BMC Cancer 2009, 9:153 http://www.biomedcentral.com/1471-2407/9/153 Table 4: Patients with grade 3 or 4 anaemia, leucopenia or thrombocytopenia by demographic, treatment and clinical variables. Number (per cent). Category n Grade 3/4 leucopenia p Grade 3/4 anaemia p Grade 3/4 thrombocytopenia Variable B symptoms Sex Age GCSF Stage Chemotherapy Performance status LDH (mU/L) Bone marrow aspirate Negative Positive Bone marrow Trephine * Fisher exact p No Yes Female Male 311 124 (39.9) 353 203 (57.5) 311 159 (51.1) 353 168 (47.6) < 75 years 496 226 (45.6) ≥ 75 years 168 101 (60.1) CHOP 334 129 (38.6) PMitCEBO 330 198 (60.0) No Yes Stage 0–2 Stage 3–4 Level 0–1 Level 2–4 Normal Elevated Negative Positive 330 184 (55.8) 334 143 (42.8) 246 99 (40.2) 418 228 (54.5) 470 197 (41.9) 183 125 (68.3) 216 96 (44.4) 381 203 (53.3) 508 248 (48.8) 57 39 (68.4) 487 228 (46.8) 89 58 (65.2 ing CRP or cytokines such as IL-6. The availability of mul- tiplex bead cytokine analyses that permit simultaneous measurement of multiple cytokines should facilitate such research. These findings may also be applicable to other malignancies where it is likely that inflammation is responsible for a significant proportion of the variability in toxicity from chemotherapy. However, as overall sur- vival has consistently been lower in patients with elevated inflammatory markers [7-10] it would be potentially haz- ardous to manage an increased risk of toxicity by dose reduction as this could further compromise response and survival. It may also be possible to use inflammatory markers to more appropriately guide the use of colony stimulating factors in patients with solid tumours. In addition to providing prognostic information, the inflammatory proteins provide a potential target for novel therapies aimed at reversing the inflammatory effects, improving drug handling and reducing toxicity. A number of antibodies have been developed to target pro-inflam- matory cytokines, including TNF-α, IL-6 and IL-6 recep- < 0.001 14 (4.5) 34 (9.6) 0.363 0.001 25 (8.0) 23 (6.5) 33 (6.7) 15 (8.9) < 0.001 27 (8.1) 21 (6.4) < 0.001 14 (4.2) 34 (10.2) < 0.001 14 (5.7) 34 (8.1) < 0.001 27 (5.7) 21 (11.5) 0.038 0.005 0.001 7 (3.2) 34 (8.9) 31 (6.1) 8 (14.0) 30 (6.2) 10 (11.2) 0.011 17 (5.5) 48 (13.6) 0.450 33 (10.6) 32 (9.1) 0.324 40 (8.1) 25 (14.9) 0.392 40 (12.0) 25 (7.6) 0.003 25 (7.6) 40 (12.0) 0.240 11 (4.5) 54 (12.9) 0.012 25 (5.3) 39 (21.3) 0.008 5 (2.3) 52 (13.6) 0.046* 45 (8.9) 12 (21.1) 0.083 40 (8.2) 18 (20.2) tor, and these should be investigated for their potential to reverse tumour-associated impairment of drug metabo- lism. There are preliminary data to suggest that this approach might also help to overcome tumour resistance. However, these data require confirmation in prospective clinical studies that also involve the collection of plasma for measurement of acute phase proteins and cytokines. Conclusion This study shows that patients with aggressive non-Hodg- kin lymphoma who have B symptoms experience signifi- cantly more myelosuppression than those without inflammatory symptoms. The toxicities were less in patients who had received G-CSF. These data support the hypothesis that patients with a cancer induced inflamma- tory reaction have reduced hepatic metabolism of cyto- toxic drugs which results in the increased toxicity. These results might help explain some of the substantial inter- patient differences in toxicity from chemotherapy. Page 7 of 10 (page number not for citation purposes) p < 0.001 0.504 0.010 0.056 0.056 < 0.001 < 0.001 < 0.001 0.004 0.001