Saturday, May 18, 2013
Series of Case Studies Invite Further Investigation of TNF-α in CRPS
After the tragic intrusion of the recent dying gasps of CALMARE/"Scrambler" into our usual CRPS research fun here at elle est belle la seine la seine elle est belle (which some idjit over at the CTTC investment message board called... hold on to your berets... an ITALIAN blog), I've had the urge to see what's new over at PubMed.
I don't need to repeat what I've often repeated to you, if you're one of my CRPS brethren or sistren, that you must do your own due diligence, that you must separate wheat from chaff (and determine whether it's the chaff or the wheat that's of value!), and that you should consult with legitimate experts in the field, though they be few and hard to find. There, no need for repeating what is simple common sense, even to people who may not have slept longer than 90 minutes at a stretch in, oh, a decade -- or whose pain levels would reduce CALMARE investors into absolute idjitness, such that we'd likely have to lock them in an isolated tower somewhere (maybe Italy?) so that they won't disturb the rest of us as we go about the business of living.
Just a reminder that TNF-alpha research is being driven by some solid basic science done as far back as 2001, with the publication of "The important role of neuropeptides in complex regional pain syndrome" as well as the seminal 2005 publication, in the journal PAIN, of "Changes in cerebrospinal fluid levels of pro-inflammatory cytokines in CRPS," that included Dr. Robert Schwartzman as a researcher. It concludes: "These results are consistent with studies that suggest that the pathogenesis of CRPS is due in part to central neuroimmune activation." "These results" refer to demonstration via ELISA assay of "elevated pro-inflammatory cytokines," one of which is, of course,TNF-α. It is all part and parcel of the major drive in [legitimate] research that follows the multifactorial role of neurogenic inflammation.
So, while keeping in mind that this is "just" a "case series," it does participate in a distinguished lineage.
The Rappaport Faculty of Medicine, Technion, Israel Institute of Technology, Haifa, Israel; Institute of Pain Medicine, Rambam Health Care Campus, Haifa, Israel.
Evidence suggests tumor necrosis factor-alpha (TNF-α) mediates, at least in part, symptoms and signs in complex regional pain syndrome (CRPS). Here, we present a case series of patients with CRPS type 1, in whom the response to the anti-TNF-α adalimumab was assessed.
Ten patients with CRPS type 1 were recruited. Assessments were performed before treatment, at 1 week, and 1, 3, and 6 months following 3 biweekly subcutaneous injections (40 mg/0.8 mL) adalimumab (Humira® ) and included the followings: Pain intensity using a 0-10 cm visual analog scale; the Short Form of the McGill Pain Questionnaire; the Beck Depression Inventory; the SF-36 questionnaire and mechanical and thermal thresholds (Von frey hair and Thermal Sensory Analyzer, respectively). In addition to the description of individual patient responses, both intention to treat (ITT) and per-protocol (PP) analyses were performed for the entire group.
Three subgroups of patients were identified (3 patients in each): "nonresponders", "partial responders", and "robust responders" in whom improvement in almost all parameters was noted. Both the ITT and PP analyses demonstrated only a trend toward improvement in mechanical pain thresholds following treatment (ITT χ² = 13.83, P = 0.008; PP χ² = 10.29, P = 0.036).
These results suggest adalimumab, and possibly other anti-TNF-α, can be potentially useful in some (although not in all) patients with CRPS type 1. These preliminary results along with the growing body of evidence which points to the involvement of TNF-α in the pathogenesis ofCRPS justify further studies in this area.
Pain Pract. 2013 May 13. doi: 10.1111/papr.12070. [Epub ahead of print]