目的 探讨儿童重症肺炎继发噬血细胞性淋巴组织细胞增生症（HLH）的危险因素。方法 回顾性分析2012年10月1日至2019年12月31日住院治疗并明确诊断为重症肺炎继发HLH（观察组）患儿的临床资料。随机选取2019年住院就诊的重症肺炎患儿作为对照组。比较两组间临床特征，分析不同指标对于重症肺炎继发HLH的预测价值。结果 观察组38例，对照组96例。与对照组相比，观察组年龄较大，6月龄~2岁比例较高，发热、嗜睡、反应差和烦躁比例较高，中位热程较长，肝、脾、淋巴结肿大，皮疹，浮肿的比例较高，肺部听诊中细湿啰音、气促和/或发绀的比例较低，差异有统计学意义（P<0.05）。与对照组相比，观察组丙氨酸氨基转移酶（ALT）、天冬氨酸氨基转移酶（AST）、乳酸脱氢酶（LDH）异常升高，白蛋白<30 g/L，C反应蛋白（CRP）>8 mg/L，降钙素原（PCT）>0.15 ng/mL的比例较高，腺病毒和真菌检出比例较高而RNA病毒检出比例较低，差异有统计学意义（P<0.05）。观察组胸腔积液、肺实变/肺不张、双肺广泛病变发生率均高于对照组，住院天数长于对照组，病死率和ICU入住率高于对照组，差异有统计学意义（P<0.05）。LDH对于重症肺炎继发HLH的预测价值较高，曲线下面积（AUC）为0.93（0.88~0.98），截断值为804.35 IU/L。结论 重症肺炎继发HLH患儿较未继发HLH者起病年龄大，住院天数长、病死率更高，LDH升高及白蛋白降低更明显。腺病毒感染、存在胸腔积液的重症肺炎患儿更易继发HLH。

Objective To explore the risk factors of hemophagocytic lymphohistiocytosis (HLH) secondary to severe pneumonia in children. Methods The clinical data of children hospitalized from October 1, 2012 to December 31, 2019 and diagnosed with severe pneumonia secondary to HLH (observation group) were retrospectively analyzed. Children with severe pneumonia hospitalized in 2019 were randomly selected as the control group. Clinical characteristics, laboratory tests and treatment results between the two groups were compared, and the predictive value of different indicators for HLH secondary to severe pneumonia were analyzed. Results There were 38 cases in the observation group and 96 cases in the control group. Compared with the control group, the observation group had a higher age of onset, a higher proportion of 6 months to 2 years old, a higher proportion of fever, lethargy, poor reaction and irritability, a longer median heat course, a higher proportion of liver, spleen, lymph node swelling, rash and edema, and a lower proportion of fine wet rales, shortness of breath and / or cyanosis in lung auscultation (all P< 0.05). In the observation group, ALT, AST and LDH were abnormally elevated, the proportion of albumin < 30 g/L, CRP > 8 mg/L, and PCT > 0.15 ng/mL was higher, the proportion of adenovirus and fungi was higher, and the proportion of RNA virus was lower. The difference was statistically significant (P<0.05). The incidence of pleural effusion, lung consolidation/atelectasis and extensive lesions of both lungs in the observation group were higher than that in the control group (all P<0.05), the length of hospitalization was longer than that in the control group, and the mortality and ICU occupancy rate were higher than that in the control group (all P<0.05). Lactate dehydrogenase has a high predictive value for HLH secondary to severe pneumonia. The area under the curve is 0.93 (0.88-0.98), and the cutoff value is 804.35 IU/L. Conclusion Compared with those without HLH, children with HLH secondary to severe pneumonia have older onset age, longer hospitalization time, higher mortality, higher lactate dehydrogenase and lower albumin. Children with severe pneumonia with adenovirus infection and pleural effusion are more likely to develop HLH.