393例过敏性紫癜患者临床及肾脏损害危险因素分析

目的:明确过敏性紫癜(HSP)的临床特点及肾脏损害的危险因素。方法:回顾性分析393例HSP住院患者的临床资料,对发病年龄、病程等与肾脏损害的关系进行单因素和多因素分析。结果:(1)发病年龄主要在4~18岁,占75.32%,发病月份以1月和3月最多,上呼吸道感染是主要诱因(24.42%);(2)紫癜累及双下肢392例(99.74%),臀部及外阴165例(41.98%)、双上肢115例(29.26%);272例(69.21%)患者皮损在1个月内消失;(3)136例患者有关节症状(34.61%),193例(49.11%)有胃肠道症。212例(53.94%)出现肾脏损害,临床上多表现为血尿和蛋白尿;(4)年龄≥10岁、皮疹反复≥1个月及IgA升高与肾脏损害存在正相关(P0.05)。结论:HSP有年龄、季节特点,发病诱因常见于上呼吸道感染,发病年龄≥10岁、紫癜反复≥1个月、IgA升高是肾脏损害的危险因素。

Analysis of 393 patients with Henoch-Schonlein purpura and the risk factors of renal damage

Objective: To determine the clinical characteristics of 393 inpatients with Henoch-Schonlein purpura (HSP) and to analyze the risk factors of renal damage.Methods: The date of 393 patients with HSP was analyzed retrospectively and the relationship among the age at onset, the duration of course, the onset time and renal damage was analyzed by the univariate and multivariate analysis.Results: ① The age at onset ranged from 4 to 18 years old in 296 patients (75.32%).The onset time of HSP was in January and March in majority of the patients.Many patients (24.42%) had an upper respiratory tract infection before the onset of the disease.② The lesions of purpura located on lower limbs in 392 patients (99.74%), followed by hip and vulva in 165 (41.98%), upper limbers in 115 (29.26%).The lesions in 272 (69.21%) patients disappeared within one month.③ One hundred and thirty six patients (34.61%) presented with the joint symptoms, 193 (49.11%) with gastrointestinal symptoms, 212 (53.94%) with renal damage manifested with hematuria and proteinuria.④ The univariate and multivariate analysis showed that renal damage was associated with the age at onset ≥10 years old, the duration of the purpura for more than one month and the high level of IgA (P<0.05).Conclusion: HSP has age and season predilection.The most important inducing factor was upper respiratory tract infection.The risk factors of renal damage included the age at onset ≥10 years old, the duration of the purpura for more than one month and high level of IgA.