Dear Deb -

If the relationship between CRPS and Interleukin 6 holds up then I too fear that you are dead on the money, so to speak. That said, you should be aware that the most recent study was not quite as conclusive as the first. See "Changes in immune and glial markers in the CSF of patients with Complex Regional Pain Syndrome," Guillermo M. Alexander, Marielle J. Perreault, Erin R. Reichenberger, Robert J. Schwartzman, Brain Behav. Immun. (2006), doi:10.1016/j.bbi.2006.10.009:

Abstract

Complex Regional Pain Syndrome is a severe chronic pain condition characterized by sensory, autonomic, motor and dystrophic signs and symptoms. The pain in CRPS is continuous, it worsens over time, and it is usually disproportionate to the severity and duration of the inciting event. This study compares cerebrospinal fluid (CSF) levels of pro- and anti-inflammatory cytokines, chemokines and several biochemical factors (glial fibrillary acidic protein (GFAP), the nitric oxide metabolites (nitrate plus nitrite), the excitatory amino acid neurotransmitter glutamate, calcium, total protein and glucose) in patients afflicted with CRPS to levels found in patients suffering with other non-painful or painful conditions. The aim of the study is to determine the degree of involvement of glial cells and immune system mediators in the pathophysiology of CRPS. There was no elevation or reduction of a CSF marker that was specific for CRPS patients. However, there were several patterns of markers that could be helpful in both elucidating the mechanisms involved in the disease process and supporting the diagnosis of CRPS. The most common pattern was found in 50% (11 out of 22) of the CRPS patients and consisted of; elevated IL-6, low levels of IL-4or IL-10, increased GFAP or MCP1 and increases in at least two of the following markers NO metabolites, calcium or glutamate. The results from this and other similar studies may aid in elucidating the mechanisms involved in the pathophysiology of CRPS. A better understanding of these mechanisms may lead to novel treatments for this very severe, life-altering illness.

(I will be happy to email anyone a copy of this study that wants to see it; just send me a pm with your email address.)

For the earlier study by largely the same authors, showing a stronger link between IL6 and CRPS, see "Changes in Cerebrospinal Fluid Levels of Pro-inflammatory Cytokines in CRPS," Alexander GM, van Rijn MA, van Hilten JJ, Perreault MJ, Schwartzmann RJ, Pain. 2005; 116:213-219 (finding of significant increases in interleukin-1β (IL-1β) and interleukin-6 (IL-6) in the CSF of patients with CRPS-I: the mean CSF value of IL-6 in the CRPS group was significantly more (P < 0.005) than that seen in the control group; CSF level of IL-6 in all patients exceeded the sensitivity (0.039 pg/ml) of the ELISA assay by a factor of at least 25) [free full text pdf file accessible on RSDSA Medical Articles Archive, alphabetically listed by author under "Research" heading at http://www.rsds.org/2/library/articl...ve/index.html].

Finally, for the most depressing link between IL6 and coronary heart disease, see, e.g., "Relative Value of Multiple Plasma Biomarkers as Risk Factors for Coronary Artery Disease and Death in an Angiography Cohort," Kenny W.J. Lee, at al., Canadian Medical Association Journal, 2006 February 14; 174(4): 461– 466 (identifying IL-6 as one of the strongest independent predictors of CAD-related death) [for free full text pdf file, block and copy title of article and search PubMed at http://www.pubmedcentral.gov/].

Mike