Paediatric Allergy and Immunology, University of Manchester, Manchester, Manchester, UK.
UKPIN UKPID Registry Team, UKPIN, London, UK.
Clin Exp Immunol. 2018 Feb;191(2):212-219. doi: 10.1111/cei.13068. Epub 2017 Nov 3.
Immunoglobulin replacement therapy enhances survival and reduces infection risk in patients with agammaglobulinaemia. We hypothesized that despite regular immunoglobulin therapy, some patients will experience ongoing respiratory infections and develop progressive bronchiectasis with deteriorating lung function. One hundred and thirty-nine (70%) of 199 patients aged 1-80 years from nine cities in the United Kingdom with agammaglobulinaemia currently listed on the UK Primary Immune Deficiency (UKPID) registry were recruited into this retrospective case study and their clinical and laboratory features analysed; 94% were male, 78% of whom had Bruton tyrosine kinase (BTK) gene mutations. All patients were on immunoglobulin replacement therapy and 52% had commenced therapy by the time they were 2 years old. Sixty per cent were also taking prophylactic oral antibiotics; 56% of patients had radiological evidence of bronchiectasis, which developed between the ages of 7 and 45 years. Multivariate analysis showed that three factors were associated significantly with bronchiectasis: reaching 18 years old [relative risk (RR) = 14·2, 95% confidence interval (CI) = 2·7-74·6], history of pneumonia (RR = 3·9, 95% CI = 1·1-13·8) and intravenous immunoglobulin (IVIG) rather than subcutaneous immunoglobulin (SCIG) = (RR = 3·5, 95% CI = 1·2-10·1), while starting immunoglobulin replacement after reaching 2 years of age, gender and recent serum IgG concentration were not associated significantly. Independent of age, patients with bronchiectasis had significantly poorer lung function [predicted forced expiratory volume in 1 s 74% (50-91)] than those without this complication [92% (84-101)] (P < 0·001). We conclude that despite immunoglobulin replacement therapy, many patients with agammaglobulinaemia can develop chronic lung disease and progressive impairment of lung function.
免疫球蛋白替代疗法可提高丙种球蛋白缺乏症患者的生存率并降低其感染风险。我们假设,尽管接受了常规免疫球蛋白治疗,但仍有部分患者会持续发生呼吸道感染,并逐渐发展为支气管扩张,肺功能逐渐恶化。本回顾性病例研究共纳入了来自英国 9 个城市的 199 名 1-80 岁丙种球蛋白缺乏症患者(英国原发性免疫缺陷登记处 UKPID 注册患者),这些患者均定期接受免疫球蛋白治疗;其中 70%(139 名)患者入组。分析了这些患者的临床和实验室特征;94%为男性,78%的患者存在 Bruton 酪氨酸激酶(BTK)基因突变。所有患者均接受免疫球蛋白替代治疗,52%的患者在 2 岁之前开始接受治疗。60%的患者还预防性服用口服抗生素;56%的患者存在支气管扩张的影像学证据,其发病年龄为 7-45 岁。多因素分析显示,3 个因素与支气管扩张显著相关:年龄达到 18 岁(RR=14.2,95%CI=2.7-74.6)、肺炎史(RR=3.9,95%CI=1.1-13.8)和静脉注射免疫球蛋白(IVIG)而非皮下免疫球蛋白(SCIG)(RR=3.5,95%CI=1.2-10.1),而在 2 岁后开始接受免疫球蛋白替代治疗、性别和近期血清 IgG 浓度与支气管扩张无显著相关性。与无支气管扩张的患者相比(74%[50-91]),支气管扩张患者的肺功能明显更差(预计 1 秒用力呼气量 74%[50-91])(P<0.001)。结论:尽管接受了免疫球蛋白替代治疗,但许多丙种球蛋白缺乏症患者仍可能发生慢性肺部疾病和肺功能进行性下降。