mice, this association is bidirectional: allergen inhalation affects serum adiponectin, and exogenous adiponectin administration affects asthma. We sought to evaluate whether allergen inhalation affects serum adiponectin in human asthma.
Methods: This study included eight sensitized subjects with mild asthma and six healthy control subjects. Asthmatic subjects were challenged with inhaled specific allergen (positive allergen skin test), methacholine, and irrelevant allergen (negative allergen skin test). Control subjects were challenged with irrelevant allergen. Sequential serum samples were obtained before and nine times after each challenge. Serum adiponectin- (primary outcome), leptin-, adiponectin-to-leptin ratio-, eotaxin-, and tumor necrosis factor-α–response curves, area under the curves, and baseline and peak concentrations were evaluated. Statistical analysis used repeated-measures analysis of variance and paired t tests.
Results: There were no significant differences in outcome measures among the challenges in asthmatic subjects or when compared to control subjects. Type II error is an unlikely explanation for these findings because the study was adequately powered to detect changes in serum adiponectin, as reported in the literature. Further, pooled data showed that serum adiponectin diurnal variation curves were lower in asthmatic subjects than in control subjects.
Conclusions: Serum adiponectin concentrations are lower in asthmatic subjects than in control subjects. Specific allergen inhalation in asthmatic subjects does not acutely affect serum adiponectin concentrations. The reverse association (ie, effect of adiponectin on asthma) needs further study. If future studies prove adiponectin to be a protective factor for asthma, modulating adiponectin may open a new approach toward managing asthma.
