慢性阻塞性肺疾病患者血浆瘦素和生长激素释放肽水平研究

目的探讨血浆瘦素和生长激素释放肽ghrelin与慢性阻塞性肺疾病（COPD）患者的营养状况和循环炎症因子水平的关系，以及排除营养因素的影响后，瘦素和ghrelin是否与COPD有关。方法检测53例稳定期COPD患者和26名健康对照者的血浆瘦素、总ghrelin、活性ghrelin、肿瘤坏死因子α（TNF-α）和白细胞介素6（IL-6）水平，评价去脂组织和脂肪组织重量。结果低体重COPD患者血浆瘦素水平[2．6（2．0-4．4）ng／L]显著低于正常体重的COPD患者[6．1（5．1-7．8）ng／L]和健康对照者[4．8（3．3-6．1）ng／L]，COPD患者的瘦素含量与脂肪组织重量和TNF-a水平呈显著正相关；校正脂肪组织重量等影响因素后，COPD患者血浆瘦素含量显著高于对照组，且与TNF-α水平显著相关。低体重COPD患者血浆总ghrelin和活性ghrelin水平[1090（860-2838）ng／L和63（50-97）ng／L]均显著高于正常体重的COPD患者[765（651-941）ng／L和47（41-56）ng／L]和健康对照者[844（676-1045）ng／L和54（41-60）ng／L]，COPD患者的总ghrelin水平、活性ghrelin水平均与体重指数呈显著负相关。结论营养不良的稳定期COPD患者血浆瘦素水平降低，总ghrdin和活性ghrelin水平升高，3种激素受营养状态影响，并且对稳定期COPD患者的营养状态起着生理性调节作用。在排除营养因素的影响后，COPD患者瘦素水平相对升高，并与TNF-α水平呈显著正相关，提示瘦素可能与COPD的疾病本身和全身炎症反应有关。

Circulating leptin and ghrelin in patients with chronic obstructive pulmonary disease

OBJECTIVE: To investigate the potential roles of leptin and ghrelin in malnutrition in patients with chronic obstructive pulmonary disease (COPD). METHODS: Plasma leptin, total ghrelin and active ghrelin, TNF-alpha and IL-6 levels were determined in 53 patients with COPD and 26 control subjects. Body compositions were assessed by bioelectrical impedance analysis. RESULTS: Plasma leptin levels were significantly lower in underweight patients than those in normal weight patients and in healthy controls [2.6 (2.0 - 4.4) vs. 6.1 (5.1 - 7.8) vs. 4.8 (3.3 - 6.1) ng/L]. The leptin level was associated positively with fat mass (r = 0.662, P = 0.000) and TNF-alpha (r = 0.431, P = 0.001) in the patients. By a stepwise multiple regression analysis, fat mass, TNF-alpha, presence of COPD, smoking and sex were found to affect leptin level (R(2) = 0.635). Both plasma total ghrelin levels and active ghrelin levels were significantly higher in underweight patients than those in normal weight patients and in healthy controls [total ghrelin: 1090 (860 - 2838) vs. 765 (651 - 941) vs. 844 (676 - 1045) ng/L; active ghrelin: 63 (50 - 97) vs. 47 (41 - 56) vs. 54 (41 - 60) ng/L]. Plasma total ghrelin and active ghrelin were associated negatively with BMI respectively (total ghrelin: r = -0.517, P = 0.000; active ghrelin: r = -0.417, P = 0.002). CONCLUSIONS: Plasma leptin levels were decreased, while plasma total ghrelin and active ghrelin levels were elevated in underweight patients with COPD, and the levels were associated with nutritional parameters. The plasma levels of leptin and ghrelin may be a compensatory mechanism in malnutritional status of COPD. After adjustment for nutritional parameters, leptin levels were elevated in COPD patients and correlated to TNF-alpha. The result suggests that leptin may play a role in systemic inflammation of COPD.