Sakiyama T
Department of 1st Pathology, St. Marianna University School of Medicine.
Nihon Rinsho. 1996 Dec;54(12):3328-32.
The clinical manifestation, diagnosis, pathogenesis, pathophysiology and treatment of purine nucleoside phosphorylase (PNP) deficiency is overviewed. Among the severe combined immunodeficiency syndrome (SCID), PNP deficiency was 2ndly found as an autosomal recessively heritable purine metabolic disease. This disease is characterized by severe T-cell immunodysfunction accompanied by marked low level of uricemia and uricosuria. In addition, this concurrence strongly suggests the diagnosis of PNP deficiency. Neurological manifestations are found in two-third of the reported cases. About 30 cases have been reported worldwide. Their ages at onset varied from birth to 6 years and their outcome is usually fatal terminating in viral infection or lymphoma. Our first case and her sister died with varicella and lymphoma, respectively. No clinical benefit was found with normalized uricemia after erythrocyte transfusion in our case. Bone marrow transplantation and future gene therapy are reviewed.
本文综述了嘌呤核苷磷酸化酶(PNP)缺乏症的临床表现、诊断、发病机制、病理生理学及治疗。在严重联合免疫缺陷综合征(SCID)中,PNP缺乏症是第二常见的常染色体隐性遗传嘌呤代谢疾病。该疾病的特征是严重的T细胞免疫功能障碍,伴有明显的低尿酸血症和低尿酸尿症。此外,这种并发情况强烈提示PNP缺乏症的诊断。在三分之二的报道病例中发现有神经学表现。全球已报道约30例。发病年龄从出生到6岁不等,其结局通常是致命的,最终死于病毒感染或淋巴瘤。我们的首例病例及其妹妹分别死于水痘和淋巴瘤。在我们的病例中,红细胞输血后尿酸血症恢复正常,但未发现临床益处。本文还综述了骨髓移植及未来的基因治疗。