| pubmed-article:7942811 | pubmed:abstractText | During episodes of acute infection there is a reduced response to epoetin therapy. It is well known that "endogenous pyrogens," such as interleukin-1 (IL-1) and tumor necrosis factor, inhibit erythropoiesis when administered exogenously. To determine whether there is a relationship between these observations, serum samples were obtained from nine patients with chronic renal failure maintained by continuous ambulatory peritoneal dialysis, during and after recovery from bacterial peritonitis, to study the effect of circulating factors on erythropoiesis. Normal human bone marrow-derived erythroid progenitors were cultured in vitro in 5% and 10% patient serum. Depression of the growth of late progenitors, colony-forming units-erythroid (at 10% serum, P = 0.005; 95% confidence intervals, 6.2 and 24.4, respectively), was observed but there was no effect on the earlier progenitors, burst-forming units-erythroid (at 10% serum, P = 0.7; 95% confidence intervals, -18.5 and 13, respectively). The effect was not prevented by antisera to IL-1. Similarly, when added to cultures, IL-1 inhibited the colony-forming units-erythroid and the effect was abrogated by IL-1 antisera. These findings suggest that a circulating soluble factor that is inhibitory to erythropoiesis and may contribute to loss of response to epoetin therapy, is present in cases of peritonitis in continuous ambulatory peritoneal dialysis patients. | lld:pubmed |
