ABSTRACT
Fibromyalgia or fibromyalgia syndrome (FMS) is defined as a central sensitization syndrome characterized by the dysfunction of neurocircuits detecting, transmitting and processing nociceptive stimuli; the prevalent manifestation is musculoskeletal pain. In addition to pain, there are multiple accompanying symptoms, in common with other algo-dysfunctional syndromes, which are reflected in a broad spectrum of somatic, neurocognitive and neuro-vegetative manifestations. An evidence-based approach is essential in FMS management, in order to improve patient health and to reduce its social burden. Since in the last ten years new international guidelines for clinical practice (Clinical Practice Guidelines or CPGs) concerning FMS diagnosis and pharmacological/ non-pharmacological management have been published, the Italian Society of Rheumatology (SIR) has decided to adapt them to the Italian national setting. The framework of the Guidelines International Network Adaptation Working Group was adopted to identify, appraise (AGREE II), synthesize, and customize the most recent CPGs on FMS to the needs of the Italian healthcare context. A working group of rheumatologists from SIR epidemiology unit and FMS experts identified relevant clinical questions to guide the systematic review of the literature. The target audience of these CPGs included physicians and healthcare professionals who manage FMS. The adapted recommendations were finally assessed by an external multidisciplinary panel. From the systematic search in databases (Pubmed/Medline, Embase) and grey literature, 6 CPGs were selected and appraised by two independent raters. The combination of the scientific evidence underlying the original CPGs with expert opinion lead to the development of 17 recommendations. The quality of evidence for each recommendation was reported and their potential impact on clinical practice was assessed. These SIR recommendations are expected to be a valuable aid in the diagnosis and treatment of FMS, as they will contribute to disseminate the best practice on the basis of the current scientific evidence.
Subject(s)
Fibromyalgia , Rheumatology , Fibromyalgia/diagnosis , Fibromyalgia/therapy , Humans , ItalyABSTRACT
The aim of this study was to evaluate the accuracy of synovial fluid analysis in the identification of calcium pyrophosphate dihydrate crystals compared to microscopic analysis of joint tissues as the reference standard. This is an ancillary study of an international, multicentre cross-sectional study performed by the calcium pyrophosphate deposition disease (CPPD) subgroup of the OMERACT Ultrasound working group. Consecutive patients with knee osteoarthritis (OA) waiting for total knee replacement surgery were enrolled in the study from 2 participating centres in Mexico and Romania. During the surgical procedures, synovial fluid, menisci and hyaline cartilage were collected and analysed within 48 hours from surgery under transmitted light microscopy and compensated polarised light microscopy for the presence/absence of calcium pyrophosphate crystals. All slides were analysed by expert examiners on site, blinded to other findings. A dichotomic score (absence/ presence) was used for scoring both synovial fluid and tissues. Microscopic analysis of knee tissues was considered the gold standard. Sensitivity, specificity, accuracy, positive and negative predictive values of synovial fluid analysis in the identification of calcium pyrophosphate crystals were calculated. 15 patients (53% female, mean age 68 yo ± 8.4) with OA of grade 3 or 4 according to Kellgren-Lawrence scoring were enrolled. 12 patients (80%) were positive for calcium pyrophosphate crystals at the synovial fluid analysis and 14 (93%) at the tissue microscopic analysis. The overall diagnostic accuracy of synovial fluid analysis compared with histology for CPPD was 87%, with a sensitivity of 86% and a specificity of 100%, the positive predictive value was 100% and the negative predictive value was 33%. In conclusion synovial fluid analysis proved to be an accurate test for the identification of calcium pyrophosphate dihydrate crystals in patients with advanced OA.
Subject(s)
Chondrocalcinosis , Osteoarthritis, Knee , Aged , Calcium Pyrophosphate , Chondrocalcinosis/diagnostic imaging , Cross-Sectional Studies , Female , Humans , Male , Osteoarthritis, Knee/diagnostic imaging , Synovial FluidABSTRACT
Klotho is a transmembrane and soluble glycoprotein that governs vascular integrity. Previous studies have demonstrated reduced serum klotho concentrations in patients with systemic sclerosis (SSc), and it is known that klotho deficiency can impair the healing of digital ulcers related to microvessel damage. The aim of this study was to evaluate the association between serum klotho levels and nailfold capillaroscopic abnormalities in SSc patients. We retrospectively enrolled 54 consecutive patients with SSc diagnosed on the basis of the 2013 EULAR/ACR criteria [11 with diffuse SSc; 47 females; median age 68.0 years (IQ 18); median disease duration 11.0 years (IQ 7)]. Serum klotho concentrations were determined by means of an enzyme-linked immunosorbent assay. On the basis of the 2000 classification of Cutolo et al., 14 patients had normal nailfold capillaroscopic findings, 8 had an early scleroderma pattern, 21 an active scleroderma pattern, and 11 a late scleroderma pattern. The median serum klotho concentration was 0.29 ng/mL (IQ 1). Regression analysis of variation showed an inverse correlation between serum klotho concentrations and the severity of the capillaroscopic pattern (p=0.02; t -2.2284), which was not influenced by concomitant treatment. Logistic regression did not reveal any significant association between the risk of developing digital ulcers and nailfold capillaroscopic patterns, serum klotho levels, or concomitant medications. The presence of avascular areas significantly correlated with calcinosis (p=0.006). In line with previous studies, our findings confirm that klotho plays a role in preventing microvascular damage detected with nailfold capillaroscopy.
Subject(s)
Calcinosis/complications , Glucuronidase/blood , Microscopic Angioscopy , Nail Diseases/blood , Nails/blood supply , Scleroderma, Systemic/blood , Adult , Aged , Antibodies, Antinuclear/blood , Biomarkers/blood , Female , Humans , Klotho Proteins , Male , Middle Aged , Nail Diseases/etiology , Regression Analysis , Retrospective Studies , Ulcer/etiologyABSTRACT
OBJECTIVE: The original European League Against Rheumatism recommendations for managing fibromyalgia assessed evidence up to 2005. The paucity of studies meant that most recommendations were 'expert opinion'. METHODS: A multidisciplinary group from 12 countries assessed evidence with a focus on systematic reviews and meta-analyses concerned with pharmacological/non-pharmacological management for fibromyalgia. A review, in May 2015, identified eligible publications and key outcomes assessed were pain, fatigue, sleep and daily functioning. The Grading of Recommendations Assessment, Development and Evaluation system was used for making recommendations. RESULTS: 2979 titles were identified: from these 275 full papers were selected for review and 107 reviews (and/or meta-analyses) evaluated as eligible. Based on meta-analyses, the only 'strong for' therapy-based recommendation in the guidelines was exercise. Based on expert opinion, a graduated approach, the following four main stages are suggested underpinned by shared decision-making with patients. Initial management should involve patient education and focus on non-pharmacological therapies. In case of non-response, further therapies (all of which were evaluated as 'weak for' based on meta-analyses) should be tailored to the specific needs of the individual and may involve psychological therapies (for mood disorders and unhelpful coping strategies), pharmacotherapy (for severe pain or sleep disturbance) and/or a multimodal rehabilitation programme (for severe disability). CONCLUSIONS: These recommendations are underpinned by high-quality reviews and meta-analyses. The size of effect for most treatments is relatively modest. We propose research priorities clarifying who will benefit from specific interventions, their effect in combination and organisation of healthcare systems to optimise outcome.
Subject(s)
Activities of Daily Living , Fatigue/therapy , Fibromyalgia/therapy , Practice Guidelines as Topic , Sleep , Acupuncture Therapy , Amitriptyline/analogs & derivatives , Amitriptyline/therapeutic use , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Anticonvulsants/therapeutic use , Antidepressive Agents, Tricyclic/therapeutic use , Biofeedback, Psychology , Capsaicin/therapeutic use , Cognitive Behavioral Therapy , Europe , Evidence-Based Medicine , Exercise Therapy , Fatigue/physiopathology , Fibromyalgia/physiopathology , Human Growth Hormone/therapeutic use , Humans , Hydrotherapy , Hypnosis , Manipulation, Chiropractic , Massage , Mind-Body Therapies , Mindfulness , Monoamine Oxidase Inhibitors/therapeutic use , Pain/physiopathology , S-Adenosylmethionine/therapeutic use , Sensory System Agents/therapeutic use , Selective Serotonin Reuptake Inhibitors/therapeutic use , Serotonin and Noradrenaline Reuptake Inhibitors/therapeutic use , Societies, Medical , Sodium Oxybate/therapeutic use , Treatment OutcomeABSTRACT
The aim was to evaluate the role of klotho in the pathogenesis of systemic sclerosis (SSc), through the measurement of its serum concentration in SSc patients compared to healthy controls, and to assess the association with cutaneous and visceral involvement. Blood samples obtained from both SSc patients and healthy controls were analysed by an ELISA assay for the detection of human klotho. SSc patients were globally evaluated for disease activity and assessed through the modified Rodnan's Skin Score, Medsger's scale, pulmonary function tests, 2D-echocardiography, nailfold capillaroscopy and laboratory tests. Our cohort consisted of 69 SSc patients (61 females, mean age 64.5±12.5 years, median disease duration 9.0 (IQR 8) years) and 77 healthy controls (28 females, mean age 49.7±10.2 years). In the group of SSc patients, 19 (27.5%) suffered from a diffuse form of SSc. All patients were receiving IV prostanoids, and some of them were concomitantly treated with immunosuppressive drugs (prednisone, hydroxychloroquine, mofetil mycophenolate, methotrexate, cyclosporin A and azathioprine). The median serum concentration of klotho was significantly lower in patients compared to controls (0.23 ng/mL vs 0.60 ng/mL; p<0.001). However, Spearman's test showed no significant association between klotho serum levels and disease activity, concerning either clinical, laboratory or instrumental findings. Our data show a significant deficit of klotho in SSc patients although any significant association was detected between klotho serum concentration and the clinical, laboratory or instrumental features of the disease. However, due to the limits of the study, further investigations are required.
Subject(s)
Glucuronidase/physiology , Scleroderma, Systemic/blood , Adult , Aged , Biomarkers , Female , Glucuronidase/blood , Humans , Immunosuppressive Agents/therapeutic use , Klotho Proteins , Lung/pathology , Male , Microscopic Angioscopy , Middle Aged , Osteoporosis/etiology , Prostaglandins/therapeutic use , Scleroderma, Systemic/complications , Scleroderma, Systemic/drug therapy , Scleroderma, Systemic/pathology , Statistics, NonparametricABSTRACT
It is still unknown whether there is an association between the use of certolizumab pegol (CZP) in rheumatic patients and the onset of cardiac arrhythmias. We describe the cases of two patients with rheumatoid arthritis (RA) treated with CZP as the first-line biological drug and methotrexate (MTX), who developed an arrhythmic event. The first was a 60-year-old, hypertensive male smoker, the second a 66-year-old dyslipidemic female non-smoker. Both were diagnosed as having RA in 2010, and started treatment with MTX plus CZP. The first patient developed undatable atrial fibrillation, which was resistant to pharmacological treatment and electrical cardioversion. The second patient developed an atrial flutter, which was treated with a betablocker. In both cases, we set a cautious interval between two consecutive administrations of CZP and, in the first case, also reduced the dose of MTX without any worsening of RA activity. Although many studies have shown that tumor necrosis factor (TNF)-alpha plays a pathogenetic role in inducing an arrhythmogenic substrate that is apparently rescued by anti-TNF drugs, there is still a lack of conclusive data. We suggest caution in any patient developing a cardiac event (including rhythm disorders) during treatment with a conventional or biological disease-modifying anti-rheumatic drug.
Subject(s)
Antirheumatic Agents/adverse effects , Arrhythmias, Cardiac/chemically induced , Certolizumab Pegol/adverse effects , Aged , Antirheumatic Agents/administration & dosage , Arrhythmias, Cardiac/drug therapy , Arthritis, Rheumatoid/drug therapy , Bisoprolol/therapeutic use , Certolizumab Pegol/administration & dosage , Drug Therapy, Combination , Female , Fibrinolytic Agents/therapeutic use , Humans , Hypertension/complications , Male , Middle Aged , Pyrazoles/therapeutic use , Pyridones/therapeutic use , Risk Factors , Smoking/adverse effects , Sympatholytics/therapeutic use , Treatment OutcomeABSTRACT
The aim of this study was to determine the prevalence of T helper 9 (Th9) lymphocytes in rheumatoid arthritis (RA) patients and to identify a possible association between the percentage of Th9 and the discontinuation of a biological treatment with an anti-tumor necrosis factor (TNF) (infliximab). We collected peripheral blood mononuclear cells (PBMCs) from 55 consecutive RA outpatients and 10 healthy controls. Among RA patients, 15 were not receiving any immunosuppressive drug, 20 were successfully treated with infliximab and 20 discontinued infliximab because of adverse events or inefficacy and were treated with other biological agents. PBMCs were cultured with/without infliximab 50 mg/L for 18 h, and the percentage of Th9 cells was assessed by means of flow cytometry. Th9 lymphocytes were identified as interferon gamma, interleukin (IL)4-, IL17-, IL9-secreting cluster of differentiation 4 (CD4)+ T cells. Cytometric analysis revealed no significant decrease in the percentage of Th9 cells after infliximab exposure in any of the groups, although it was lower in healthy controls than RA patients either before and after the infliximab stimulation assay. Th9 cells are IL-9-secreting T helper lymphocytes whose role in RA is still poorly known. IL-9 levels are increased in RA patients, in whom this cytokine plays a crucial role. Th9 cells are the major producers of IL-9, and their prevalence is higher in RA patients than in healthy subjects; however our experiment in vitro does not demonstrate an association between Th9 lymphocytes and the response to infliximab. Further studies are required to evaluate the real involvement of Th9 population in the immunogenicity of anti-TNF agents.
Subject(s)
Antirheumatic Agents/therapeutic use , Arthritis, Rheumatoid/diagnosis , Arthritis, Rheumatoid/drug therapy , Infliximab/therapeutic use , Interleukin-9/blood , Tumor Necrosis Factor-alpha/antagonists & inhibitors , Adult , Arthritis, Rheumatoid/blood , Arthritis, Rheumatoid/immunology , Biomarkers/blood , Body Mass Index , Case-Control Studies , Female , Humans , In Vitro Techniques , Leukocytes, Mononuclear/drug effects , Leukocytes, Mononuclear/immunology , Male , Middle Aged , Outpatients , Predictive Value of Tests , Sensitivity and SpecificityABSTRACT
OBJECTIVES: To compare the effectiveness of rituximab versus an alternative tumour necrosis factor (TNF) inhibitor (TNFi) in patients with rheumatoid arthritis (RA) with an inadequate response to one previous TNFi. METHODS: SWITCH-RA was a prospective, global, observational, real-life study. Patients non-responsive or intolerant to a single TNFi were enrolled ≤4â weeks after starting rituximab or a second TNFi. Primary end point: change in Disease Activity Score in 28 joints excluding patient's global health component (DAS28-3)-erythrocyte sedimentation rate (ESR) over 6â months. RESULTS: 604 patients received rituximab, and 507 an alternative TNFi as second biological therapy. Reasons for discontinuing the first TNFi were inefficacy (n=827), intolerance (n=263) and other (n=21). A total of 728 patients were available for primary end point analysis (rituximab n=405; TNFi n=323). Baseline mean (SD) DAS28-3-ESR was higher in the rituximab than the TNFi group: 5.2 (1.2) vs 4.8 (1.3); p<0.0001. Least squares mean (SE) change in DAS28-3-ESR at 6â months was significantly greater in rituximab than TNFi patients: -1.5 (0.2) vs -1.1 (0.2); p=0.007. The difference remained significant among patients discontinuing the initial TNFi because of inefficacy (-1.7 vs -1.3; p=0.017) but not intolerance (-0.7 vs -0.7; p=0.894). Seropositive patients showed significantly greater improvements in DAS28-3-ESR with rituximab than with TNFi (-1.6 (0.3) vs -1.2 (0.3); p=0.011), particularly those switching because of inefficacy (-1.9 (0.3) vs -1.5 (0.4); p=0.021). The overall incidence of adverse events was similar between the rituximab and TNFi groups. CONCLUSIONS: These real-life data indicate that, after discontinuation of an initial TNFi, switching to rituximab is associated with significantly improved clinical effectiveness compared with switching to a second TNFi. This difference was particularly evident in seropositive patients and in those switched because of inefficacy.
Subject(s)
Antibodies, Monoclonal, Murine-Derived/therapeutic use , Antirheumatic Agents/therapeutic use , Arthritis, Rheumatoid/drug therapy , Tumor Necrosis Factor-alpha/antagonists & inhibitors , Adrenal Cortex Hormones/therapeutic use , Adult , Aged , Drug Substitution , Drug Therapy, Combination , Female , Humans , Male , Methotrexate/therapeutic use , Middle Aged , Prospective Studies , Rituximab , Treatment Failure , Treatment OutcomeABSTRACT
OBJECTIVES: We investigated sub-clinical cardiovascular involvement in primary Sjögren's syndrome (pSS) patients by means of ADMA, coronary flow reserve (CFR), intima media thickness (cIMT), pulse wave velocity (PWV) and myocardial deformation. METHODS: The study involved 22 outpatients with pSS (6 males, 16 females; mean age 60.14±7.81 years) and no documentable cardiovascular disease, and 22 age- and gender-matched controls. Dipyridamole transthoracic stress echocardiography was used to evaluate wall motion and CFR. A CFR value of <2.5 was considered a sign of impaired coronary function. We also evaluated cIMT arterial stiffness PWV and plasma ADMA levels, and made a speckle tracking echocardiography (STE) analysis. RESULTS: All of the patients were affected by pSS. Although within the normal range, the patients' CFR was lower than that of the controls (median 2.70; IQR 2.40-2.90 vs. 3.20; IQR 3.06-3.33; p<0.0001), whereas their ADMA levels were significantly higher (median 0.81 µM; IQR 0.79-0.85 µM vs. 0.54 µM; IQR 0.52-0.58 µM; p<0.0001). Both left and right PWV values were significantly higher in the patients than in the controls (median 8.8 m/s right and 8.9 m/s left vs. 6.86 and 6.89 m/s), whereas QIMT was substantially similar in the two groups. CONCLUSIONS: Higher ADMA levels suggest the presence of endothelial dysfunction and sub-clinical atherosclerosis in pSS patients, even in the case of a normal CFR. This finding is supported by the PWV values, which were higher in the pSS patients. ADMA levels and PWV values may be useful markers for identifying early endothelial dysfunction in pSS patients.
Subject(s)
Atherosclerosis/diagnostic imaging , Atherosclerosis/epidemiology , Echocardiography , Sjogren's Syndrome/diagnostic imaging , Sjogren's Syndrome/epidemiology , Aged , Arginine/analogs & derivatives , Arginine/blood , Atherosclerosis/physiopathology , Carotid Intima-Media Thickness , Coronary Circulation/physiology , Endothelium, Vascular/physiopathology , Female , Humans , Male , Middle Aged , Pilot Projects , Pulse Wave Analysis , Risk Factors , Sjogren's Syndrome/physiopathology , Vascular Stiffness/physiologyABSTRACT
Pain, a complex phenomenon influenced by a series of genetic, biological, psychological and social factors, is a major component of many rheumatological conditions and the result of physiological interactions between central and peripheral nervous system signalling. It may be acute or chronic (generally defined as lasting ≥ three months): acute pain is often primarily attributable to inflammation and/or damage to peripheral structures (i.e. nociceptive input), whereas chronic pain is more likely to be due to input from the central nervous system (CNS). The many different aspects of pain mean that rheumatologists and other clinicians need to have enough expertise to diagnose the type of pain correctly and treat it appropriately. However, most rheumatologists receive little formal training concerning contemporary theories of pain processing or management, and this may affect the clinical results of any specific target therapy.
Subject(s)
Pain/etiology , Rheumatic Diseases/physiopathology , Analgesics/therapeutic use , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Central Nervous System Sensitization , Combined Modality Therapy , Exercise Therapy , Fibromyalgia/physiopathology , Humans , Neurotransmitter Agents/physiology , Pain/diagnosis , Pain/physiopathology , Pain Management , Pain Perception , Quality of Life , Rheumatic Diseases/immunologyABSTRACT
Medically unexplained symptoms are considered 'somatoform disorders' in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV). The introduction of this nosographic category has been helpful in drawing attention to a previously neglected area, but has not been successful in promoting an understanding of the disorders' biological basis and treatment implications, probably because of a series of diagnostic shortcomings. The newly proposed DSM-V diagnostic criteria try to overcome the limitations of the DSM-IV definition, which was organised centrally around the concept of medically unexplained symptoms, by emphasising the extent to which a patient's thoughts, feelings and behaviours concerning their somatic symptoms are disproportionate or excessive. This change is supported by a growing body of evidence showing that psychological and behavioural features play a major role in causing patient disability and maintaining high level of health care use. Pain disorders is the sub-category of DSM-IV somatoform disorders that most closely resembles fibromyalgia. Regardless of the diagnostic changes recently brought about by DSM-V, neuroimaging studies have identified important components of the mental processes associated with a DSM- IV diagnosis of pain disorder.
Subject(s)
Chronic Pain/etiology , Diagnostic and Statistical Manual of Mental Disorders , Fibromyalgia/diagnosis , Musculoskeletal Pain/etiology , Pain Perception , Rheumatic Diseases/psychology , Somatoform Disorders/diagnosis , Chronic Pain/diagnosis , Chronic Pain/psychology , Diagnosis, Differential , Fibromyalgia/complications , Fibromyalgia/psychology , Humans , Hyperalgesia/diagnosis , Hyperalgesia/etiology , Hyperalgesia/psychology , Musculoskeletal Pain/diagnosis , Musculoskeletal Pain/psychology , Neuroimaging , Pain Measurement , Rheumatic Diseases/complications , Rheumatic Diseases/diagnosis , Somatoform Disorders/classification , Somatoform Disorders/etiology , Somatoform Disorders/psychology , Symptom AssessmentABSTRACT
Pain is the main manifestation of many rheumatic diseases (be they overtly inflammatory such as rheumatoid arthritis or dysfunctional such as fibromyalgia) but, at least initially, the mechanisms involved in the genesis, amplification and chronicisation of the persistent pain characterising the various conditions can be very different. The main peripheral mechanism underlying acute nociceptive pain is a change in the activity of the nociceptors located in the affected anatomical structures (joints, tendons and ligaments), which makes them more sensitive to normally painful stimuli (hyperalgesia) or normally non-painful stimuli (allodynia). This physiopathological mechanism of peripheral sensitisation plays a primary role in rheumatic diseases characterised by acute inflammation, such as the arthritides due to microcrystals. In the case of chronic rheumatic diseases that do not regress spontaneously, functional and structural central nervous system changes cause a generalised reduction in the pain threshold that is not limited to the anatomical structures involved, thus leading to the appearance of hyperalgesia and allodynia in many, if not all body districts. This is the physiopathological basis of chronic, widespread musculoskeletal pain.
Subject(s)
Central Nervous System Sensitization/physiology , Chronic Pain/physiopathology , Nociceptors/physiology , Rheumatic Diseases/physiopathology , Adaptation, Psychological , Autonomic Nervous System/physiopathology , Chronic Pain/immunology , Chronic Pain/psychology , Depression/complications , Depression/physiopathology , Humans , Hyperalgesia/physiopathology , Musculoskeletal Pain/immunology , Musculoskeletal Pain/physiopathology , Musculoskeletal Pain/psychology , Musculoskeletal Pain/therapy , Nerve Growth Factors/physiology , Neuroimmunomodulation/physiology , Neurotransmitter Agents/physiology , Pain Management , Pain Perception/physiology , Peripheral Nervous System/physiopathology , Posterior Horn Cells/physiology , Rheumatic Diseases/immunology , Rheumatic Diseases/psychologyABSTRACT
Chronic pain is a healthcare problem that significantly affects the mental health, and the professional and private life of patients. It can complicate many disorders and represents a common symptom of rheumatologic diseases, but the data on its prevalence is still limited. Pain is a ubiquitous problem in systemic sclerosis (SSc). SSc-related pain has been studied on the basis of biomedical models and is considered a symptom caused by the disease activity or previous tissue damage. Effective pain management is a primary goal of the treatment strategy, although this symptom in SSc has not yet been investigated in detail. However, these patients do not all respond adequately to pharmacological pain therapies, therefore in these cases a multimodal approach needs to be adopted. This paper must be considered as retracted due to a plagiarism misconduct. See the Retraction note at: https://doi.org/10.4081/reumatismo.2018.1171
Subject(s)
Chronic Pain/etiology , Musculoskeletal Pain/etiology , Scleroderma, Systemic/complications , Analgesics/therapeutic use , Autoantibodies/immunology , Bursitis/etiology , Bursitis/physiopathology , Centromere/immunology , Chronic Pain/epidemiology , Chronic Pain/physiopathology , Chronic Pain/psychology , Chronic Pain/therapy , Cognitive Behavioral Therapy , Combined Modality Therapy , Emotions , Fibromyalgia/etiology , Fibromyalgia/physiopathology , Humans , Models, Biological , Musculoskeletal Pain/epidemiology , Musculoskeletal Pain/physiopathology , Musculoskeletal Pain/psychology , Musculoskeletal Pain/therapy , Pain Management , Prevalence , Scleroderma, Systemic/immunology , Scleroderma, Systemic/physiopathology , Scleroderma, Systemic/psychology , Social SupportABSTRACT
Pain is the hallmark symptom of fibromyalgia (FM) and other related syndromes, but quite different from that of other rheumatic diseases, which depends on the degree of damage or inflammation in peripheral tissues. Sufferers are often defined as patients with chronic pain without an underlying mechanistic cause, and these syndromes and their symptoms are most appropriately described as "central pain", "neuropathic pain", "nonnociceptive pain" or "central sensitivity syndromes". The pain is particular, regional or widespread, and mainly relates to the musculoskeletal system; hyperalgesia or allodynia are typical. Its origin is currently considered to be distorted pain or sensory processing, rather than a local or regional abnormality. FM is probably the most important and extensively described central pain syndrome, but the characteristics and features of FM-related pain are similar in other disorders of particular interest for rheumatologists, such as myofascial pain syndromes and temporo-mandibular joint disorders, and there is also an intriguing overlap between FM and benign joint hypermobility syndrome. This suggests that the distinctive aspects of pain in these idiopathic or functional conditions is caused by central nervous system hypersensitivity and abnormalities. Pharmacological and non-pharmacological therapies have been suggested for the treatment of these conditions, but a multidisciplinary approach is required in order to reduce the abnormal cycle of pain amplification and the related maladaptive and self-limiting behaviours.
Subject(s)
Chronic Pain/etiology , Fibromyalgia/physiopathology , Myofascial Pain Syndromes/physiopathology , Neuralgia/physiopathology , Analgesics/therapeutic use , Central Nervous System Sensitization , Chronic Pain/physiopathology , Chronic Pain/psychology , Chronic Pain/therapy , Combined Modality Therapy , Fatigue/etiology , Fibromyalgia/diagnosis , Fibromyalgia/psychology , Humans , Hyperalgesia/etiology , Hyperalgesia/physiopathology , Models, Neurological , Neuralgia/etiology , Neuralgia/psychology , Neuralgia/therapy , Pain Management , Pain Perception/physiology , Sleep Disorders, Intrinsic/complications , Sleep Disorders, Intrinsic/physiopathology , Stress, Psychological/complications , Stress, Psychological/physiopathology , Temporomandibular Joint Dysfunction Syndrome/physiopathologyABSTRACT
Chronic pain has been identified as an important issue related to various rheumatic diseases. At the time of a major government spending review, it is appropriate to discuss the pain characterising rheumatic diseases and its related costs. It is clearly essential for healthcare authorities to rationalise their policies on the basis of the increasing expectations of the users of healthcare services while simultaneously balancing their books. There are few published studies concerning the costs of pain of any kind, and the same is true of the costs of the chronic pain associated with diseases such as rheumatoid arthritis, osteoarthritis, and fibromyalgia.
Subject(s)
Chronic Pain/economics , Cost of Illness , Musculoskeletal Pain/economics , Rheumatic Diseases/economics , Acute Pain/economics , Acute Pain/etiology , Analgesics/economics , Analgesics/therapeutic use , Antirheumatic Agents/economics , Antirheumatic Agents/therapeutic use , Arthritis, Rheumatoid/complications , Arthritis, Rheumatoid/economics , Chronic Pain/etiology , Drug Costs , Europe , Fibromyalgia/complications , Fibromyalgia/economics , Health Expenditures , Health Policy , Health Resources/statistics & numerical data , Health Services Needs and Demand , Humans , Italy/epidemiology , Musculoskeletal Pain/etiology , Osteoarthritis/complications , Osteoarthritis/economics , Prescription Fees , Quality of Life , Rheumatic Diseases/complications , Rheumatic Diseases/epidemiology , United StatesABSTRACT
Patients with rheumatoid arthritis (RA) are frequently afflicted by pain, which may be caused by joint inflammation (leading to structural joint damage) or secondary osteoarthritis, and may be increased by central sensitisation. Non-inflammatory pain may also confuse the assessment of disease activity, and so the aim of treatment is not only to combat inflammatory disease, but also relieve painful symptoms. In order to ensure effective treatment stratification, it is necessary to record a patients medical history in detail, perform a physical examination, and objectively assess synovitis and joint damage. The management of pain requires various approaches that include pharmacological analgesia and biological and non-biological treatments. Although joint replacement surgery can significantly improve RA-related pain, it may only be available to patients with the most severe advanced disease.
Subject(s)
Chronic Pain/physiopathology , Musculoskeletal Pain/physiopathology , Analgesics/therapeutic use , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Antirheumatic Agents/therapeutic use , Arthritis, Rheumatoid/immunology , Arthritis, Rheumatoid/physiopathology , Central Nervous System Sensitization , Chronic Pain/diagnosis , Chronic Pain/psychology , Chronic Pain/therapy , Cognitive Behavioral Therapy , Combined Modality Therapy , Exercise Therapy , Fibromyalgia/complications , Fibromyalgia/drug therapy , Fibromyalgia/physiopathology , Humans , Inflammation , Musculoskeletal Pain/diagnosis , Musculoskeletal Pain/psychology , Musculoskeletal Pain/therapy , Neurotransmitter Agents/physiology , Osteoarthritis/complications , Osteoarthritis/physiopathology , Pain Management , Pain Measurement , Pain Perception , Pain Threshold/physiologyABSTRACT
The pain associated with spondyloarthritis (SpA) can be intense, persistent and disabling. It frequently has a multifactorial, simultaneously central and peripheral origin, and may be due to currently active inflammation, or joint damage and tissue destruction arising from a previous inflammatory condition. Inflammatory pain symptoms can be reduced by non-steroidal anti-inflammatory drugs, but many patients continue to experience moderate pain due to alterations in the mechanisms that regulate central pain, as in the case of the chronic widespread pain (CWP) that characterises fibromyalgia (FM). The importance of distinguishing SpA and FM is underlined by the fact that SpA is currently treated with costly drugs such as tumour necrosis factor (TNF) inhibitors, and direct costs are higher in patients with concomitant CWP or FM than in those with FM or SpA alone. Optimal treatment needs to take into account symptoms such as fatigue, mood, sleep, and the overall quality of life, and is based on the use of tricyclic antidepressants or selective serotonin reuptake inhibitors such as fluoxetine, rather than adjustments in the dose of anti-TNF agents or disease-modifying drugs.
Subject(s)
Chronic Pain/etiology , Musculoskeletal Pain/etiology , Spondylarthritis/physiopathology , Analgesics/therapeutic use , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Antidepressive Agents/therapeutic use , Antirheumatic Agents/therapeutic use , Arthritis, Psoriatic/diagnosis , Arthritis, Psoriatic/physiopathology , Central Nervous System Sensitization/physiology , Chronic Pain/drug therapy , Chronic Pain/economics , Chronic Pain/physiopathology , Chronic Pain/psychology , Cross-Sectional Studies , Diagnosis, Differential , Fatigue/etiology , Fibromyalgia/diagnosis , Fibromyalgia/physiopathology , Humans , Musculoskeletal Pain/drug therapy , Musculoskeletal Pain/economics , Musculoskeletal Pain/physiopathology , Musculoskeletal Pain/psychology , Pain Management , Pain Measurement , Quality of Life , Sleep Disorders, Intrinsic/etiology , Spondylarthritis/diagnosis , Spondylarthritis/drug therapy , Spondylarthritis/economicsABSTRACT
Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by heterogeneous clinical manifestations involving virtually the entire body. The pain in SLE can have different causes. The SLE classification criteria include mainly the musculoskeletal manifestations of pain, which are commonly reported as initial symptoms of SLE, such as arthralgia, arthritis and/or myalgia. Chronic widespread pain, which is typical of fibromyalgia (FM), is frequently associated with SLE. The aim of this review is to describe widespread pain and fatigue in SLE, and the association of SLE and FM. Although secondary FM is not correlated with the disease activity, it may interfere with the daily activities of SLE patients. Therefore it is necessary to identify its symptoms and treat them promptly to improve the quality of life of patients. In conclusion, it is essential to identify the origin of pain in SLE in order to avoid dangerous over-treatment in patients with co-existing widespread pain and FM.
Subject(s)
Lupus Erythematosus, Systemic/physiopathology , Pain/etiology , Analgesics/therapeutic use , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Anticonvulsants/therapeutic use , Antidepressive Agents/therapeutic use , Central Nervous System Sensitization , Comorbidity , Diagnosis, Differential , Fatigue/etiology , Fibromyalgia/complications , Fibromyalgia/diagnosis , Fibromyalgia/physiopathology , Fibromyalgia/psychology , Humans , Lupus Erythematosus, Systemic/diagnosis , Lupus Erythematosus, Systemic/immunology , Pain/diagnosis , Pain/drug therapy , Pain/physiopathology , Pain/psychology , Pain Management , Pain Perception , Quality of LifeABSTRACT
Temporomandibular joint (TMJ) involvement is common but usually delayed in patients with juvenile idiopathic arthritis (JIA). We describe the case of a JIA patient with bilateral TMJ involvement, mandibular retrognathia, bone erosion, and severely restricted mouth opening. The use of cone beam computed tomography and a 3D diagnostic protocol in young patients with JIA provides reliable, accurate and precise quantitative data and images of the condylar structures and their dimensional relationships. Analgesics and conventional disease modifying antirheumatic drugs were ineffective, but interdisciplinary treatment with etanercept and a Herbst functional appliance improved functional TMJ movement and bone resorption.
Subject(s)
Arthritis, Juvenile/complications , Cone-Beam Computed Tomography , Imaging, Three-Dimensional , Temporomandibular Joint Disorders/diagnostic imaging , Temporomandibular Joint Disorders/etiology , Adolescent , Humans , MaleABSTRACT
OBJECTIVE: We aimed to compare a chemiluminescent immunoassay (CIA, QUANTA Flash) on BIO-FLASH with a multiplex flow immunoassay (MFI) on BioPlex 2200 for the detection of antibodies to Ro60, Ro52, and SS-B. METHODS: The study included 241 samples, from patients suffering from systemic autoimmune diseases (n = 108) as well as disease controls (n = 133). All samples were tested for anti-Ro52, anti-Ro60, and anti-SS-B (La) antibodies on QUANTA Flash (INOVA Diagnostics, San Diego, USA) and BioPlex 2200 (Bio-Rad Laboratories Inc., Hercules, USA). Discrepant samples were tested by two independent methods: BlueDot/ANA and QUANTRIX Microarray (both D-tek, Belgium). RESULTS: The overall qualitative agreements were 95.4% (95% confidence interval, CI 92.0-97.7%) for anti-Ro52, 98.8% (95% CI 96.4-99.7%) for anti-Ro60, and 91.7% (95% CI 87.5-94.9%) for anti-SS-B antibodies. There were 34 discrepant samples among all assays (20 anti-SS-B, 11 anti-Ro52, 3 anti-Ro60). 30/33 of retested samples (by D-tek dot blot) agreed with the QUANTA Flash results. Similar findings were obtained with QUANTRIX Microarray kit. CONCLUSION: QUANTA Flash and BioPlex 2200 show good qualitative agreement. The clinical performances were similar for anti-Ro52 and anti-Ro60 autoantibodies while differences were observed for anti-SS-B (La) antibodies.