Variation in C - reactive protein response according to host and mycobacterial characteristics in active tuberculosis.

Variation in C - reactive protein response according to host and mycobacterial characteristics in active tuberculosis.
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DOI:
10.1186/s12879-016-1612-1
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发表时间:
2016-06-10
影响因子:
3.7
通讯作者:
Lipman M
Lipman M
中科院分区:
医学3区
文献类型:
--
作者:
Brown J;Clark K;Smith C;Hopwood J;Lynard O;Toolan M;Creer D;Barker J;Breen R;Brown T;Cropley I;Lipman M

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通常在活动性结核病 (TB) 患者中测量 C 反应蛋白 (CRP) 反应,但对其与 TB 临床特征的关系,或者不同种族或不同结核分枝杆菌 (M.tb) 菌株类型之间的反应是否存在差异,人们知之甚少。我们报告了结核病低发病率地区结核病居民的大都市人群治疗前基线血清 CRP 与疾病特征之间的关系。对 2003 年至 2014 年间在英国伦敦四个地点接受结核病治疗的患者进行了评估并收集了以下特征的数据:基线 CRP 水平;人口统计(种族、性别和年龄);艾滋病毒状况;结核病部位;痰涂片(肺部病例)和培养结果。还使用 VNTR 分型数据评估了培养阳性肺部病例中结核菌菌株类型的影响。分析纳入了 3222 名患者,其中 72% 的患者在开始结核病治疗前 4 周或 4 周内具有基线 CRP。与培养阴性病例相比,培养阳性病例的 CRP 结果显着更高:中位数 49 mg/L (16–103 mg/L) vs 19 mg/L (IQR 5–72 mg/L),p = <0.001。在患有肺部疾病的患者中,涂片阳性病例的 CRP 高于涂片阴性病例:67 mg/L (31–122 mg/L) vs 24 mg/L (7–72 mg/L),p<0.001。 HIV 阳性病例的基线 CRP 高于 HIV 阴性病例:75 mg/L (26–136 mg/L) vs 37 mg/L (10–88 mg/L),p <0.001。不同的疾病部位与基线 CRP 的差异相关:预计分枝杆菌负荷较高的部位(例如肺部疾病和播散性疾病)的 CRP 显着高于皮肤、淋巴结或中枢神经系统疾病等部位,而这些部位的分枝杆菌负荷在 HIV 阴性受试者中通常较低。在针对宿主特征和 M.tb 菌株类型进行调整的多变量对数尺度线性回归模型中,东非印度菌株的感染与基线 CRP 显着降低相关(CRP 倍数变化为 0.51 (0.34–0.77),p<0.01)。宿主和分枝杆菌因素与结核病的基线 CRP 反应密切相关。该分析表明,根据种族、结核分枝杆菌菌株类型和疾病部位,先天免疫反应存在重要差异。这可能反映了不同的分枝杆菌负荷或宿主免疫反应。本文的在线版本 (doi:10.1186/s12879-016-1612-1) 包含补充材料,可供授权用户使用。
The C - reactive protein (CRP) response is often measured in patients with active tuberculosis (TB) yet little is known about its relationship to clinical features in TB, or whether responses differ between ethnic groups or with different Mycobacterium tuberculosis (M.tb) strain types. We report the relationship between baseline serum CRP prior to treatment and disease characteristics in a metropolitan population with TB resident in a low TB incidence region. People treated for TB at four London, UK sites between 2003 and 2014 were assessed and data collected on the following characteristics: baseline CRP level; demographics (ethnicity, gender and age); HIV status; site of TB disease; sputum smear (in pulmonary cases) and culture results. The effect of TB strain-type was also assessed in culture-positive pulmonary cases using VNTR typing data. Three thousands two hundred twenty-two patients were included in the analysis of which 72 % had a baseline CRP at or within 4 weeks prior to starting TB treatment. CRP results were significantly higher in culture positive cases compared to culture negative cases: median 49 mg/L (16–103 mg/L) vs 19 mg/L (IQR 5–72 mg/L), p = <0.001. In those with pulmonary disease, smear positive cases had a higher CRP than smear negative cases: 67 mg/L (31–122 mg/L) vs 24 mg/L (7–72 mg/L), p < 0.001. HIV positive cases had higher baseline CRPs than HIV negative cases: 75 mg/L (26–136 mg/L) vs 37 mg/L (10–88 mg/L), p <0.001. Differing sites of disease were associated with differences in baseline CRP: locations that might be expected to have a high mycobacterial load (e.g. pulmonary disease and disseminated disease) had a significantly higher CRP than those such as skin, lymph node or CNS disease, where the mycobacterial load is typically low in HIV negative subjects. In a multivariable log-scale linear regression model adjusting for host characteristics and M.tb strain type, infection with the East African Indian strain was associated with significantly lower baseline-CRP (fold-change in CRP 0.51 (0.34–0.77), p < 0.01). Host and mycobacterial factors are strongly associated with baseline CRP response in tuberculosis. This analysis suggests that there are important differences in innate immune response according to ethnicity, Mtb strain type and site of disease. This may reflect differing mycobacterial loads or host immune responses. The online version of this article (doi:10.1186/s12879-016-1612-1) contains supplementary material, which is available to authorized users.