10.07.2015 Views

1813 01 REUMA3 Editoriale - ME/CFS Australia

1813 01 REUMA3 Editoriale - ME/CFS Australia

1813 01 REUMA3 Editoriale - ME/CFS Australia

SHOW MORE
SHOW LESS

Create successful ePaper yourself

Turn your PDF publications into a flip-book with our unique Google optimized e-Paper software.

The evaluation of the fibromyalgia patients 37SerumCompared to healthy subjects or patients with otherdiseases, FM patients present with high antipolymerantibodies (APA) (12) and antiserotoninantibody (13) values, with contrasting results inthe Italian population. The APA positivity in a recentwork appears to be less than that evidenced inthe USA, and it appears to correlate with the severityof the disease; this result could be due to a differentethnic origin of the populations studied. Otherantibodies (antiganglioside and antiphospholipids)were identified in FM patients compared tohealthy subjects, but the sensitivity and specificitywas not clear. Patients with FM have a higher frequencyof anti-thyroid antibodies, and their valuesseem to be correlated with the presence of certainsymptoms (14). Recent studies have shown higherhyaluronic acid values in FM patients compared tohealthy controls, but this data has not been confirmed(15, 16). Alterations of branched-chainamino acids (valine, leucine, isoleucine), phenycriteriadiagnostic criteria for FM are based uponchronic widespread pain and tenderness in 11 of 18defined muscular sites (1). Recent evidence suggeststhat the tenderness component of FM is notconfined to these sites; rather, it is present throughoutthe body, including non-muscular sites such asthe thumb. The widespread nature of spontaneouspain in FM implicates general mechanisms that mayinvolve spinal or supraspinal modulation of normalperipheral input, or effector mechanisms that alterpain sensitivity at the periphery. These mechanismsare likely observed at supraspinal sites. Functionalneuroimaging of the brain has opened a window intothe supraspinal processes in health and disease(5). With a few exceptions, these methods inferneural activity in the brain by changes in regionalcerebral blood flow (rCBF). This inference is basedon the principle that localized brain activity signalsa discreet increase in rCBF to meet the metabolicdemands of this increase in neural activity. The increasein rCBF occurs after a hemodynamic delayof a few seconds and is closely coupled to the magnitudeand duration of the activity. Most functionalimaging methods are based on the evaluation ofthe time course of changes in rCBF throughout thebrain (6).The absence of anatomopathological lesions andbiohumoral abnormalities, demonstrated with classicalinstrumental methods, has led to considerabledifficulties in diagnosis. The diagnostic criteria frequentlyoverlap with those of other diseases; infact, some patients with chronic fatigue syndrome(<strong>CFS</strong>) meet the criteria for FM, and an FM-likeframework may be present even in non-rheumaticdiseases.For example, patients with hypothyroidism showmusculoskeletal pain that is similar FM. The diagnosisbased on the ACR criteria, therefore, must beaccompanied by the exclusion of diseases that havesymptoms, but not causes, in common with FM asevidenced by the evaluation of markers and humoralscans (miositis, rheumatic polmyalgia,spondyloarthritis, etc.) (7). Often, FM is comorbidwith other diseases that act as confounding and aggravatingfactors (Sjögren, systemic lupus eriythematosus(SLE), rheumtoid arthritis (RA), thyroiddisease). There are no instrumental tests to confirmthe diagnosis of FM; and many differential diagnosesmay be excluded by an extensive clinicalexamination and patient history. Considering theoverlap of FM with other medical conditions, treatingphysicians should be vigilant: chest-X-rays andabdominal ultrasonography are the first steps to-ward general evaluation of all patients with suspectedFM. An individualized, multidisciplinaryrange of treatments should be employed to treatthe various symptoms that patients experience. Althoughsome of these therapies have been tested inrandomized controlled trials (RCT), there has beenlittle standardization in the approach to these trialsand in the outcome measures used. Evaluating therapeuticeffects in FM patients is difficult becauseof the many facets of the syndrome. To address theidentification of core outcome domains, the Initiativeon Methods, Measurement, and Pain Assessmentin Clinical Trials (IMMPACT) (8) and OutcomeMeasures in Rheumatoid Arthritis ClinicalTrials (O<strong>ME</strong>RACT) (9) workshop convened ameeting to develop consensus recommendationsfor chronic pain clinical trials.LABORATORY AND INSTRU<strong>ME</strong>NTALEVALUATIONS IN PATIENTS WITH FMIn clinical studies and observational research studies,FM is usually diagnosed by application of theACR criteria (1). Moreover, diagnosis is made by acombination of patient history, physical examination,laboratory evaluations and exclusion of othercauses for symptoms attributed to FM (10, 11).BIOMARKERS IN FM

Hooray! Your file is uploaded and ready to be published.

Saved successfully!

Ooh no, something went wrong!