Chronic fatigue syndrome (CFS) may be alleviated by the anti-cancer drug Rituximab, suggesting that the source of the disease could lie in the immune system, according to a new study published Oct. 19 in the online journal PLoS ONE. Uncertainty about the cause of CFS, which is characterized by extreme, unexplained exhaustion, among other symptoms, has led to much debate, but the authors of this recent study believe they may have found the answer.
The work, led by Drs. Oystein Fluge and Olav Mella of Haukeland University Hospital in Norway, was initiated when the researchers noticed a patient with both chronic fatigue syndrome (CFS) and Hodgkin's lymphoma who showed marked recovery from CFS symptoms upon treatment with chemotherapy.
The investigators reasoned that the effect could be mediated through B-lymphocyte depletion, and to further investigate this connection they conducted first a pilot case series, and then a double-blind, placebo-controlled phase II trial with 30 CFS patients, and found that the Rituximab treatment was associated with significant, but generally transient, improvement in CFS symptoms.
Rituximab is a B-lymphocyte depleting agent. It acts as an antibody against a protein found primarily on the surface these cells, which are a component of the immune system. According to the authors, "the delay of clinical responses after the initial and rapid B-cell depletion suggests to us that CFS/ME, which is often preceded by an infection, may be a form of autoimmune disease in which B-cells are important". Thus, this study reveals a potential new direction for CFS research.
Citation: Fluge Ø, Bruland O, Risa K, Storstein A, Kristoffersen EK, et al. (2011) Benefit from B-Lymphocyte Depletion Using the Anti-CD20 Antibody Rituximab in Chronic Fatigue Syndrome. A Double-Blind and Placebo-Controlled Study. PLoS ONE 6(10): e26358. doi:10.1371/journal.pone.0026358
Financial Disclosure: The work received financial support from Helse Vest grant no 911557, and also from the legacy of Torstein Hereid. These funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing Interest Statement: Haukeland University Hospital has patents and pending patent applications on the issue of B-cell depletion therapy for chronic fatigue syndrome. Family members of WO2009083602 A1 are pending, as well as granted US 12/348024. The two authors ØF and OM are named as inventors in these applications. This does not alter the authors' adherence to all the PLoS ONE policies on sharing data and materials.
PLEASE LINK TO THE SCIENTIFIC ARTICLE IN ONLINE VERSIONS OF YOUR REPORT (URL goes live after the embargo ends): http://dx.plos.org/10.1371/journal.pone.0026358
Disclaimer: This press release refers to upcoming articles in PLoS ONE. The releases have been provided by the article authors and/or journal staff. Any opinions expressed in these are the personal views of the contributors, and do not necessarily represent the views or policies of PLoS. PLoS expressly disclaims any and all warranties and liability in connection with the information found in the release and article and your use of such information.
About PLoS ONE
PLoS ONE is the first journal of primary research from all areas of science to employ a combination of peer review and post-publication rating and commenting, to maximize the impact of every report it publishes. PLoS ONE is published by the Public Library of Science (PLoS), the open-access publisher whose goal is to make the world's scientific and medical literature a public resource.
All works published in PLoS ONE are Open Access. Everything is immediately available—to read, download, redistribute, include in databases and otherwise use—without cost to anyone, anywhere, subject only to the condition that the original authors and source are properly attributed. For more information about PLoS ONE relevant to journalists, bloggers and press officers, including details of our press release process and our embargo policy, see the everyONE blog at http://everyone.plos.org/media.