Hershfield M S
Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710, USA.
Hum Mutat. 1995;5(2):107-12. doi: 10.1002/humu.1380050202.
PEG-ADA is a long-circulating form of adenosine deaminase (ADA) that has been in use for > 8 years as replacement therapy for severe combined immunodeficiency disease due to ADA deficiency. Treatment with PEG-ADA almost completely corrects metabolic abnormalities, allowing the recovery of a variable degree of immune function. Although not normal, the level of function achieved has in most cases been sufficient to protect against opportunistic and life-threatening infections. PEG-ADA has been used as an alternative for patients who lack an HLA-identical bone marrow donor, but are judged to be at too high a risk for undergoing HLA-haploidentical marrow transplantation. To date, mortality and morbidity with PEG-ADA have been less than for the latter procedure. PEG-ADA has also been an important adjunct to attempts to develop somatic cell gene therapy for ADA deficiency, although its continued use poses a problem for evaluation of the benefit of gene therapy. As a true "orphan drug" developed to treat a very small patient population, the cost per patient of PEG-ADA is very high.
聚乙二醇化腺苷脱氨酶(PEG-ADA)是腺苷脱氨酶(ADA)的一种长效循环形式,作为ADA缺乏所致重症联合免疫缺陷病的替代疗法已使用超过8年。PEG-ADA治疗几乎能完全纠正代谢异常,使免疫功能恢复到不同程度。虽然未恢复正常,但在大多数情况下所达到的功能水平足以预防机会性感染和危及生命的感染。PEG-ADA已被用作缺乏人类白细胞抗原(HLA)匹配骨髓供体但被判定接受HLA单倍型骨髓移植风险过高的患者的替代疗法。迄今为止,PEG-ADA治疗的死亡率和发病率低于后者。PEG-ADA也是开发ADA缺乏体细胞基因治疗的重要辅助手段,尽管其持续使用给评估基因治疗的益处带来了问题。作为一种为治疗极少数患者群体而开发的真正“孤儿药”,PEG-ADA的每位患者治疗成本非常高。