Anticoagulant therapy for idiopathic pulmonary fibrosis
Anticoagulant therapy for idiopathic pulmonary fibrosis
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DOI：
10.1378/chest.128.3.1475
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发表时间：
2005-09-01
期刊：
影响因子：
9.6
通讯作者：
Sasaki, H
中科院分区：
文献类型：
--
作者：
Kubo, H;Nakayama, K;Sasaki, H
研究目的：评估抗凝治疗对特发性肺纤维化 (IPF) 患者生存的影响。设计：前瞻性研究。地点：位于日本宫城县的五家医院，包括一家大学医院、一家红十字会医院、两家公立综合医院和一家市立医院。患者：收治 56 名 IPF 患者（平均年龄，69.4 岁；范围，47 至 89） 2001 年 4 月至 2004 年 4 月在医院进行治疗。 干预措施：患者被分配接受单独泼尼松龙治疗或泼尼松龙联合抗凝治疗。抗凝药物包括门诊口服华法林和重新住院的严重进行性呼吸衰竭患者使用低分子肝素。测量和结果：非抗凝组和抗凝组的基线特征，包括年龄、性别、临床状况、肺功能、血浆d-二聚体水平没有差异。评估总生存期和无住院期。非抗凝组和抗凝组的生存曲线存在显着差异，风险比为2.9（p = 0.04，Cox回归模型）。组间无住院期的概率没有显着差异。在本研究中，临床恶化的主要原因是随访期间的急性加重。因此，还评估了急性加重患者的死亡率和血浆 d-二聚体水平。与非抗凝剂组相比，抗凝剂组与 IPF 急性加重相关的死亡率显着降低（分别为 18% 和 71%；p = 0.008，Fisher Exact 检验）。此外，在 IPF 急性加重期间，死亡患者的血浆 d-二聚体水平显着高于幸存者（3.3 +/- 2.3 μg/mL vs 0.9 +/- 0.7 μg/mL，p < 0.0001）。对非抗凝组中因 IPF 恶化而死亡的 3 名患者进行的组织学分析显示了普通间质性肺炎和急性肺损伤的特征。结论：我们的数据表明，血浆 d-二聚体水平与 IPF 急性恶化患者的死亡率相关，抗凝治疗对 IPF 患者的生存有有益影响。
Study objective: To evaluate the effect of anticoagulant therapy on the survival of patients with idiopathic pulmonar fibrosis (IPF).Design: Prospective study.Setting: Five hospitals located in the Miyagi prefecture in Japan, including a university hospital, a Red Cross hospital, two public general hospitals, and a municipal hospital.Patients: Fifty-six patients with IPF (mean age, 69.4 years; range, 47 to 89) admitted to the hospitals from April 2001 to April 2004.Interventions: Patients were assigned to receive prednisolone alone or prednisolone plus anticoagulant therapy. The anticoagulants included oral warfarin in an outpatient setting and low-molecular-weight heparin for rehospitalized patients with severely progressive respiratory failure.Measurements and results: There was no difference in baseline characteristics, including age, gender, clinical condition, pulmonary, function, and plasma d-dimer level between the nonanticoagulant group and the anticoagulant group. The overall survival and hospitalization-free periods were assessed. There was a significant difference between survival curves of the nonanticoagulant group and the anticoagulant group, with a 2.9 hazard ratio (p = 0.04, Cox regression model). There was no significant difference in the probability, of a hospitalization-free period between groups. The major cause of clinical deterioration was acute exacerbation during follow-up in the present study. Therefore, the mortality, and plasma d-dimer levels in patients with an acute exacerbation were also assessed. The mortality, associated with acute exacerbations of IPF in the anticoagulant group was significantly reduced compared to that in the nonanticop agulant group (18% vs 71%, respectively; p = 0.008, Fisher Exact Test). Furthermore, the plasma d-dimer levels in patients who died were significantly higher than those in survivors during acute exacerbation of IPF (3.3 +/- 2.3 mu g/mL vs 0.9 +/- 0.7 mu g/mL, p < 0.0001). Histologic analysis performed in three patients who died due to an exacerbation of IPF in the nonanticoagulant group demonstrated the features of usual interstitial pneumonia and acute lung injury.Conclusions: Our data suggested that plasma d-dimer levels are associated with mortality in patients with an acute exacerbation of IPF, and that anticoagulant therapy has a beneficial effect on survival in patients with IPF.