The erythrocyte sedimentation rate (ESR) remains a commonly measured indicator of disease, but is subject to several non-disease influences. The haemoglobin concentration (Hb) and ESR were measured in 1249 consecutive patients (492 men, 757 women) from primary care practices. An inverse correlation was found between Hb and ESR throughout the range of measured Hb, and in particular there was a significant difference in the median ESR of patients in the highest and lowest quartile for non-anaemic Hb (P< 0.001). These results indicate that correct clinical analysis of an ESR result should take into account the Hb, both in anaemic and in non-anaemic patients. Interpretative difficulties due to external influences on the measured ESR could be resolved by replacement of this test with plasma viscosity estimation.

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We have studied the effects of interferons gamma (IFN‐γ) and alpha (IFN‐α), and tumour‐necrosis factor‐alpha (TNF) on circulating 14‐day erythroid progenitor cell (BFU‐E) growth in vitro from patients with non‐leukaemic myeloproliferative disorders (MPD) compared with normal controls. IFN‐γ (1000 U/ml) inhibited BFU‐E growth in all controls studied (mean growth ± SE = 61 % ± 6%, n = 10). In 7 of 11 MPD studied there was no inhibition, and in some cases clear enhancement of BFU‐E growth by IFN‐γ. When cultured in the presence of recombinant erythropoietin (rEpo) 1 U/ml, both IFN‐α and TNF (at 100 and 1000 U/ml) produced a similar degree of inhibition of BFU‐E growth in MPD and controls. The inhibition by 100 U/ml IFN‐α was abrogated, partially in controls but completely in MPD, by increasing the dose of rEpo to 5 U/ml. Similarly, the increase in rEpo dose enhanced BFU‐E growth in cultures with 100 U/ml TNF, but had little effect on cultures containing 1000 U/ml of either IFN‐α or TNF. The aberrant in vitro response to IFN‐γ demonstrated in some of these patients may be of relevance to the pathophysiology of MPD. These results fail to demonstrate a differential in vitro effect for IFN‐α on MPD BFU‐E growth compared with controls and suggest that the in vitro suppression of haemopoiesis by IFN‐α when used in MPD treatment is non‐specific.

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