Biology and therapy of fibromyalgia. Evidence-based biomarkers for fibromyalgia syndrome

Abstract

Researchers studying fibromyalgia strive to identify objective, measurable biomarkers that may identify susceptible individuals, may facilitate diagnosis, or that parallel activity of the disease. Candidate objective measures range from sophisticated functional neuroimaging to office-ready measures of the pressure pain threshold. A systematic literature review was completed to assess highly investigated, objective measures used in fibromyalgia studies. To date, only experimental pain testing has been shown to coincide with improvements in clinical status in a longitudinal study. Concerted efforts to systematically evaluate additional objective measures in research trials will be vital for ongoing progress in outcome research and translation into clinical practice. IntroductionFibromyalgia (FM) is a chronic condition characterized by widespread pain and tenderness on examination, along with symptoms of nonrestorative sleep, fatigue, and cognitive difficulties. Recent familial studies have suggested an underlying genetic susceptibility on which environmental factors trigger the expression of symptoms [1,2]. Despite the myalgias that patients experience, no abnormality in muscle has been reliably found [3]. Instead, aberrant pain and sensory processing probably caused by alterations in the central nervous system function are being consistently recognized in FM and related syndromes. Investigations into the autonomic nervous system and the hypothalamic-pituitary-adrenal axis also suggest a role of these stress-response systems in vulnerability to FM or in symptom expression in FM.Our improved understanding of FM has stimulated the search for biomarkers to be used to identify individuals susceptible to the syndrome, for the diagnosis of FM, for objective measures of disease activity, or as surrogate endpoints of GeneticsIncreasing evidence supports a genetic predisposition to FM. First-degree relatives of individuals with FM display an eightfold greater risk of developing the syndrome than those in the general population [1]. As such, a genetic study using multicase families has been completed that identified an HLA linkage not yet replicated [4].Polymorphisms in the serotonergic 5-hydroxy tryptamine 2A receptor (T/T phenotype), the serotonin transporter, the dopamine 4 receptor and the catecholamine o-methyl transferase enzyme have also been evaluated in patients with FM [5][6][7][8][9][10]. Notably, these polymorphisms all affect the metabolism or transport of monoamines, compounds that have a critical role in both sensory processing and the human stress response. With the exception of the catecholamine omethyl transferase finding and the dopamine-4-receptor gene polymorphism, however, which have not been replicated or

Primary attributions in women suffering fibromyalgia emphasize the perception of a disruptive onset for a long-lasting pain problem

“…A majority of patients also complain of fatigue and nonrestorative sleep, memory or concentration problems, stiffness, and mood disturbances. A number of studies also point to central sensitization in patients with FM [3,4]. Attempts have been made to elucidate etiological mechanisms underlying FM.…”

Fibromialgia: diagnóstico, fisiopatologia e tratamentos

“…A participação de fatores genéticos, endócrinos, imunológicos, neurológicos e ou comportamentais na gênese e evolução da FM é alvo frequente de investigações científicas, contudo os resultados são divergentes e não conclusivos (DADABHOY et al, 2008;DI FRANCO et al, 2010).…”

Predictors of pain and functioning over time in fibromyalgia syndrome: An autoregressive path analysis

“…FMS is perhaps one of the most difficult conditions to manage for both patients and practitioners because of the uncertainty of the diagnosis and management of the disease. Although many theories have been proposed and have received some level of empirical support (including genetic, neuroendocrine, neurologic, and psychological theories [1][2][3][4]), the true etiopathogenesis of FMS remains unknown. Therefore, researchers and clinicians continue to assess the proper means of and targets for effective intervention and treatment.…”