RESUMEN
Pain is a significant issue in rheumatoid arthritis (RA) and psoriatic arthritis (PSA) and can have a negative impact on patients' quality of life. Despite optimal control of inflammatory disease, residual chronic pain remains a major unmet medical need in RA. Pain in RA can be secondary to inflammation but can also generate neuroendocrine responses that initiate neurogenic inflammation and enhance cytokine release, leading to persistent hyperalgesia. In addition to well-known cytokines such as TNFα and IL-6, other cytokines and the JAK-STAT pathway play a role in pain modulation and inflammation. The development of chronic pain in RA involves processes beyond inflammation or structural damage. Residual pain is often observed in patients even after achieving remission or low disease activity, suggesting the involvement of non-inflammatory and central sensitization mechanisms. Moreover, fibromyalgia syndrome (FMS) is prevalent in RA patients and may contribute to persistent pain. Factors such as depression, sleep disturbance, and pro-inflammatory cytokines may contribute to the development of fibromyalgia in RA. It is essential to identify and diagnose concomitant FMS in RA patients to better manage their symptoms. Further research is needed to unravel the complexities of pain in RA. Finally, recent studies have shown that JAK inhibitors effectively reduce residual pain in RA patients, suggesting pain-reducing effects independent of their anti-inflammatory properties.
Asunto(s)
Artritis Reumatoide , Humanos , Artritis Reumatoide/complicaciones , Artritis Reumatoide/tratamiento farmacológico , Artritis Reumatoide/fisiopatología , Fibromialgia/diagnóstico , Fibromialgia/fisiopatología , Fibromialgia/inmunología , Dolor Crónico/fisiopatología , Dolor Crónico/etiología , Dolor Crónico/tratamiento farmacológico , Inflamación , Artritis Psoriásica/tratamiento farmacológico , Artritis Psoriásica/complicaciones , Artritis Psoriásica/fisiopatología , Artritis Psoriásica/diagnóstico , Citocinas , Diagnóstico DiferencialRESUMEN
Fibromyalgia (FM) is a chronic disease characterized by widespread musculoskeletal pain of unknown etiology. The condition is commonly associated with other symptoms, including fatigue, sleep disturbances, cognitive impairment, and depression. For this reason, FM is also referred to as FM syndrome. The nature of the pain is defined as nociplastic according to the latest international classification and is characterized by altered nervous sensitization both centrally and peripherally. Psychosocial conditions have traditionally been considered critical in the genesis of FM. However, recent studies in animal models and humans have provided new evidence in favor of an inflammatory and/or autoimmune pathogenesis. In support of this hypothesis are epidemiological data of an increased female prevalence, similar to that of autoimmune diseases, and the frequent association with immune-mediated inflammatory disorders. In addition, the observation of an increased incidence of this condition during long COVID revived the hypothesis of an infectious pathogenesis. This narrative review will, therefore, discuss the evidence supporting the immune-mediated pathogenesis of FM in light of the most current data available in the literature.
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Autoinmunidad , COVID-19 , Fibromialgia , Inflamación , Animales , Humanos , Enfermedades Autoinmunes/inmunología , Enfermedades Autoinmunes/complicaciones , COVID-19/inmunología , COVID-19/complicaciones , COVID-19/virología , Fibromialgia/inmunología , Inflamación/inmunología , SARS-CoV-2/inmunologíaRESUMEN
INTRODUCTION: Post-Covid Syndrome, Sick Building Syndrome, Silicone Breast Syndrome, Choric Fatigue Syndrome, Fibromyalgia -Autoimmunity to the Autonomic Nervous System.
Asunto(s)
COVID-19 , Fibromialgia , Humanos , Fibromialgia/inmunología , Femenino , COVID-19/inmunología , Siliconas/efectos adversos , Síndrome Post Agudo de COVID-19 , Sistema Nervioso Autónomo/fisiopatología , Implantes de Mama/efectos adversos , Autoinmunidad , Enfermedades del Sistema Nervioso Autónomo/etiología , Enfermedades del Sistema Nervioso Autónomo/inmunología , Enfermedades del Sistema Nervioso Autónomo/fisiopatologíaRESUMEN
Fibromyalgia (FM) remains a condition with a pathogenesis that is not completely understood, affecting a significant portion of the global population. This article summarises the main advances in FM during the last year. Even in 2023, research on FM was notably active. From a clinimetric perspective, studies have been conducted to evaluate the possibilities of interchanging the primary indices of disease severity, primarily for studies with substantial case numbers. Regarding FM pathogenesis, ongoing research focuses on small fiber neuropathy: some studies have documented its association with central sensitisation, while others have revealed distinct sensory profiles in patients with FM and small fiber neuropathy compared to those solely with small fiber neuropathy. Dorsal root ganglia seem to play a crucial role in the pathogenesis of FM as they host satellite glial cells, which are targeted by pain-driving immunoglobulin G. These antibodies have been identified in a subset of patients exhibiting high symptom severity. An important study conducted on animal models confirmed the role of neuroinflammation at the level of dorsal root ganglia, in this case mediated by polymorphonuclear neutrophils. Mounting evidence underscores the link between COVID-19 and the persistence of FM symptoms after recovery. In identifying potential biomarkers aiding FM diagnosis, research has also concentrated on studying the expression of specific circulating microRNAs. Recent discoveries have unveiled novel therapeutic strategies for FM, especially focused in non-pharmacological interventions. This includes a focus on non-invasive brain stimulation and exercise programs, all directed towards relieving symptoms and improving functionality in individuals affected by the condition.
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COVID-19 , Fibromialgia , Fibromialgia/diagnóstico , Fibromialgia/terapia , Fibromialgia/fisiopatología , Fibromialgia/inmunología , Humanos , COVID-19/complicaciones , COVID-19/inmunología , COVID-19/diagnóstico , Animales , SARS-CoV-2/inmunología , Ganglios Espinales/fisiopatología , Ganglios Espinales/inmunología , Ganglios Espinales/metabolismo , Índice de Severidad de la Enfermedad , Biomarcadores/sangreRESUMEN
Fibromyalgia syndrome (FMS) is characterized by widespread pain and tenderness, and patients typically experience fatigue and emotional distress. The etiology and pathophysiology of fibromyalgia are not fully explained and there are no effective drug treatments. Here we show that IgG from FMS patients produced sensory hypersensitivity by sensitizing nociceptive neurons. Mice treated with IgG from FMS patients displayed increased sensitivity to noxious mechanical and cold stimulation, and nociceptive fibers in skin-nerve preparations from mice treated with FMS IgG displayed an increased responsiveness to cold and mechanical stimulation. These mice also displayed reduced locomotor activity, reduced paw grip strength, and a loss of intraepidermal innervation. In contrast, transfer of IgG-depleted serum from FMS patients or IgG from healthy control subjects had no effect. Patient IgG did not activate naive sensory neurons directly. IgG from FMS patients labeled satellite glial cells and neurons in vivo and in vitro, as well as myelinated fiber tracts and a small number of macrophages and endothelial cells in mouse dorsal root ganglia (DRG), but no cells in the spinal cord. Furthermore, FMS IgG bound to human DRG. Our results demonstrate that IgG from FMS patients produces painful sensory hypersensitivities by sensitizing peripheral nociceptive afferents and suggest that therapies reducing patient IgG titers may be effective for fibromyalgia.
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Fibromialgia/inmunología , Fibromialgia/fisiopatología , Animales , Estudios de Casos y Controles , Modelos Animales de Enfermedad , Femenino , Fibromialgia/etiología , Ganglios Espinales/fisiopatología , Humanos , Inmunización Pasiva , Inmunoglobulina G/administración & dosificación , Inmunoglobulina G/sangre , Masculino , Ratones , Ratones Endogámicos C57BL , Nociceptores/inmunología , Nociceptores/fisiología , Dolor/fisiopatología , Umbral del Dolor/fisiologíaRESUMEN
INTRODUCTION: The impact of sex, age, body mass index (BMI) in fibromyalgia is still unclear. A systematic review was conducted to investigate whether sex, age and BMI influence the clinical outcomes and rate of adverse events. METHODS: The present study was performed according to the PRISMA guidelines. The literature search was performed in February 2021. All the RCTs investigating pharmacological strategies for fibromyalgia were accessed. RESULTS: Data from 51 RCTs (17,311 patients) were collected. Short Form 36 emotional, Social function and physical role subscales showed evidence of a negative association with BMI (P = 0.02, P = 0.002 and P = 0.0001, respectively). Depression and anxiety subscales of the Hospital Anxiety and Depression score demonstrated evidence of a positive association with age (P = 0.04 and P = 0.001, respectively) and sex (P = 0.00005 and P = 0.0001, respectively). Visual analog scale evidenced a positive association with BMI (P = 0.04). Clinical Global Impression Severity scale demonstrated evidence of a negative association with BMI (P = 0.02). CONCLUSION: Irrespective from the pharmacological approach, a higher BMI is negatively associated with a favorable outcome in patients with fibromyalgia. The association with sex and age remains controversial. LEVEL OF EVIDENCE: I, systematic review of RCTs.
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Índice de Masa Corporal , Fibromialgia/tratamiento farmacológico , Fibromialgia/inmunología , Factores de Edad , Fibromialgia/fisiopatología , Fibromialgia/psicología , Humanos , Ensayos Clínicos Controlados Aleatorios como Asunto , Índice de Severidad de la Enfermedad , Factores Sexuales , Resultado del TratamientoAsunto(s)
Alergia e Inmunología , Analgésicos Opioides/uso terapéutico , Encéfalo/inmunología , Fibromialgia/inmunología , Microbiota/inmunología , Trastornos Relacionados con Opioides/inmunología , Dolor/inmunología , Animales , Fibromialgia/tratamiento farmacológico , Humanos , Inflamación Neurogénica , Dolor/tratamiento farmacológicoRESUMEN
Data on the association between fibromyalgia syndrome (FMS) and psoriasis are scarce. We aimed to examine the association between FMS and psoriasis using a large-scale observational population-based study. This cross-sectional study analyzed data from a big computerized database to evaluate potential differences in the prevalence of psoriasis between patients with FMS and matched control subjects. The study included 18,598 patients with FMS and 36,985 controls. The prevalence of psoriasis was increased in patients with FMS as compared with control subjects (6.7% vs. 4.8%, respectively; OR, 1.4; 95% CI, 1.3-1.5; P < 0.001). This association was robust to multivariate analysis adjustment for sex, age, ancestry, socioeconomic status, and healthcare utilization (OR, 1.3; 95% CI, 1.2-1.4; P < 0.001). When compared with patients with only FMS, patients with a dual diagnosis of FMS and psoriasis presented with FMS at a significantly older age, had a higher mean BMI, and a higher frequency of smoking. To conclude, we found a significant association between FMS and psoriasis. More extensive cooperation between dermatologists and rheumatologists is suggested to enable early identification of their co-occurrence.
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Fibromialgia/complicaciones , Psoriasis/epidemiología , Adolescente , Adulto , Anciano , Anciano de 80 o más Años , Macrodatos , Estudios de Casos y Controles , Estudios Transversales , Bases de Datos Factuales/estadística & datos numéricos , Femenino , Fibromialgia/inmunología , Humanos , Israel/epidemiología , Masculino , Persona de Mediana Edad , Prevalencia , Psoriasis/inmunología , Factores de Riesgo , Índice de Severidad de la Enfermedad , Adulto JovenRESUMEN
Advancements in nucleic acid sequencing technology combined with an unprecedented availability of metadata have revealed that 45% of the human genome constituted by transposable elements (TEs) is not only transcriptionally active but also physiologically necessary. Dysregulation of TEs, including human retroviral endogenous sequences (HERVs) has been shown to associate with several neurologic and autoimmune diseases, including Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). However, no study has yet addressed whether abnormal expression of these sequences correlates with fibromyalgia (FM), a disease frequently comorbid with ME/CFS. The work presented here shows, for the first time, that, in fact, HERVs of the H, K and W types are overexpressed in immune cells of FM patients with or without comorbid ME/CFS. Patients with increased HERV expression (N = 14) presented increased levels of interferon (INF-ß and INF-γ) but unchanged levels of TNF-α. The findings reported in this study could explain the flu-like symptoms FM patients present with in clinical practice, in the absence of concomitant infections. Future work aimed at identifying specific genomic loci differentially affected in FM and/or ME/CFS is warranted.
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Elementos Transponibles de ADN/genética , Fibromialgia/genética , Fibromialgia/inmunología , Leucocitos/metabolismo , Adulto , Anciano , Citocinas/sangre , Retrovirus Endógenos , Fatiga/genética , Femenino , Fibromialgia/sangre , Humanos , Modelos Lineales , Masculino , Persona de Mediana Edad , Modelos Biológicos , ARN de Transferencia/genética , Encuestas y CuestionariosRESUMEN
Fibromyalgia is one of the most important "rheumatic" disorders, after osteoarthritis. The etiology of the disease is still not clear. At the moment, the most defined pathological mechanism is the alteration of central pain pathways, and emotional conditions can trigger or worsen symptoms. Increasing evidence supports the role of mast cells in maintaining pain conditions such as musculoskeletal pain and central sensitization. Importantly, mast cells can mediate microglia activation through the production of proinflammatory cytokines such as IL-1ß, IL-6, and TNFα. In addition, levels of chemokines and proinflammatory cytokines are enhanced in serum and could contribute to inflammation at systemic level. Despite the well-characterized relationship between the nervous system and inflammation, the mechanism that links the different pathological features of fibromyalgia, including stress-related manifestations, central sensitization, and dysregulation of the innate and adaptive immune responses is largely unknown. This review aims to provide an overview of the current understanding of the role of adaptive immune cells, in particular T cells, in the physiopathology of fibromyalgia. It also aims at linking the latest advances emerging from basic science to envisage new perspectives to explain the role of T cells in interconnecting the psychological, neurological, and inflammatory symptoms of fibromyalgia.
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Fibromialgia/fisiopatología , Inflamación/fisiopatología , Linfocitos T/patología , Inmunidad Adaptativa , Animales , Citocinas/análisis , Citocinas/inmunología , Fibromialgia/inmunología , Fibromialgia/patología , Humanos , Inmunidad Celular , Inflamación/inmunología , Inflamación/patología , Linfocitos T/inmunologíaRESUMEN
Since the first discovery that the bioactive lipid, lysophosphatidic acid (LPA) and LPA1 receptor signaling play a role in the initiation of neuropathic pain (NeuP), accumulated reports have supported the original findings and extended the study toward possible therapeutic applications. The present review describes beneficial roles of LPA receptor signaling in a variety of chronic pain, such as peripheral NeuP induced by nerve injury, chemotherapy and diabetes, central NeuP induced by cerebral ischemia with hemorrhage and spinal cord injury, and fibromyalgia-like wide spread pain induced by repeated cold, psychological and muscular acidic stress. Emerging mechanistic findings are the feed-forward amplification of LPA production through LPA1, LPA3 and microglia and the evidence for maintenance of chronic pain by LPA receptor signaling.
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Dolor Crónico , Fibromialgia , Lisofosfolípidos/metabolismo , Neuralgia , Receptores del Ácido Lisofosfatídico/antagonistas & inhibidores , Receptores del Ácido Lisofosfatídico/metabolismo , Transducción de Señal , Animales , Dolor Crónico/tratamiento farmacológico , Dolor Crónico/inmunología , Dolor Crónico/metabolismo , Fibromialgia/tratamiento farmacológico , Fibromialgia/inmunología , Fibromialgia/metabolismo , Humanos , Neuralgia/tratamiento farmacológico , Neuralgia/inmunología , Neuralgia/metabolismo , Transducción de Señal/efectos de los fármacosRESUMEN
Fibromyalgia (FM) is a disease characterized by chronic widespread pain, fatigue, aches, joint stiffness, depression, cognitive dysfunction, and nonrestorative sleep. In FM, neurotransmission and glial activation can occur with an increase in inflammatory cytokines and involvement of mast cells (MCs) in the skin. FM skin biopsies show an increase in the number of MCs, as well as the production of corticotropin releasing hormone and substance P (SP) by the neurons, which in turn activate MCs to release neurosensitizing proinflammatory substances, such as cytokines, secreted preformed mediators, and lipids, which can exacerbate low-grade inflammation. In fact, certain proinflammatory cytokines are higher in FM and mediate muscle pain, the mechanism of which is not yet clear. MC-derived tumor necrosis factor (TNF) induces nerve growth factor (NGF) and participates in nerve fiber elongation in skin hypersensitivity. IL-37 is an inhibitor of proinflammatory IL-1 family members, which are generated and released by MCs. The goal of this article is to demonstrate that inflammatory cytokines and MC products play a role in FM and that inflammation may be inhibited by IL-37. Here, we propose IL-37 as a cytokine that contributes to improve the pathogenesis of FM by blocking IL-1 family members.
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Fibromialgia/fisiopatología , Inflamación/patología , Mastocitos/inmunología , Animales , Enfermedad Crónica , Citocinas/inmunología , Fibromialgia/inmunología , Humanos , Inflamación/inmunología , Interleucina-1/inmunología , Piel/inmunología , Piel/patologíaRESUMEN
OBJECTIVE: Rheumatoid arthritis (RA) patients with concomitant fibromyalgia (FM) exhibit alterations in brain connectivity synonymous with central sensitization. This study was undertaken to investigate how peripheral inflammation, the principal nociceptive stimulus in RA, interacts with brain connectivity in RA patients with FM. METHODS: RA patients with concomitant FM and those without FM (FM+ and FM-, respectively; n = 27 per group) underwent functional connectivity magnetic resonance imaging. Seed-to-whole-brain functional connectivity analyses were conducted using seeds from the left mid/posterior insula and left inferior parietal lobule (IPL), which are regions that have been previously linked to FM symptoms and inflammation, respectively. The association between functional connectivity and erythrocyte sedimentation rate (ESR) was assessed in each group separately, followed by post hoc analyses to test for interaction effects. Cluster-level, family-wise error (FWE) rates were considered significant if the P value was less than 0.05. RESULTS: The group of RA patients with FM and those without FM did not differ by age, sex, or ESR (P > 0.2). In FM+ RA patients, increased functional connectivity of the insula-left IPL, left IPL-dorsal anterior cingulate, and left IPL-medial prefrontal cortex regions correlated with higher levels of ESR (all FWE-corrected P < 0.05). Post hoc interaction analyses largely confirmed the relationship between ESR and connectivity changes as FM scores increased. CONCLUSION: We report the first neurobiologic evidence that FM in RA may be linked to peripheral inflammation via pronociceptive patterns of brain connectivity. In patients with such "bottom-up" pain centralization, concomitant symptoms may partially respond to antiinflammatory treatments.
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Artritis Reumatoide/inmunología , Encéfalo/diagnóstico por imagen , Sensibilización del Sistema Nervioso Central , Fibromialgia/inmunología , Nocicepción , Adulto , Anciano , Sedimentación Sanguínea , Encéfalo/fisiopatología , Corteza Cerebral/diagnóstico por imagen , Corteza Cerebral/fisiopatología , Femenino , Neuroimagen Funcional , Humanos , Inflamación/inmunología , Imagen por Resonancia Magnética , Masculino , Persona de Mediana Edad , Vías Nerviosas/diagnóstico por imagen , Vías Nerviosas/fisiopatología , Lóbulo Parietal/diagnóstico por imagen , Lóbulo Parietal/fisiopatologíaRESUMEN
BACKGROUND: Fatigue is a common symptom of systemic autoimmune rheumatic disease (SARD). Patients with SARD have a protracted pre-clinical phase during which progressive immunologic derangements occur culminating in disease. In this study, we sought to determine when fatigue develops and whether its presence correlates with inflammatory factors or predicts disease progression. METHODS: Anti-nuclear antibody (ANA)-negative healthy controls (HCs) and ANA-positive participants with no criteria, at least one clinical criteria (undifferentiated connective tissue disease, UCTD), or meeting SARD classification criteria were recruited. Fatigue was assessed using a modified version of the FACIT-F questionnaire and the presence of fibromyalgia determined using a questionnaire based on the modified 2010 ACR criteria. Peripheral blood expression of five IFN-induced genes was quantified by NanoString and the levels of IL-1ß, IL-6, or TNF-α by ELISA. RESULTS: Fatigue was as prevalent and severe in individuals lacking SARD criteria as it was in UCTD and SARD. Overall, ~ 1/3 of ANA+ subjects met fibromyalgia criteria, with no differences between sub-groups. Although fatigue was more severe in these individuals, those lacking fibromyalgia remained significantly more fatigued than ANA- HC. However, even in these subjects, fatigue correlated with the widespread pain index and symptom severity scores on the fibromyalgia questionnaire. Fatigue was not associated with elevated cytokine levels in any of the ANA+ sub-groups and did not predict imminent disease progression. CONCLUSIONS: Fatigue is common in ANA+ individuals lacking sufficient criteria for a SARD diagnosis, correlates with fibromyalgia-related symptoms, and is not associated with inflammation or predictive of disease progression.
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Anticuerpos Antinucleares/sangre , Citocinas/sangre , Progresión de la Enfermedad , Fatiga/sangre , Enfermedades Reumáticas/sangre , Índice de Severidad de la Enfermedad , Adulto , Anciano , Anticuerpos Antinucleares/inmunología , Autoanticuerpos/sangre , Autoanticuerpos/inmunología , Enfermedades Autoinmunes/sangre , Enfermedades Autoinmunes/diagnóstico , Enfermedades Autoinmunes/inmunología , Citocinas/inmunología , Fatiga/diagnóstico , Fatiga/inmunología , Femenino , Fibromialgia/sangre , Fibromialgia/diagnóstico , Fibromialgia/inmunología , Predicción , Humanos , Mediadores de Inflamación/sangre , Mediadores de Inflamación/inmunología , Masculino , Persona de Mediana Edad , Enfermedades Reumáticas/diagnóstico , Enfermedades Reumáticas/inmunología , Conducta de Reducción del Riesgo , Adulto JovenRESUMEN
Fibromyalgia (FM) is a chronic syndrome characterized by widespread musculoskeletal pain, and physical and emotional symptoms. Although its pathophysiology is largely unknown, immune-inflammatory pathways may be involved. We examined serum interleukin (IL)-6, high sensitivity C-reactive protein (hs-CRP), CXCL-8, and IL-10 in 67 female FM patients and 35 healthy women while adjusting for age, body mass index (BMI), and comorbid disorders. We scored the Fibromyalgia Severity Score, Widespread Pain Index (WPI), Symptom Severity Scale (SSS), Hospital Anxiety (HADS-A), and Depression Scale and the Perceived Stress Scale (PSS-10). Clinical rating scales were significantly higher in FM patients than in controls. After adjusting for covariates, IL-6, IL-10, and CXCL-8 were lower in FM than in HC, whereas hs-CRP did not show any difference. Binary regression analyses showed that the diagnosis FM was associated with lowered IL-10, quality of sleep, aerobic activities, and increased HADS-A and comorbidities. Neural networks showed that WPI was best predicted by quality of sleep, PSS-10, HADS-A, and the cytokines, while SSS was best predicted by PSS-10, HADS-A, and IL-10. Lowered levels of cytokines are associated with FM independently from confounders. Lowered IL-6 and IL-10 signaling may play a role in the pathophysiology of FM.
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Fibromialgia/sangre , Fibromialgia/inmunología , Aprendizaje Automático , Transducción de Señal/inmunología , Ansiedad/sangre , Ansiedad/psicología , Proteína C-Reactiva/metabolismo , Citocinas/sangre , Citocinas/inmunología , Depresión/sangre , Depresión/psicología , Femenino , Fibromialgia/psicología , Humanos , Mediadores de Inflamación/sangre , Mediadores de Inflamación/inmunología , Persona de Mediana Edad , Análisis Multivariante , Dolor/sangre , Dolor/diagnóstico , Escalas de Valoración Psiquiátrica , Calidad de Vida , Índice de Severidad de la Enfermedad , Encuestas y CuestionariosRESUMEN
Fibromyalgia (FM) is a highly prevalent and disabling syndrome characterized by chronic widespread musculoskeletal pain and a broad range of cognitive and affective symptoms. Up to now, the pathogenesis of FM is unknown although a peripheral and central sensitization involving an imbalance on immune biomarkers appears to have a relevant role in its aetiology. The aim of this study was to extend previous clinical findings of Mindfulness-Based Stress Reduction (MBSR) to both its impact on clinical symptomatology and immune biomarkers (IL-6, CXCL8, IL-10 and hs-CRP), and also to explore the role of biomarkers as predictors of efficacy. METHODS: A total of 70 female patients with FM were randomly assigned to two treatment modalities, namely Treatment as Usual (TAU) plus MBSR (nâ¯=â¯35) or TAU alone (nâ¯=â¯35). This study is embedded within a larger RCT (nâ¯=â¯225) that includes three study arms (TAU; TAU plus MBSR; and TAU plus the psychoeducative intervention FibroQoL), and a 12-month follow-up (clinical trial registration: NCT02561416). Blood cytokine assays and clinical assessment were conducted at baseline and post-treatment. Treatment effects were analysed using linear mixed models with intention to treat and per protocol analyses. In order to evaluate the balance between pro- and anti-inflammatory pathways, ratios of pro-inflammatory IL-6, CXCL8 and hs-CRP with the anti-inflammatory cytokine IL-10 were calculated (i.e. IL-6/IL-10, CXCL8/IL10 and hs-CRP/IL-10). RESULTS: The results show that MBSR is an efficacious intervention to reduce clinical severity of patients with FM. MBSR also prevents the tendency of IL-10 to decrease as observed in the TAU group. Higher levels of baseline CXCL8 levels attenuate the beneficial effect of MBSR practice on clinical symptomatology, including pain, energy, stiffness or quality of sleep. Furthermore, higher baseline IL-6/IL-10 and CXCL8/IL-10 ratios were associated with less improvement in psychological inflexibility following MBSR treatment. DISCUSSION: Our results show that mindfulness training has clinical efficacy in patients with FM. The results suggest that MBSR has significant immune regulatory effects in FM patients, while immune-inflammatory pathways may in part predict the clinical efficacy of MBSR. These cytokines and chemokines may be adequate biomarkers to monitor responsivity to MBSR.
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Fibromialgia/inmunología , Fibromialgia/terapia , Atención Plena/métodos , Adulto , Biomarcadores/sangre , Proteína C-Reactiva/análisis , Citocinas/sangre , Citocinas/inmunología , Femenino , Humanos , Interleucina-10/sangre , Interleucina-10/inmunología , Interleucina-6/sangre , Interleucina-6/inmunología , Interleucina-8/sangre , Interleucina-8/inmunología , Meditación/métodos , Persona de Mediana Edad , Estrés Psicológico/psicología , Resultado del TratamientoRESUMEN
Fibromyalgia is a multifaceted disease. The clinical picture of fibromyalgia covers numerous comorbidities. Each comorbidity stands as a distinct condition. However, common pathophysiologic factors are occupied in their background. Along with the genetic, environmental and neuro-hormonal factors, inflammation has been supposed to have role in the pathogenesis of fibromyalgia. The aim of the present article was to review the current literature regarding the potential role of inflammation in the pathogenesis and treatment of fibromyalgia. A literature search was conducted through PubMed/MEDLINE and Web of Science databases using relevant keywords. Recent evidence on this highly studied topic indicates that fibromyalgia has an immunological background. Cytokines/chemokines, lipid mediators, oxidative stress and several plasma-derived factors underlie the inflammatory state in fibromyalgia. There are potential new therapeutic options targeting inflammatory pathways in fibromyalgia patients. In conclusion, there is evidence to support the inflammation-driven pathways in the pathogenesis of fibromyalgia. However, further research is required to fully understand the network of inflammation and its possible role in diagnosis and/or treatment of fibromyalgia.