Humoral suppression of erythropoiesis in systemic lupus erythematosus (SLE) and rheumatoid arthritis

Nicholas Dainiak, John Hardin, Vicki Floyd, Maureen Callahan, Ronald Hoffman

Research output: Contribution to journalArticle

27 Scopus citations

Abstract

Anemia due to inadequate red cell production often accompanies systemic lupus erythematosus and rheumatoid arthritis. We investigated its pathogenesis in 17 patients with these disorders, using a plasma clot culture system. In serum from normal donors and nonanemic patients CFU-E derived colony formation was not significantly altered by normal marrow cells (mean 74±12 colonies/6 × 104 cells), whereas colony formation was inhibited (mean 36 ± 6 colonies/6 × 104 cells) in serum from 10 anemic patients. In serum from anemic patients proliferation of the more primitive BFU-E was also reduced in three cases. In two patients with a humoral inhibitor, colony growth was suppressed by autologous marrow cells. In another patient without an inhibitor, colony formation was not suppressed by autologous bone marrow. The physical properties of this inhibitor are compatible with those of an immunoglobulin. Moreover, its presence is related to disease activity and it can be removed by successful therapy with either corticosteroids or plasma exchange. Circulating inhibitors of erythropoiesis may play an important role in causing severe anemia in patients with these rheumatic diseases.

Original languageEnglish (US)
Pages (from-to)537-544
Number of pages8
JournalThe American Journal of Medicine
Volume69
Issue number4
DOIs
StatePublished - Oct 1980

ASJC Scopus subject areas

  • Medicine(all)

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