ARTHROPATHY IN THALASSEMIA PATIENTS RECEIVING DEFERIPRONE

被引:59
作者
BERKOVITCH, M
LAXER, RM
INMAN, R
KOREN, G
PRITZKER, KPH
FRITZLER, MJ
OLIVIERI, NF
机构
[1] HOSP SICK CHILDREN,DEPT PEDIAT,HAEMOGLOBINOPATHY PROGRAM,TORONTO M5G 1X8,ON,CANADA
[2] UNIV TORONTO,TORONTO HOSP,DEPT MED,TORONTO,ON,CANADA
[3] UNIV TORONTO,MT SINAI HOSP,DEPT PATHOL,TORONTO M5G 1X5,ON,CANADA
[4] UNIV ALBERTA,MCCALG CTR JOINT INJURY & ARTHRITIS RES,CALGARY,AB,CANADA
关键词
D O I
10.1016/S0140-6736(94)92585-2
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The iron chelator deferiprone (L1) reduces tissue iron stores in iron-loaded patients. Three of sixteen patients treated with deferiprone developed joint pain and swelling without evidence of systemic lupus erythematosus (SLE). Articular cartilage, synovial hypertrophy and iron deposition, and synovial lining cell proliferation, with no inflammatory or allergic reaction, were observed on synovial exploration and biopsy. Symptoms resolved partly or completely during continued drug administration. We hypothesise that deferiprone-induced shifts of iron to synovium resulted in tissue damage, accelerated by free-radical formation during incomplete complexation of iron and this bidentate chelator. This deferiprone-associated symptom complex is not associated with drug-induced SLE, and does not progress in severity during continued therapy.
引用
收藏
页码:1471 / 1472
页数:2
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