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In this study, 100 synovial fluid (SF) samples from patients with a variety of arthritides were assayed for levels of colony-stimulating factors (CSFs) using a human bone-marrow bioassay and enzyme immunoassays for granulocyte (G-) and granulocyte-macrophage (GM-) CSFs. GM-CSF was found more frequently in samples from rheumatoid arthritis (RA) subjects (49%) than in non-RA samples (29%). Absence of GM- but not G- or bioassay CSFs characterised samples from subjects with psoriatic arthritis and ankylosing spondylitis (n = 14). There was strong evidence of an antagonistic relationship between levels of G- and GM-CSFs in samples from RA patients, an effect independent of drug treatment. However, treatment with non-steroidal anti-inflammatory agents (NSAIDs) may affect reported CSF concentrations: G-CSF levels were significantly lower in samples from subjects not taking NSAIDs. These results suggest that SF-CSF estimations using commercially available assays could provide useful diagnostic clues for clinicians, but careful interpretation is warranted particularly in patients on long-term NSAID treatment.

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Summary. Granulocyte colony‐stimulating factor (G‐CSF) levels were studied in 23 patients (10 myeloma, 13 relapsed Hodgkin's disease, non‐Hodgkin's lymphoma or germ cell tumours), post autologous peripheral blood stem cell transplantation (PBSCT). The two groups had similar previous chemotherapy and numbers of CD34+ cells transplanted. All patients received G‐CSF by injection starting 8 d post transplantation. Twenty out of 23 patients showed raised endogenous levels of G‐CSF before cytokine administration. Myeloma patients showed significantly lower levels of endogenous G‐CSF than the other patients (0·767 versus 3·262 ng/ml, P < 0·05). Further rises in G‐CSF levels were seen following the administration of exogenous G‐CSF which then fell, despite ongoing administration of G‐CSF, as neutrophil recovery occurred.

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