Increased serum HO-1 in hemophagocytic syndrome and adult-onset Still's disease: use in the differential diagnosis of hyperferritinemia.
Increased serum HO-1 in hemophagocytic syndrome and adult-onset Still's disease: use in the differential diagnosis of hyperferritinemia.
复制标题
血清HO-1在嗜血型综合征和成人疾病中的血清HO-1疾病：用于高铁蛋白血症的鉴别诊断。
DOI：
10.1186/ar1721
复制
发表时间：
2005
影响因子：
4.9
通讯作者：
Ishigatsubo, Yoshiaki
中科院分区：
文献类型：
--
作者：
Kirino, Yohei;Takeno, Mitsuhiro;Iwasaki, Mika;Ueda, Atsuhisa;Ohno, Shigeru;Shirai, Akira;Kanamori, Heiwa;Tanaka, Katsuaki;Ishigatsubo, Yoshiaki
血红素加氧酶-1（HO-1）是一种诱导型血红素降解酶，由巨噬细胞和内皮细胞在各种应激反应中表达。由于铁蛋白的合成是由亚铁离子，这是血红素降解的产物刺激，我们研究了HO-1和铁蛋白水平的噬血细胞综合征（HPS），成人型斯蒂尔病（ASD），和其他疾病，可能会导致高铁蛋白血症患者的血清中的关系。HPS患者7例，ASD患者10例，其他风湿性疾病患者73例，肝病患者20例，因血液系统疾病反复输血者10例，健康志愿者22例。ELISA法测定血清HO-1和铁蛋白水平。分别采用实时PCR和免疫细胞化学技术检测外周血单个核细胞（PBMCs）HO-1 mRNA和蛋白的表达。活动期HPS和ASD患者血清HO-1水平显著高于其他各组（P < 0.01）。HO-1水平在其他原因引起的高铁蛋白血症患者中不升高，但在皮肌炎/多发性肌炎患者中中度升高。在HPS和ASD患者中，血清HO-1水平与血清铁蛋白水平密切相关，经治疗缓解后两者均恢复正常。部分HPS和ASD患者PBMC中HO-1 mRNA表达增加。高铁蛋白血症与HPS和ASD患者血清HO-1水平升高密切相关，但与其他疾病无关，这表明血清HO-1和铁蛋白水平的测定有助于高铁蛋白血症的鉴别诊断，也可能有助于监测HPS和ASD的疾病活动。
Heme oxygenase-1 (HO-1), an inducible heme-degrading enzyme, is expressed by macrophages and endothelial cells in response to various stresses. Because ferritin synthesis is stimulated by Fe2+, which is a product of heme degradation, we examined the relation between HO-1 and ferritin levels in the serum of patients with hemophagocytic syndrome (HPS), adult-onset Still's disease (ASD), and other diseases that may cause hyperferritinemia. Seven patients with HPS, 10 with ASD, 73 with other rheumatic diseases, 20 with liver diseases, 10 recipients of repeated blood transfusion because of hematological disorders, and 22 healthy volunteers were enrolled. Serum HO-1 and ferritin levels were determined by ELISA. Expression of HO-1 mRNA and protein by peripheral blood mononuclear cells (PBMCs) was determined by real-time PCR and immunocytochemical techniques, respectively. Serum levels of HO-1 were significantly higher in patients with active HPS and ASD than in the other groups (P < 0.01). HO-1 levels were not elevated in patients with other causes of hyperferritinemia but were moderately elevated in patients with dermatomyositis/polymyositis. Among patients with HPS and ASD, serum HO-1 levels correlated closely with serum ferritin levels, and the levels of both returned to normal after therapy had induced remission. Increased expression of HO-1 mRNA was confirmed in PBMCs from some patients with HPS and ASD. Hyperferritinemia correlated closely with increased serum HO-1 in patients with HPS and ASD but not other conditions, indicating that measurement of serum HO-1 and ferritin levels would be useful in the differential diagnosis of hyperferritinemia and perhaps also in monitoring disease activity in HPS and ASD.