中山大学附属第一医院MICU,广东 广州 510080
吴燕茹,硕士生,研究方向:呼吸与危重症,E-mail:wuyanru3@mail2.sysu.edu.cn
纸质出版日期:2022-11-20,
收稿日期:2022-06-30,
扫 描 看 全 文
吴燕茹,曾勉.免疫抑制宿主肺炎与淋巴细胞的相关性及激素对重症患者结局的影响[J].中山大学学报(医学科学版),2022,43(06):976-984.
WU Yan-ru,ZENG Mian.Correlation Between Immunocompromised Host Pneumonia and Lymphocyte and Influence of Glucocorticoid on Outcome of Severe Patients[J].Journal of Sun Yat-sen University(Medical Sciences),2022,43(06):976-984.
吴燕茹,曾勉.免疫抑制宿主肺炎与淋巴细胞的相关性及激素对重症患者结局的影响[J].中山大学学报(医学科学版),2022,43(06):976-984. DOI: 10.13471/j.cnki.j.sun.yat-sen.univ(med.sci).2022.0613.
WU Yan-ru,ZENG Mian.Correlation Between Immunocompromised Host Pneumonia and Lymphocyte and Influence of Glucocorticoid on Outcome of Severe Patients[J].Journal of Sun Yat-sen University(Medical Sciences),2022,43(06):976-984. DOI: 10.13471/j.cnki.j.sun.yat-sen.univ(med.sci).2022.0613.
目的
2
探究免疫抑制宿主肺炎患者外周血中淋巴细胞与疾病严重程度的相关性,和不同剂量激素使用方案对重症患者临床结局的影响。
方法
2
收集免疫抑制宿主肺炎患者的临床资料,根据ATS/IDSA指南重症肺炎标准,将患者分为重症组和非重症组。采用logistic回归分析筛出与免疫抑制宿主肺炎患者发展为重症肺炎相关的危险因素,并绘制受试者工作曲线(ROC)以评估各危险因素对重症免疫抑制宿主肺炎的预测价值。同时,根据重症组的激素使用情况,将重症患者分为重症+高剂量激素组(泼尼松龙用量≥1 mg·kg
-1
·d
-1
或等效剂量激素)、重症+低剂量激素组(泼尼松龙用量<1 mg·kg
-1
·d
-1
或等效剂量激素)、重症+未使用激素组,对比三组患者28 d存活率,以评估激素治疗对重症患者结局的影响。
结果
2
重症组淋巴细胞绝对值、T淋巴细胞百分比、T淋巴细胞绝对值、CD4
+
T淋巴细胞绝对值均低于非重症组患者(
P
<0.05)。重症组IL-2、IL-4、IL-6高于非重症组患者,IFN-γ低于非重症组患者(
P
<0.05)。logistic 回归分析:CRP及PCT的升高、PT的延长是与免疫抑制宿主肺炎患者发展为重症肺炎相关的独立危险因素,而血小板、T淋巴细胞绝对值的升高为免疫抑制宿主肺炎的独立保护因素。ROC曲线分析显示,相比于其他危险因素,T淋巴细胞绝对值计数对免疫抑制宿主肺炎患者发展至重症的风险评估具有较好的预测价值。当T淋巴细胞绝对值计数低于874.65个/μL,判断重症型的敏感度90.9%,特异度43.5%。曲线下面积(AUC)为0.723[95%CI (0.649,0.797)]。重症+高剂量激素组、重症+低剂量激素组、重症+未使用激素组3组28d存活率分别为45.5%、66.7%、25.0%,重症+低剂量激素组患者28 d存活率高于重症+未使用激素组(
P
<0.05);重症+低剂量激素组患者28 d存活率高于重症+高剂量激素组患者,但差异无统计学意义(
P
>0.05)。
结论
2
外周血T淋巴细胞绝对值的升高为免疫抑制宿主肺炎的独立保护因素,T淋巴细胞绝对值对患者发展为重症肺炎具有良好预测价值。当T淋巴细胞绝对值计数低于874.65个/μL,预测患者发展为重症免疫抑制宿主肺炎的敏感性达90.9%,低剂量激素治疗可提高重症免疫抑制宿主肺炎的28 d存活率。
Objective
2
The purpose of this article is to explore the relationship between lymphocyte and the severity of immunocompromised host pneumonia, and to examine the effect of different doses of glucocorticoid on the survival outcome of severe group.
Methods
2
The clinical data of immunocompromised host pneumonia patients were collected. The patients were divided into severe group and non-severe group according to the official clinical practice guideline of the ATS/IDSA. Logistic regression analysis was used to search for independent risk factors of severe immunocompromised host pneumonia. Meanwhile, the receiver operating characteristic curves
(
ROCs) were created to evaluate the predictive value of each risk factor. Furthermore, the severe group were divided into three sub-groups according to the dose of glucocorticoid during hospitalization: severe+ high-dose glucocorticoid group (≥1 mg·kg
-1
·d
-1
prednisolone or other equivalent dose of glucocorticoid), severe+ low-dose glucocorticoid group (<1 mg·kg
-1
·d
-1
prednisolone or other equivalent dose of glucocorticoid), and severe+ non-glucocorticoid group. The 28-day survival rates of the three groups were compared to evaluate the effect of glucocorticoid on severe immunocompromised host pneumonia.
Results
2
The levels of lymphocyte absolute value, T lymphocytes percentage, T lymphocyte absolute value, CD4
+
T lymphocyte absolute value in severe pneumonia group were lower than those in non-severe pneumonia group. The results of logistic regression showed that the increase of CRP and PCT and the prolongation of PT were independent risk factors for the severe immunocompromised host pneumonia, while the increase of platelet and T lymphocyte absolute value were independent protective factors for the severe immunocompromised host pneumonia. The ROCs analysis showed that compared with other risk factors, the decrease of T lymphocyte absolute value had better predictive value for the risk assessment of immunocompromised host pneumonia. When the absolute value of T lymphocytes was lower than 874.65 cells /μL, the sensitivity and specificity were 90.9% and 43.5%, respectively. The area under the curve (AUC) was 0.723 [95% confidence interval (0.649, 0.797)]. The survival rate of the severe + high-dose glucocorticoid group was 45.5%. The survival rate of the severe + low-dose glucocorticoid group was 66.7%. The survival rate of the severe + non-dose glucocorticoid group was 25.0%. The survival rate of the severe + low-dose glucocorticoid group was higher than the survival rate of the severe + non-dose(
P
<0.05). Meanwhile, the survival rate of the severe + low-dose glucocorticoid group was higher than the survival rate of the severe + high-dose glucocorticoid group, but no statistically significant difference was found (
P
>
0.05).
Conclusions
2
The increase of T lymphocyte absolute value is the independent protective factor for immunocompromised host pneumonia. The absolute value of T lymphocytes have a good predictive value for the severity of immunocompromised host pneumonia. When the absolute value of T lymphocytes is lower than 874.65 cells/μL, the sensitivity is up to 90.9% . Low-dose glucocorticoid therapy can improve the 28-day survival rate of patients with severe immunosuppressive host pneumonia.
免疫抑制宿主肺炎T淋巴细胞高危因素糖皮质激素
immunocompromised hostpneumoniaT lymphocytesrisk factorsglucocorticoid
Azoulay E, Russel L, Van De Louw A, et al. Diagnosis of severe respiratory infections in immunocompromised patients[J]. Intensive Care Medicine, 2020, 46(2): 298-314.
Ramirez JA, Musher DM, Evans SE, et al. Treatment of community-acquired pneumonia in immunocompromised adults: a consensus statement regarding initial strategies[J]. Chest, 2020,158(5): 1896-1911.
Vila-Corcoles A, Ochoa-Gondar O, Rodriguez-Blanco T, et al. Epidemiology of community-acquired pneumonia in older adults: a population-based study[J]. Respir Med, 2009, 103(2): 309-316.
Letourneau AR, Issa NC, Baden LR. Pneumonia in the immunocompromised host[J]. Curr Opin Pulm Med, 2014, 20(3): 272-279.
Gonzalez C, Johnson T, Rolston K, et al. Predicting pneumonia mortality using CURB-65, PSI, and patient characteristics in patients presenting to the emergency department of a comprehensive cancer center[J]. Cancer medicine, 2014, 3(4): 962-970.
瞿介明, 曹彬. 中国成人社区获得性肺炎诊断和治疗指南(2016年版)[J]. 中华结核和呼吸杂志, 2016, 39(4): 253-279.
Qu JM, Cao B. Guidelines for diagnosis and treatment of community-acquired pneumonia in Chinese adults (2016 ed.) [J].Chin J Tuberc Respir Dis, 2016, 39(4): 253-279.
施毅. 中国成人医院获得性肺炎与呼吸机相关性肺炎诊断和治疗指南(2018年版)[J]. 中华结核和呼吸杂志, 2018,41(4): 255-280.
Shi Y. Guidelines for diagnosis and treatment of hospital acquired pneumonia and ventilator associated pneumonia in adults in China[J]. Chin J Tuberc Respir Dis, 2018, 41(4): 255-280.
Metlay JP, Waterer GW, Long AC, et al. Diagnosis and treatment of adults with community-acquired pneumonia. an official clinical practice guideline of the American thoracic society and infectious diseases society of America[J]. Am J Respir Crit Care Med, 2019, 200(7): e45-e67.
Kuang Z, Yang Y, Wei W, et al. Clinical characteristics and prognosis of community-acquired pneumonia in autoimmune disease-induced immunocompromised host: a retrospective observational study[J]. World J Emerg Med, 2020, 11(3): 145-151.
Rivers EP, Mccord J, Otero R, et al. Clinical utility of b-type natriuretic peptide in early severe sepsis and septic shock[J]. J Intensive Care Med, 2007, 22(6): 363-373.
Saini K, Bolia R, Bhat NK. Incidence, predictors and outcome of sepsis-associated liver injury in children: a prospective observational study[J]. Eur J Pediatr, 2022, 181(4): 1699-1707.
Dhainaut J, Marin N, Mignona A, et al. Hepatic response to sepsis: interaction between coagulation and inflammatory processes[J]. Crit Care Med, 2001,29(7 Suppl):S42-47.
李晟, 刘启明, 孙波, 等. 老年感染所致血小板减少症23例临床分析[J]. 广东医学, 2017, 38(S1): 153-154.
Li S, Liu QM, Sun B, et al. Clinical analysis of 23 cases of senile thrombocytopenia caused by infection[J]. J Guangdong Med, 2017, 38(S1): 153-154.
Iba T, Levy JH. Inflammation and thrombosis: roles of neutrophils, platelets and endothelial cells and their interactions in thrombus formation during sepsis[J]. J Thromb Haemost, 2018,16(2): 231-241.
Stearns-Kurosawa DJ, Osuchowski MF, Valentine C, et al. The pathogenesis of sepsis[J]. Annu Rev Pathol, 2011, 6: 19-48.
Sanson E, Trautwein C. Hepatocytes clear platelets and are key regulators of disseminated intravascular coagulation during sepsis[J]. J Hepatol, 2009,50(5): 1060-1061.
Ware J, Corken A, Khetpal R. Platelet function beyond hemostasis and thrombosis[J]. Curr Opin Hematol, 2013, 20(5): 451-456.
周志刚, 谢云, 冯铁男, 等. 血小板计数短期动态变化对ICU脓毒症患者预后的临床预测价值:一项成人的回顾性队列研究[J]. 中华危重病急救医学, 2020(3): 301-306.
Zhou ZG, Xie Y, Feng TN, et al. The clinical predictive value of short-term dynamic changes of platelet count on the prognosis of patients with sepsis in ICU : an adult retrospective cohort study[J]. Chin Crit Care Med, 2020(3): 301-306.
Tan L, Wang Q, Zhang D, et al. Lymphopenia predicts disease severity of COVID-19: a descriptive and predictive study[J]. Signal Transduct Target Ther, 2020,5(1): 33.
Inoue N, Fushimi K. Adjunctive corticosteroids decreased the risk of mortality of non-HIV pneumocystis pneumonia[J]. Int J Infect Dis, 2019, 79: 109-115.
Lemiale V, Debrumetz A, Delannoy A, et al. Adjunctive steroid in HIV-negative patients with severe pneumocystis pneumonia[J]. Respir Res, 2013,14(1): 87.
Annane D, Bellissant E, Bollaert PE, et al. Corticosteroids for treating sepsis in children and adults[J]. Cochrane Database Syst Rev, 2019, 12(12): D2243.
Lionakis MS, Kontoyiannis DP. Glucocorticoids and invasive fungal infections[J]. Lancet, 2003, 362(9398): 1828-1838.
Park YJ, Lee MJ, Bae J, et al. Effects of glucocorticoid therapy on sepsis depend both on the dose of steroids and on the severity and phase of the animal sepsis model[J]. Life (Basel), 2022, 12(3): 421.
0
浏览量
0
下载量
0
CSCD
关联资源
相关文章
相关作者
相关机构