哮喘儿童血清维生素D水平下降与皮质激素使用增加相关
2010/08/11
背景：目前，有关哮喘儿童维生素D（vitD）缺陷的相关临床变量了解较少。目的：本试验在哮喘儿童中研究与VitD缺陷相关的疾病变量，以及VitD与皮质激素介导的抗炎反应之间的作用。
方法：对100名哮喘儿童检测血清25羟维生素D水平，研究25羟维生素D水平与患者特征之间的关系。此外，我们检测了VitD对地塞米松（DEX）诱导的PBMC内丝裂原活化蛋白激酶磷酸酶1和IL-10产生的影响。
结果：血清25羟基维生素D的平均水平为31 ng/mL。47％的患者VitD水平不足（<30 ng/mL），17％的患者存在VitD缺陷（<20 ng/mL）。Log(10) IgE (P = .01, rho = -0.25)和阳性气源性过敏原皮肤针刺反应（P = .02, rho = -0.23）与VitD水平呈现显著负相关。FEV(1)预测值（P = .004, rho = 0.34）和FEV1/用力肺活量比值（P = .01, rho = 0.30）均与VitD水 平正相关。激素吸入使用（P = .0475）、口服激素使用（P = .02）和激素总使用剂量（P = .001）与VitD水平成显著负相关。VitD与DEX在诱导丝裂原活化蛋白激酶磷酸酶1和IL-10 mRNA表达上显著强于单用DEX（P < .01）。在激素抵抗的试验模型中，DEX单用不能抑制T细胞增加，额外给予DEX后能以剂量依赖的方式抑制细胞增殖。
结论：哮喘患者的皮质激素使用和气道受限加重与血清VitD水平较低有关。在哮喘患者中，VitD能增加糖皮质激素对PBMCs的作用，增加DEX的体外免疫抑制作用。
（苏楠 审校）
J Allergy Clin Immunol. 2010 May;125(5):995-1000. Epub 2010 Apr 9.
Decreased serum vitamin D levels in children with asthma are associated with increased corticosteroid use.
Searing DA, Zhang Y, Murphy JR, Hauk PJ, Goleva E, Leung DY.
Division of Allergy and Immunology, Department of Pediatrics, National Jewish Health, Denver, CO 80206, USA.
Abstract
BACKGROUND: There is little knowledge about clinical variables associated with vitamin D (VitD) insufficiency in asthmatic children.
OBJECTIVE: We sought to investigate disease variables associated with VitD insufficiency in patients with childhood asthma and interaction of VitD with corticosteroid-mediated anti-inflammatory responses.
METHODS: We analyzed 25-hydroxyvitamin D serum levels in 100 asthmatic children to investigate relationships between 25-hydroxyvitamin D levels and patients’ characteristics. We determined VitD’s effects on dexamethasone (DEX) induction of mitogen-activated protein kinase phosphatase 1 and IL-10 in PBMCs.
RESULTS: The median 25-hydroxyvitamin D serum level was 31 ng/mL. Forty-seven percent of subjects had VitD levels in the insufficient range (<30 ng/mL), whereas 17% were VitD deficient (<20 ng/mL). Log(10) IgE (P = .01, rho = -0.25) and the number of positive aeroallergen skin prick test responses (P = .02, rho = -0.23) showed a significant inverse correlation with VitD levels, whereas FEV(1) percent predicted (P = .004, rho = 0.34) and FEV(1)/forced vital capacity ratio (P = .01, rho = 0.30) showed a significant positive correlation with VitD levels. The use of inhaled steroids (P = .0475), use of oral steroids (P = .02), and total steroid dose (P = .001) all showed significant inverse correlations with VitD levels. The amount of mitogen-activated protein kinase phosphatase 1 and IL10 mRNA induced by VitD plus DEX was significantly greater than that induced by DEX alone (P < .01). In an experimental model of steroid resistance in which DEX alone did not inhibit T-cell proliferation, addition of VitD to DEX resulted in significant dose-dependent suppression of cell proliferation.
CONCLUSIONS: Corticosteroid use and worsening airflow limitation are associated with lower VitD serum levels in asthmatic patients. VitD enhances glucocorticoid action in PBMCs from asthmatic patients and enhances the immunosuppressive function of DEX in vitro.
J Allergy Clin Immunol. 2010 May;125(5):995-1000. Epub 2010 Apr 9.
方法：对100名哮喘儿童检测血清25羟维生素D水平，研究25羟维生素D水平与患者特征之间的关系。此外，我们检测了VitD对地塞米松（DEX）诱导的PBMC内丝裂原活化蛋白激酶磷酸酶1和IL-10产生的影响。
结果：血清25羟基维生素D的平均水平为31 ng/mL。47％的患者VitD水平不足（<30 ng/mL），17％的患者存在VitD缺陷（<20 ng/mL）。Log(10) IgE (P = .01, rho = -0.25)和阳性气源性过敏原皮肤针刺反应（P = .02, rho = -0.23）与VitD水平呈现显著负相关。FEV(1)预测值（P = .004, rho = 0.34）和FEV1/用力肺活量比值（P = .01, rho = 0.30）均与VitD水 平正相关。激素吸入使用（P = .0475）、口服激素使用（P = .02）和激素总使用剂量（P = .001）与VitD水平成显著负相关。VitD与DEX在诱导丝裂原活化蛋白激酶磷酸酶1和IL-10 mRNA表达上显著强于单用DEX（P < .01）。在激素抵抗的试验模型中，DEX单用不能抑制T细胞增加，额外给予DEX后能以剂量依赖的方式抑制细胞增殖。
结论：哮喘患者的皮质激素使用和气道受限加重与血清VitD水平较低有关。在哮喘患者中，VitD能增加糖皮质激素对PBMCs的作用，增加DEX的体外免疫抑制作用。
（苏楠 审校）
J Allergy Clin Immunol. 2010 May;125(5):995-1000. Epub 2010 Apr 9.
Decreased serum vitamin D levels in children with asthma are associated with increased corticosteroid use.
Searing DA, Zhang Y, Murphy JR, Hauk PJ, Goleva E, Leung DY.
Division of Allergy and Immunology, Department of Pediatrics, National Jewish Health, Denver, CO 80206, USA.
Abstract
BACKGROUND: There is little knowledge about clinical variables associated with vitamin D (VitD) insufficiency in asthmatic children.
OBJECTIVE: We sought to investigate disease variables associated with VitD insufficiency in patients with childhood asthma and interaction of VitD with corticosteroid-mediated anti-inflammatory responses.
METHODS: We analyzed 25-hydroxyvitamin D serum levels in 100 asthmatic children to investigate relationships between 25-hydroxyvitamin D levels and patients’ characteristics. We determined VitD’s effects on dexamethasone (DEX) induction of mitogen-activated protein kinase phosphatase 1 and IL-10 in PBMCs.
RESULTS: The median 25-hydroxyvitamin D serum level was 31 ng/mL. Forty-seven percent of subjects had VitD levels in the insufficient range (<30 ng/mL), whereas 17% were VitD deficient (<20 ng/mL). Log(10) IgE (P = .01, rho = -0.25) and the number of positive aeroallergen skin prick test responses (P = .02, rho = -0.23) showed a significant inverse correlation with VitD levels, whereas FEV(1) percent predicted (P = .004, rho = 0.34) and FEV(1)/forced vital capacity ratio (P = .01, rho = 0.30) showed a significant positive correlation with VitD levels. The use of inhaled steroids (P = .0475), use of oral steroids (P = .02), and total steroid dose (P = .001) all showed significant inverse correlations with VitD levels. The amount of mitogen-activated protein kinase phosphatase 1 and IL10 mRNA induced by VitD plus DEX was significantly greater than that induced by DEX alone (P < .01). In an experimental model of steroid resistance in which DEX alone did not inhibit T-cell proliferation, addition of VitD to DEX resulted in significant dose-dependent suppression of cell proliferation.
CONCLUSIONS: Corticosteroid use and worsening airflow limitation are associated with lower VitD serum levels in asthmatic patients. VitD enhances glucocorticoid action in PBMCs from asthmatic patients and enhances the immunosuppressive function of DEX in vitro.
J Allergy Clin Immunol. 2010 May;125(5):995-1000. Epub 2010 Apr 9.
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