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ObjectiveTo determine if fibromyalgia (FM) or fibromyalgia-ness (the tendency to respond to illness and psychosocial stress with fatigue, widespread pain, general increase in symptoms, and similar factors) is increased in patients with compared to those without systemic lupus erythematosus (SLE); to determine whether FM or fibromyalgia-ness biases the SLE Activity Questionnaire (SLAQ); and to determine if the SLAQ is overly sensitive to FM symptoms.MethodsWe developed a 16-item SLE Symptom Scale (SLESS) modeled on the SLAQ and used that scale to investigate the relation between SLE symptoms and fibromyalgia-ness in 23,321 patients with rheumatic disease. FM was diagnosed by survey FM criteria, and fibromyalgia-ness was measured using the Symptom Intensity (SI) Scale. As comparison groups, we combined patients with rheumatoid arthritis and noninflammatory rheumatic disorders into an “arthritis” group and also utilized a physician-diagnosed group of patients with FM.ResultsFM was identified in 22.1% of SLE and 17.0% of those with arthritis. The SI scale was minimally increased in SLE. The correlation between SLAQ and SLESS was 0.738. SLESS/SLAQ scale items (Raynaud’s phenomenon, rash, fever, easy bruising, hair loss) were significantly more associated with SLE than FM, while the reverse was true for headache, abdominal pain, paresthesias/stroke, fatigue, cognitive problems, and muscle pain or weakness. There was no evidence of disproportionate symptom-reporting associated with fibromyalgia-ness. Self-reported SLE was associated with an increased prevalence of FM that was unconfirmed by physicians, compared to SLE confirmed by physicians.ConclusionThe prevalence of FM in SLE is minimally increased compared with its prevalence in patients with arthritis. Fibromyalgia-ness does not bias the SLESS and should not bias SLE assessments, including the SLAQ.

Discussant_s Remarks (Renee LeBoeuf, University of Washington): I do have one burning question I have to get out of my system, and I think it would be to Dr. Moser. In the X-ALD (X-linked adrenoleukodystrophy) males, 50% have the inflammatory brain version. Is there an association with MHC class molecules like you find in diabetes? (Hugo Moser, Kennedy Krieger Institute): No, there is not. Dr. Kirby Smith and I did that, and it is not. (Arthur Spector, University of Iowa): This is a question for Nick Bazan. I didn’t understand—is the neuroprotective docosanoid present all the time or only in response to injury? The second question is if 15-lipoxygenase is involved in the pathway, arachidonic acid is a very good substrate for it. The PLA2 mechanism should release arachidonate, so are you seeing any arachidonate products of either 15-HETE or something else that might indicate whether arachidonate is being used by that pathway? (Nicolas Bazan, Louisiana State University): Thank you Art, great questions. In fact, we are very astonished by the observation that we cannot detect neuroprotectin-D1 in unstimulated cells. In mouse brain as well as in rat brain, without injury or stimulation, you have no neuroprotectinD1 as well as in all the cells that we have studied up to now. As soon as some sort of stimulation—and the same is true now with the growth factors in our growth factor experiments—as soon as you treat the system, you start to see the accumulation. Insofar as the enzymes involved, we do not know. We feel it is a fit because of the chemical structure. We feel it is a 15-like lipoxygenase. We have not explored this, and you just mentioned a very good experiment to do in parallel, the assays under the same conditions to see if there would be arachidonic acid metabolism. We have not done that yet. But the other issue might be compartmentalization. You see, we were very surprised. The first paper on the release of these two fatty acids measured by mass was in 1970, and we were very surprised that arachidonic acid will go up in the brain very rapidly and DHA will also go up rapidly but will follow a different time kinetics. We are talking about minutes of differences, but the time kinetics are different, that would be in the BBA (Biochimica Et Biophysica Acta) 1970 paper (Bazan 1970) and then the others have confirmed the same kinetics. That is where we are on those issues. (Norman Salem, National Institutes of Health/National Institute on Alcohol Abuse and Alcoholism [NIH/NIAAA]): Nicolas, that was an awesome series of experiments, congratulations. There have been two or three publications which I think you are aware of showing that preloading the diet with fish oil or DHA in animal studies helped mitigate against damage to the brain from ischemia, stroke, or experimentally-induced occlusion of the arteries and so on. Your research suggests another possibility, and now there may be a third. When this challenge is given after the preloading of DHA, is there a difference in the neuroprotectinDl? It’s a little bit hypothetical and I don’t know if you have anything to say. (Bazan): Well, it’s a great question and we are doing things along those lines to try to see if there is a correlation. Again, I believe through the data that we are generating that these are very potent metabolites. I don’t want to call them J Mol Neurosci (2007) 33:120–124 DOI 10.1007/s12031-007-0054-z

Objective Fibromyalgia (FM) in rheumatoid arthritis (RA) can cause consternation because symptoms are seen to be out of proportion to physician and laboratory assessments, and composite RA activity scores such as the 28 joint Disease Activity Score, Clinical Disease Activity Index, and Routine Assessment of Patient Index Data 3 (RAPID-3) can yield apparently “wrong” results. We explored the effect of polysymptomatic distress (PSD), a measure of fibromyalgianess and a quantity derived from the American College of Rheumatology 2010 FM diagnostic criteria, to explain the relationship of patient to physician variables. Methods We obtained PSD scores on 300 RA patients prior to ordinary clinical care, and assessed the associations of PSD with tender and swollen joints, physician global estimate of RA activity, pain, Health Assessment Questionnaire score, and composite RA activity measures during routine clinic assessments. Results PSD scores greater than the sample mean (8.8) were associated with increased patient symptoms regardless of the presence or absence of FM, while scores below the mean were associated with better patient outcomes. PSD scores predicted all patient outcomes and less strongly predicted physician outcomes. The discrepancy between patient and physician measures was greatest at low levels of physician-estimated disease activity. Conclusion PSD rather than FM diagnosis more usefully identifies and predicts disproportionate responses. Just as there are patients who lean disproportionately toward greater severity, there are also patients who disproportionately report milder symptoms. Composite measures used to assess RA are flawed, as they confound RA inflammation and patient distress, and more consideration should be given to disaggregated assessments. PSD also appears to be influenced weakly by RA disease activity.

More money than ever is flowing into impact investing, yet many social entrepreneurs creating companies that serve the poor still find it difficult to raise capital., Stanford Social Innovation Review, 11(1), 36-43

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