Arthropathy in thalassaemia patients receiving deferiprone

Matitiahu Berkovitch, Ronald M. Laxer, Robert Inman, Gideon Koren, Kenneth P.H. Pritzker, M. J. Fritzler, Nancy F. Olivieri

Research output: Contribution to journalArticlepeer-review

Abstract

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.

Original languageEnglish
Pages (from-to)1471-1472
Number of pages2
JournalThe Lancet
Volume343
Issue number8911
DOIs
StatePublished - 1 Jan 1994
Externally publishedYes

Fingerprint

Dive into the research topics of 'Arthropathy in thalassaemia patients receiving deferiprone'. Together they form a unique fingerprint.

Cite this