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ID PMID Title PublicationDate abstract
24061693 Intermediate to long-term follow-up results of INH chemoprophylaxis prior to anti-TNF-alph 2013 Oct BACKGROUND: The use of anti-TNF drugs for rheumatic diseases has increased in recent years. Several studies have reported an increased risk of reactivation of tuberculosis (TB) with anti-TNF agents. OBJECTIVES: The aim of this study was to present the follow-up results of a single center from Turkey, a country with a high rate of active and latent tuberculosis infection (LTBI), for INH chemoprophylaxis in patients receiving anti-TNF-α therapy for rheumatic diseases infection. METHODS: In this prospective observational study, consenting patients who were to be administered an anti-TNF agent for a rheumatic disease were evaluated for the presence of active infection or LTBI by a chest X-ray and a tuberculin skin test. Patients with LTBI were given chemoprophylaxis 1 month prior to commencement of anti-TNF treatment. All patients were followed-up bimonthly for any signs of pulmonary or extrapulmonary TB. RESULTS: A total of 73 patients, 23 female (31.5 %) and 50 male (68.5 %), with a mean age of 41.0 ± 13.1 years (18-78) were enrolled in the study. Overall, 44 patients (60.3 %) had ankylosing spondylitis, 18 (24.7 %) had rheumatoid arthritis, 7 (9.6 %) had juvenile rheumatoid arthritis, and 3 (4.1 %) had psoriatic arthritis. LTBI was identified in 58 patients all of whom received chemoprophylaxis for 9 months. None of the patients in the study developed any signs of tuberculosis reactivation during follow-up. CONCLUSIONS: TST is a reliable and cost-effective method for the diagnosis of LTBI in patients prior to anti-TNF therapy. Moreover, chemoprophylaxis with INH seems to be effective for the prevention of TB reactivation in individuals with LTBI.
23618995 One-year prospective outcome analysis and complications following total replacement of the 2013 Oct Total replacement of the temporomandibular joint (TMJ) is increasingly accepted as the gold standard for reconstruction of irreparably damaged or ankylosed joints. The TMJ Concepts system (TMJ Concepts, Ventura, USA) has the longest follow-up of the 2 systems used in the UK. A total of 74 patients had placement of TMJ Concepts prostheses. The primary diagnoses were degenerative disease, multiple previous operations, injury, rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and ankylosis. Of these, 12 were revisions of previous replacements (3 after multiple operations). Over the year there was a significant mean (SD) reduction in pain score (10 cm visual analogue scale) from 72 (2.5) to 8 (1.7) (p<0.0001), and mean (SD) improvements in mouth opening from 22.4 mm (9.4) to 33.7 mm (6.2) (p<0.0001), and dietary consistency (10 cm analogue liquid 0 to solid 100) from 38 (23) to 93 (16) (p<0.0001). No patient had worse symptoms postoperatively. Joints in 2 patients failed because of biofilm infections. Two patients required blood transfusion and one required ligation of the external carotid artery. Five had perioperative dislocation, which responded to elastic intermaxillary fixation for one week. A total of 31 patients had partial, and 2 had total weakness of the facial nerve. All resolved fully except weakness of the temporal branch in one patient, which required brow lift. Total TMJ replacement gives good early improvements in function and pain with few complications. Of the 74 patients, 71 were very pleased to have had the procedure. One was dissatisfied despite complete pain relief and improvement in mouth opening from 3 to 30 mm, and 2 were ambivalent (one had infection, revision, and permanent weakness of the temporal branch of the facial nerve).
24816437 Miscellaneous indications for extracorporeal photochemotherapy (ECP). 2014 Jun Extracorporeal photochemotherapy (ECP) has been applied to many T-cell mediated diseases where immunosuppressive drugs are insufficient or not tolerated. As ECP is mainly used in rare indications after failure of other therapies, controlled studies are hardly possible. In addition, the importance of the extracorporeal circuit imposes ethical doubts in organising sham ECP procedure, which explains the rarity of controlled double-blind studies. However, encouraging and even successful results have been reported in newly developed diabetes mellitus, erosive lichen planus, Crohn's disease, systemic sclerosis, nephrogenic fibrosing dermopathy, atopic dermatitis, rheumatoid arthritis, systemic lupus erythematodes, psoriasis arthritis, cutaneous mucinosis, scleromyxoedema, pemphigus vulgaris, multiple sclerosis, eosinophilic fasciitis and in the prevention of percutaneous transluminal coronary angioplasty (PTCA) restenosis. This article discusses the various levels of evidence in the above cited indications.
24338532 Autoimmune diseases, their pharmacological treatment and the cardiovascular system. 2013 Cardiovascular system involvement is a frequent complication of autoimmune diseases (AD) such as systemic lupus erythematosus, scleroderma, rheumatoid arthritis, spondyloarthropaties or psoriatic arthritis. The most common forms of such involvement are pericarditis, myocarditis, accelerated atherosclerosis resulting in myocardial infarction or stroke, arrhythmias, conduction abnormalities or congestive heart failure. Some of these manifestations may be dramatic in their course and ultimately fatal. The treatment of AD may further affect the cardiovascular system and result in a lower quality of life, higher mortality and increased cost of healthcare. The aim of this review is to discuss possible cardiac complications of various AD and the related treatment of these diseases.
23857445 Chronic pain management in pregnancy and lactation. 2014 Feb During pregnancy most of women will experience some kind of pain, either as a result of a pre-existing condition (low back pain, headache, fibromyalgia, and rheumatoid arthritis) or as a direct consequence of pregnancy (weight gain, postural changes, pelvic floor dysfunction, hormonal factors). However, chronic pain management during pregnancy and lactation remains a challenge for clinicians and pregnant women are at risk of undertreatment for painful conditions, because of fear about use of drugs during pregnancy. Few analgesic drugs have been demonstrated to be absolutely contraindicated during pregnancy and breastfeeding, but studies in pregnant women are not available for most of pain medications. The aim of this paper is to review the safety profile in pregnancy or lactation of the commonly prescribed pain medications and non-pharmacological treatments. In addition to the conventional classifications from the Food and Drug Administration and the American Academy of Paediatrics, authors analyzed the currently available clinical data from literature.
24963403 Fibroblast-like synoviocytes induce calcium mineral formation and deposition. 2014 Calcium crystals are present in the synovial fluid of 65%-100% patients with osteoarthritis (OA) and 20%-39% patients with rheumatoid arthritis (RA). This study sought to investigate the role of fibroblast-like synoviocytes (FLSs) in calcium mineral formation. We found that numerous genes classified in the biomineral formation process, including bone gamma-carboxyglutamate (gla) protein/osteocalcin, runt-related transcription factor 2, ankylosis progressive homolog, and parathyroid hormone-like hormone, were differentially expressed in the OA and RA FLSs. Calcium deposits were detected in FLSs cultured in regular medium in the presence of ATP and FLSs cultured in chondrogenesis medium in the absence of ATP. More calcium minerals were deposited in the cultures of OA FLSs than in the cultures of RA FLSs. Examination of the micromass stained with nonaqueous alcoholic eosin indicated the presence of birefringent crystals. Phosphocitrate inhibited the OA FLSs-mediated calcium mineral deposition. These findings together suggest that OA FLSs are not passive bystanders but are active players in the pathological calcification process occurring in OA and that potential calcification stimuli for OA FLSs-mediated calcium deposition include ATP and certain unidentified differentiation-inducing factor(s). The OA FLSs-mediated pathological calcification process is a valid target for the development of disease-modifying drug for OA therapy.
24498364 Myeloid deletion of SIRT1 aggravates serum transfer arthritis in mice via nuclear factor-Π2014 OBJECTIVE: SIRT1 modulates the acetylation of the p65 subunit of nuclear factor-κB (NF-κB) and plays a pivotal role in the inflammatory response. This study sought to assess the role of SIRT1 in rheumatoid arthritis (RA) using a myeloid cell-specific SIRT1 knockout (mSIRT1 KO) mouse. METHODS: mSIRT1 KO mice were generated using the loxP/Cre recombinase system. K/BxN serum transfer arthritis was induced in mSIRT1 KO mice and age-matched littermate loxP control mice. Arthritis severity was assessed by clinical and pathological scoring. The levels of inflammatory cytokines in the serum and joints were measured by ELISA. Migration, M1 polarization, cytokine production, osteoclastogenesis, and p65 acetylation were assessed in bone marrow-derived monocytes/macrophages (BMMs). RESULTS: mSIRT1 KO mice showed more severe inflammatory arthritis and aggravated pathological findings than control mice. These effects were paralleled by increases in IL-1, TNF-α, TRAP-positive osteoclasts, and F4/80⁺ macrophages in the ankles of mSIRT1 KO mice. In addition, BMMs from mSIRT1 KO mice displayed hyperacetylated p65 and increased NF-κB binding activity when compared to control mice, which resulted in increased M1 polarization, migration, pro-inflammatory cytokine production, and osteoclastogenesis. CONCLUSION: Our study provides in vivo evidence that myeloid cell-specific deletion of SIRT1 exacerbates inflammatory arthritis via the hyperactivation of NF-κB signaling, which suggests that SIRT1 activation may be beneficial in the treatment of inflammatory arthritis.
25228851 Prescription patterns for children with juvenile idiopathic arthritis in Michigan Medicaid 2014 BACKGROUND: Due to a limited number and disparate distribution of pediatric rheumatologists in the US, a variety of physician types provide care to children with rheumatologic diseases. However, little is known about how that care may differ across prescribing physician groups. Our objective was to compare medication claims for children with juvenile idiopathic arthritis (JIA) by type of prescribing physician. METHODS: We performed a retrospective cohort study of children with JIA using Michigan Medicaid data for 7/1/2005-6/30/2007, employing descriptive and bivariate analyses by age, medication type, and prescriber type. RESULTS: Among 397 children, there was no difference in the frequency of medication claims for children with internist versus pediatric rheumatologist prescribers. Children with non-rheumatologist prescribers were less likely to have claims for disease modifying anti-rheumatic drugs (DMARDs) and biologic agents. CONCLUSION: Differential use of DMARDs and biologic agents by rheumatologists indicates the importance of referring children with JIA for specialty care.
23252659 Behçet disease-associated uveitis successfully treated with golimumab. 2013 Apr Over the past decade, the off-label use of biologic agents such as TNF-α antagonists, including infliximab and adalimumab, has improved the treatment armamentarium for refractory immune-mediated uveitis, with particular success in Behçet disease-associated uveitis. Golimumab is a novel fully human anti-TNF-α monoclonal antibody that has been approved for the treatment of rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis, with very promising results. Herein, the authors present the use of GLM in a case of Behçet uveitis refractory to other TNF-α blockers. There are only two reports in the literature about the use of GLM in uveitis, describing four patients with JIA-associated uveitis and a case of idiopathic retinal vasculitis. To the authors' knowledge, this is the first report about the use of GLM in Behçet uveitis.
24356481 Effect of golimumab on carotid atherosclerotic disease measures and cardiovascular events 2014 Jan OBJECTIVE: The objective of this study was to assess the effect of golimumab on carotid ultrasound measures and cardiovascular serious adverse events (SAEs) in patients with inflammatory arthritides. METHODS: An exploratory carotid artery ultrasound substudy was performed in the GO-BEFORE study of methotrexate (MTX)-naive rheumatoid arthritis patients, with ultrasounds performed at weeks 0, 24, and 52 to measure common carotid artery intima-media thickness, distensibility coefficient, interadventitial diameter, and plaque count. Cardiovascular SAEs reported over 2 years of follow-up were assessed in 5 golimumab phase 3 clinical trials of patients with rheumatoid arthritis (GO-BEFORE, GO-FORWARD, and GO-AFTER), psoriatic arthritis (GO-REVEAL), and ankylosing spondylitis (GO-RAISE). In GO-BEFORE and GO-FORWARD, patients received placebo + MTX, golimumab 50 mg + MTX, or golimumab 100 mg +/- MTX at baseline and every 4 weeks; in the other 3 trials, patients received placebo or golimumab 50 or 100 mg. RESULTS: The carotid ultrasound substudy showed inconsistent changes in common carotid artery intima-media thickness in the golimumab + MTX groups over time, and there was large variability in the measurements. Increases in interadventitial diameter were observed in the golimumab 100 mg + placebo group, but not in the golimumab + MTX groups. There were no significant differences in the distensibility coefficient and plaque count between the golimumab and placebo groups. Very few patients overall experienced a cardiovascular SAE, and the incidence of cardiovascular SAEs was not statistically different between the golimumab and placebo groups. CONCLUSIONS: The results of the carotid ultrasound substudy were inconclusive, and no increase or decrease in cardiovascular SAEs was observed following 2 years of treatment with golimumab with or without MTX.
24871659 Effects of cichoric acid extract from Echinacea purpurea on collagen-induced arthritis in 2014 Cichoric acid extract (CAE) from Echinacea purpurea L. was used to investigate the anti-arthritic effect by using collagen-induced arthritis (CIA) rat model. The hind paw swelling volume and the body weight were measured and recorded. All the drug solutions were administered orally to rats for a total of 28 days. On day 28, the rats were anaesthetized and decapitated. The thymus and spleen were weighed for the determination of the organ index. The concentration of tumor necrosis factor alpha (TNFα), interleukin-1 beta (IL-1β) and prostaglandin E2 (PGE-2) in the serum was measured using commercially available ELISA kits. Total and phosphor-NF-κB and Cox-2 protein expression in synovial tissues were determined by histological slides quantification and western blot analysis. Our data showed that administration of all doses of CAE (8, 16, and 32 mg/kg) significantly decreased the paw swelling, restored body weight gain and decreased the organ index of the thymus and spleen compared with that of the CIA group. CAE (8, 16, and 32 mg/kg) treatment significantly reduced the levels of TNFα, IL-1β and PGE-2 in serum compared with the CIA group. Histopathological analysis demonstrated that CAE has obvious anti-arthritic activity. In addition, CAE (32 mg/kg) significantly decreased the levels of nuclear factor-κB (NF-κB), TNFα and cyclooxygenase 2 (Cox-2) in synovium tissues of the ankle joint compared with the CIA group. Furthermore, CAE administration significantly decreased the protein expression of phosphor-NF-κB and Cox-2 in synovium tissues of the knee joint compared with the CIA group. The results suggest that the anti-inflammatory activity of CAE may account for its anti-arthritic effect, and CAE could be a potential therapeutic drug for the treatment of rheumatoid arthritis (RA).
25920195 [Construction and functional analysis of a bispecific antibody that targets TNF-α and ED- 2014 Dec In order to enhance the specificity of TNF-α monoclonal antibody to inflamed site, a bispecific antibody BsDb that targets TNF-α and the extra-domain B (ED-B) of fibronectin (FN) was constructed by covalently linking the anti-TNF-α single chain Fv antibody (TNF-scFv) and the anti-ED-B scFv L19 via a flexible peptide linker deriving from human serum albumin (HSA). ED-B is an antigen specifically expressed at the inflamed site. BsDb is expressed in E. coli, identified by immunoblot, and purified with affinity chromatography. This was followed by further examination of its bioactivities and pharmacokinetics. We demonstrated that BsDb retained the immunoreactivity of its original antibodies as it could simultaneously bind to TNF-α and ED-B and neutralize the biological action of TNF-α. In the collagen-induced arthritis mice model, BsDb selectively accumulate in the inflamed joint with a maximal uptake of (12.2 ± 1.50)% ID/g in a single inflamed paw and retain in the inflamed paw for at least 72 h. In contrast, BsDb showed a short serum half-life of (0.50 ± 0.05) h and a rapid clearance from normal tissues. The findings reported herein indicate that BsDb has good specificity to the inflamed site and low toxicity to normal tissues. BsDb is therefore likely to have greater clinical applications in the treatment of rheumatoid arthritis and other autoimmune diseases. This laid a stable basis for its preclinical study.
25110599 Rapidly destructive inflammatory arthritis of the hip. 2014 Rapidly destructive coxarthrosis (RDC) is a rare syndrome that involves aggressive hip joint destruction within 6-12 months of symptom onset with no single diagnostic laboratory, pathological, or radiographic finding. We report an original case of RDC as an initial presentation of seronegative rheumatoid arthritis (RA) in a 57-year-old Caucasian woman presenting with 6 months of progressive right groin pain and no preceding trauma or chronic steroid use. Over 5 months, she was unable to ambulate and plain films showed complete resorption of the right femoral head and erosion of the acetabulum. There were inflammatory features seen on computed tomography (CT) and magnetic resonance imaging (MRI). She required a right total hip arthroplasty, but arthritis in other joints showed improvement with triple disease modifying antirheumatic drugs (DMARD) therapy and almost complete remission with the addition of adalimumab. We contrast our case of RDC as an initial presentation of RA to 8 RDC case reports of patients with established RA. Furthermore, this case highlights the importance of obtaining serial imaging to evaluate a patient with persistent hip symptoms and rapid functional deterioration.
23463583 Is tendinitis an inflammatory disease initiated and driven by pro-inflammatory cytokines s 2013 Aug Tendonitis and tendinitis are terms used to describe an inflamed and painful tendon. Tendinopathy, is a descriptive term for describing clinical conditions arising from tendon injury and overuse both within and around tendons. The aim of this mini-review is to explore the role of pro-inflammatory cytokines, particularly interleukin-1β (IL-1β) in tendon disorders. A number of investigators including our group have proposed that pro-inflammatory cytokines such as IL-1β are initiators of tendinopathies, stimulating inflammation, apoptosis and extracellular matrix (ECM) degradation. This is one of the reasons why IL-1β is frequently used in culture models of tendon inflammation to study the inflammatory and catabolic responses of tenocytes. However, some researchers oppose this view and suggest that although IL-1β may play a role in rheumatoid arthritis (RA) and osteoarthritis (OA), the involvement of IL-1β in the development of tendinopathy is questionable. This mini-review discusses the relevant papers published in this area and summarises the evidence for and against the involvement of pro-inflammatory cytokines such as IL-1β in tendonitis. Reaching a consensus will be important for the development and refinement of biomimetic models of tendon inflammation and the formulation of new therapeutic strategies for the treatment of tendon injuries.
23389765 Temporal development of muscle atrophy in murine model of arthritis is related to disease 2013 Sep BACKGROUND: Rheumatoid arthritis (RA) is an inflammatory autoimmune disease of unknown etiology, affecting mainly the joint but also other tissues. RA patients usually present weakness and muscle atrophy, nonarticular manifestations of the disease. Although causing great impact, the understanding of muscle atrophy, its development, and the mechanisms involved is still very limited. The objective of this study is to evaluate the development of muscle atrophy in skeletal muscle of a murine model of arthritis. METHODS: The experimental murine model of collagen-induced arthritis (CIA) was used. DBA/1J mice were randomly divided into three groups: control (CO, n = 25), sham arthritis (SA, n = 25), and arthritis (CIA, n = 28), analyzed in different time points: 25, 35, and 45 days after the induction of arthritis. The arthritis development was followed by clinical scores and hind paw edema three times a week. The spontaneous exploratory locomotion and weight were evaluated weekly. In all time points, serum was collected before the death of the animals for cytokine analysis, and myofiber cross-sectional areas (CSA) of gastrocnemius (GA) and tibialis anterior (TA) skeletal muscles were evaluated. RESULTS: The clinical parameters of arthritis progressively increased in CIA in all experimental times, demonstrating the greatest difference from other groups at 45 days after induction (clinical score: CO, 00 ± 00; SA, 1.00 ± 0.14; CIA, 3.28 ± 0.41 p > 0.05). The CIA animals had lower weights during all the experimentation periods with a difference of 6 % from CO at 45 days (p > 0.05). CIA animals also demonstrated progressive decrease in distance walked, with a reduction of 54 % in 35 and 74 % at 45 days. Cytokine analysis identified significant increase in IL-6 serum levels in CIA than CO and SA in all experimental times. CSA of the myofiber of GA and TA was decreased 26 and 31 % (p > 0.05) in CIA in 45 days after the induction of disease, respectively. There was significant and inverse correlation between the disease clinical score and myofiber CSA in 45 days (GA: r = -0.71; p = 0.021). CONCLUSION: Our results point to a progressive development of muscle wasting, with premature onset arthritis. These observations are relevant to understand the development of muscle loss, as well as for the design of future studies trying to understand the mechanisms involved in muscle wasting. As far as we are concerned, this is the first study to evaluate the relation between disease score and muscle atrophy in a model of arthritis.
22975756 Autophagy regulates TNFα-mediated joint destruction in experimental arthritis. 2013 May OBJECTIVES: Autophagy is a homeostatic process to recycle dispensable and damaged cell organelles. Dysregulation of autophagic pathways has recently been implicated in the pathogenesis of various diseases. Here, we investigated the role of autophagy during joint destruction in arthritis. METHODS: Autophagy in osteoclasts was analysed in vitro and ex vivo by transmission electron microscopy, Western blotting and immunohistochemistry for Beclin1 and Atg7. Small molecule inhibitors, LysMCre-mediated knockout of Atg7 and lentiviral overexpression of Beclin1 were used to modulate autophagy in vitro and in vivo. Osteoclast differentiation markers were quantified by real-time PCR. The extent of bone and cartilage destruction was analysed in human tumour necrosis factor α transgenic (hTNFα tg) mice after adoptive transfer with myeloid specific Atg7-deficient bone marrow. RESULTS: Autophagy was activated in osteoclasts of human rheumatoid arthritis (RA) showing increased expression of Beclin1 and Atg7. TNFα potently induced the expression of autophagy-related genes and activated autophagy in vitro and in vivo. Activation of autophagy by overexpression of Beclin1-induced osteoclastogenesis and enhanced the resorptive capacity of cultured osteoclasts, whereas pharmacologic or genetic inactivation of autophagy prevented osteoclast differentiation. Arthritic hTNFα tg mice transplanted with Atg7(fl/fl)×LysMCre(+) bone marrow cells (BMC) showed reduced numbers of osteoclasts and were protected from TNFα-induced bone erosion, proteoglycan loss and chondrocyte death. CONCLUSIONS: These findings demonstrate that autophagy is activated in RA in a TNFα-dependent manner and regulates osteoclast differentiation and bone resorption. We thus provide evidence for a central role of autophagy in joint destruction in RA.
25110981 Neurostimulation of the cholinergic anti-inflammatory pathway ameliorates disease in rat c 2014 INTRODUCTION: The inflammatory reflex is a physiological mechanism through which the nervous system maintains immunologic homeostasis by modulating innate and adaptive immunity. We postulated that the reflex might be harnessed therapeutically to reduce pathological levels of inflammation in rheumatoid arthritis by activating its prototypical efferent arm, termed the cholinergic anti-inflammatory pathway. To explore this, we determined whether electrical neurostimulation of the cholinergic anti-inflammatory pathway reduced disease severity in the collagen-induced arthritis model. METHODS: Rats implanted with vagus nerve cuff electrodes had collagen-induced arthritis induced and were followed for 15 days. Animals underwent active or sham electrical stimulation once daily from day 9 through the conclusion of the study. Joint swelling, histology, and levels of cytokines and bone metabolism mediators were assessed. RESULTS: Compared with sham treatment, active neurostimulation of the cholinergic anti-inflammatory pathway resulted in a 52% reduction in ankle diameter (p = 0.02), a 57% reduction in ankle diameter (area under curve; p = 0.02) and 46% reduction overall histological arthritis score (p = 0.01) with significant improvements in inflammation, pannus formation, cartilage destruction, and bone erosion (p = 0.02), accompanied by numerical reductions in systemic cytokine levels, not reaching statistical significance. Bone erosion improvement was associated with a decrease in serum levels of receptor activator of NF-κB ligand (RANKL) from 132±13 to 6±2 pg/mL (mean±SEM, p = 0.01). CONCLUSIONS: The severity of collagen-induced arthritis is reduced by neurostimulation of the cholinergic anti-inflammatory pathway delivered using an implanted electrical vagus nerve stimulation cuff electrode, and supports the rationale for testing this approach in human inflammatory disorders.
23459013 To Wnt or not to Wnt: the bone and joint health dilemma. 2013 Jun The Wnt signalling cascades have essential roles in development, growth and homeostasis of joints and the skeleton. Progress in basic research, particularly relating to our understanding of intracellular signalling cascades and fine regulation of receptor activation in the extracellular space, has provided novel insights into the roles of Wnt signalling in chronic arthritis. Cartilage and bone homeostasis require finely tuned Wnt signalling; both activation and suppression of the Wnt-β-catenin cascade can lead to osteoarthritis in rodent models. Genetic associations with the Wnt antagonist encoded by FRZB and the transcriptional regulator encoded by Dot1l with osteoarthritis further corroborate the essential part played by Wnts in the joint. In rheumatoid arthritis, inhibition of Wnt signalling has a role in the persistence of bone erosions, whereas Wnts have been associated with the ankylosing phenotype in spondyloarthritis. Together, these observations identify the Wnt pathway as an attractive target for therapeutic intervention; however, the complexity of the Wnt signalling cascades and the potential secondary effects of drug interventions targeting them highlight the need for further research and suggest that our understanding of this exciting pathway is still in its infancy.
23690825 Enteropathic spondyloarthritis: from diagnosis to treatment. 2013 Enteropathic arthritis (EA) is a spondyloarthritis (SpA) which occurs in patients with inflammatory bowel diseases (IBDs) and other gastrointestinal diseases. Diagnosis is generally established on the medical history and physical examination. It was, generally, made according to the European Spondyloarthropathy Study Group (ESSG) criteria. Rheumatic manifestations are the most frequent extraintestinal findings of IBD with a prevalence between 17% and 39%, and IBD is associated, less frequently, with other rheumatic disease such as rheumatoid arthritis, Sjogren syndrome, Takayasu arteritis, and fibromyalgia. Although the pathogenesis of EA has not been plainly clarified, the most popular theory supposes that joint inflammation occurs in genetically predisposed subjects with bacterial gut infections, provided an important evidence for a possible relationship between inflammation of the gut mucosa and arthritis. The management of patients with EA requires an active cooperation between the gastroenterologist and rheumatologist.
23494635 The comparison of efficacy of different imaging techniques (conventional radiography, ultr 2013 Jan BACKGROUND: Psoriatic arthritis (PsA) is a chronic inflammatory joint disease which develops in patients with psoriasis. The rheumatoid factor is characteristically absent in the serum of PsA patients. Etiology of the disease is still unclear but a number of genetic associations have been identified. Inheritance of the disease is multilevel and the role of environmental factors is emphasized. Immunology of PsA is also quite complex. Inflammation is caused by immunological reactions leading to a release of kinins. Destructive changes in bones usually appear after a few months from the onset of clinical symptoms. MATERIAL/METHODS: PsA typically involves joints of the axial skeleton with an asymmetrical patern. The spectrum of symptoms includes inflammatory changes in attachments of articular capsules, tendons, and ligaments to bone surface. The disease can have a diverse clinical course but usually manifests as oligoarthritis. RESULTS: Imaging plays an important role in the diagnosis of PsA. Classical radiography has been used for this purpose for over a hundred years. It allows to identify late stages of the disease, when bone tissue is affected. In the last 20 years however many new imaging modalities, such as ultrasonography (US), computed tomography (CT) and magnetic resonance (MR), have been developed and became important diagnostic tools for evaluating rheumatoid diseases. They enable the assessment and monitoring of early inflammatory changes. CONCLUSIONS: As a result, patients have earlier access to modern treatment and thus formation of destructive changes in joints can be markedly delayed or even avoided.