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Reactive arthritis: update 2018
Abstract
At this time, reactive arthritis (ReA) is considered to be part of the spectrum of the spondyloarthritis, previously known as Reiter’s syndrome, and refers to an infection induced systemic illness, characterized by a sterile synovitis occurring in a genetically predisposed individual, secondary to an infection localized in a distant organ/system, but also accompanied with multiple extra articular manifestations.
... Despite the potential for symptomatic reactive infectious arthritis of the TMJs (18), ID was previously regarded primarily as non-inflammatory disc dysfunction, even in symptomatic subjects (19). Recently, sterile synovitis emerged as one of the significant causes of pain in axial SpA (20,21,22), including the pain in the TMJ (23,24,25). Whether the ID of TMJ represents SpA activity remains unknown. ...
... Unatoč mogućnosti za simptomatski reaktivni infektivni artritis TMZ-a (18), IK TMP prije se smatrao primarno neupalnim poremećajem djelovanja pločice, čak i kod simptomatskih bolesnika (19). Odnedavno se sterilni sinovitis prepoznaje kao jedan od značajnih uzroka boli u aksijalnom SpA-u (20,21,22), uključujući i TMZ (23,24,25). Ostaje nepoznato je li IK TMP posljedica aktivnosti SpA-a. ...
Objectives
The group of spondyloarthritis (SpA) disorders shares common clinical manifestations, including internal derangement (ID) of temporomandibular joint (TMJ). This study aimed to investigate SpA activity in patients with ID of TMJ.
Materials and Methods
We assessed 200 patients with neck pain using the Assessment of Spondyloarthritis International Society (ASAS) criteria. TMJ was examined using Diagnostic Criteria for Temporomandibular Disorders (DC/TMD protocol). Patients with SpA were divided into three groups: symptomatic ID of TMJ, asymptomatic ID of TMJ, or healthy TMJ (controls). Activity of SpA was evaluated using the Ankylosing Spondylitis Disease Activity Score (ASDAS), Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), Disease Activity Index in Psoriatic Arthritis (DAPSA), patients' self-estimated SpA activity, difficulties in performing daily activities, pain intensity (visual analogue scale) and laboratory parameters.
Results
Patients with symptomatic and asymptomatic ID showed statistically significantly increased ASDAS, anti-streptolysin titer, patients' self-estimated axial pain and activity of SpA, and decreased hematocrit than the control. Patients with symptomatic ID also had statistically significant earlier onset of SpA, along with increased BASDAI and DAPSA, total body pain, difficulties in performing daily activities, platelet count, and serum alpha-amylase but lower hemoglobin concentration than controls. Patients with asymptomatic ID had higher frequencies of exacerbated axial SpA and sacroiliac joint ankylosis compared to the control.
Conclusion
All patients with SpA and ID showed increased axial disease activity.
... Synovial joints are the target of antigen-specific autoimmune responses in diseases such as rheumatoid arthritis (RA) 1 , but joint pain (arthralgia), or even overt inflammation, is a relatively common manifestation of viral and bacterial infections in distant unrelated organs (for example, bacterial enteritis or streptococcal pharyngitis). This phenomenon is thought, at least in part, to be mediated by circulating microbial antigen-IgG immune complexes (ICs) [2][3][4] . Similarly, in systemic lupus erythematosus, an autoimmune disease characterized by IgG IC deposition, arthritis is a common symptom 5 . ...
... Joint pain or inflammation is a common and early feature of several systemic diseases. These include autoimmune diseases, such as systemic lupus erythematosus, adult onset Still's disease and inflammatory bowel disease, as well as infection in organs distant to the musculoskeletal system, including enteric or genitourinary infections, streptococcal pharyngitis and viral infections, for example, parvovirus [2][3][4] . The pathogenic mediators vary, but circulating ICs or microbial antigens have been implicated 37 . ...
A wide variety of systemic pathologies, including infectious and autoimmune diseases, are accompanied by joint pain or inflammation, often mediated by circulating immune complexes (ICs). How such stimuli access joints and trigger inflammation is unclear. Whole-mount synovial imaging revealed PV1⁺ fenestrated capillaries at the periphery of the synovium in the lining–sublining interface. Circulating ICs extravasated from these PV1⁺ capillaries, and nociceptor neurons and three distinct macrophage subsets formed a sentinel unit around them. Macrophages showed subset-specific responses to systemic IC challenge; LYVE1⁺CX3CR1⁺ macrophages orchestrated neutrophil recruitment and activated calcitonin gene-related peptide⁺ (CGRP⁺) nociceptor neurons via interleukin-1β. In contrast, major histocompatibility complex class II⁺CD11c⁺ (MHCII⁺CD11c⁺) and MHCII⁺CD11c– interstitial macrophages formed tight clusters around PV1⁺ capillaries in response to systemic immune stimuli, a feature enhanced by nociceptor-derived CGRP. Altogether, we identify the anatomical location of synovial PV1⁺ capillaries and subset-specific macrophage–nociceptor cross-talk that forms a blood–joint barrier protecting the synovium from circulating immune challenges.
... [1] However, circinate balanitis may occur independently, as in our case or alongside other mucocutaneous features, including keratoderma blenorrhagicum, ulcerative vulvitis, [4] onycholysis and nail dystrophy (20%-30%), painless oral ulcers, geographic tongue, and erythema nodosum. [5,6] The primary approach to managing circinate balanitis consists of appropriate patient counseling, excluding high-risk sexual behaviors and appropriate serological testing (VDRL/rapid plasma reagin, HIV-1 and 2). Topical corticosteroid therapy, such as hydrocortisone or triamcinolone, is most commonly utilized. ...
Circinate balanitis, a common manifestation of reactive arthritis, is usually an associated finding seen with the clinical trial of arthritis, conjunctivitis, and urethritis. We hereby report a case of isolated circinate balanitis and its dermoscopic features in an adult patient. The patient responded successfully to treatment with topical tacrolimus 0.1% ointment.
YouTube is often used by patients and healthcare professionals to obtain medical information. Reactive arthritis (ReA) is a type of inflammatory arthritis triggered by infection, usually in the genitourinary or gastrointestinal tract. However, the accuracy and quality of ReA-related information on YouTube are not fully known. This study aimed to assess the reliability and quality of YouTube videos pertaining to ReA.
A YouTube search was performed on August 1, 2023, using the keywords “reactive arthritis,” “Reiter’s disease,” and “Reiter’s syndrome.” The number of days since upload; the number of views, likes, and comments; and the duration of videos were recorded. The modified DISCERN tool (mDISCERN) and the global quality scale (GQS) were used to evaluate the reliability and quality of the videos. Two physicians independently classified videos as low, moderate, or high quality and rated them on a five-point GQS (1 = poor quality, 5 = excellent quality). The source of videos was also noted.
Of the 180 videos screened, 68 met the inclusion criteria. The most common topic (61, 89.7%) was “ReA overview.” Among the 68 videos analyzed, the main source of uploads was physicians 45 (66.2%), and 66 (97%) were categorized as useful. Around half of the YouTube videos about ReA were of high quality (33, 48.5%) according to the GQS. Upon comparing videos uploaded by rheumatologists, non-rheumatology healthcare professionals, and independent users, significant differences were found in mDISCERN and GQS but not in the number of views, likes, and comments or duration. Upon comparing high-, moderate-, and low-quality videos, significant differences were found in the number of views, likes, and comments; duration; and in mDISCERN and GQS.
YouTube is a source of information on ReA of variable quality, with wide viewership and the potential to influence patients’ knowledge and behavior. Our results showed that most YouTube videos on ReA were of high quality. Videos presented by physicians had higher quality. YouTube should consider avoiding low-quality videos by using validity scales such as mDISCERN and GQS.
To report a rare case of corneal perforation in reactive arthritis and review the scientific basis for it. A case report. A 22-year-old male patient presented with redness, foreign body sensation, and blurred vision associated with knee and lumbar arthritis after an episode of urethritis was diagnosed with reactive arthritis (ReA). Ophthalmological examination revealed keratitis and corneal perforation at the time of admission. The patient received antibiotic drops and systemic steroids and underwent a corneal patch graft, which improved his visual acuity and outcome; however, he developed chronic arthritis and had to be treated with infliximab. The classical ocular manifestations of ReA are conjunctivitis, anterior uveitis, keratitis, and scleritis; however, this case report demonstrates a rare but severe presentation of ReA that should be considered.
Drug-induced gingival overgrowth occurs commonly as an adverse effect of using drugs like calcium channel blockers, immunosuppressants, and anti-epileptics. Usually, in immunosuppressants, cyclosporin is the most common cause of gingival overgrowth. But this case report illustrates a rare gingival overgrowth caused by prednisolone which may be the first of its kind. Gingival overgrowth can be treated with multiplicity of therapeutic options like gingivoplasty and/or gingivectomy by using a scalpel, or electrocautery. Other contemporary therapeutic options like lasers, and cryosurgery gained prominence lately due to lesser post-operative complications. Amid various novel approaches, lasers demonstrated better healing and enhanced aesthetic outcomes making lasers an ideal treatment option for gingivoplasty/gingivectomy in gingival hyperplasia cases.
Interleukin-17 (IL-17A) is a cytokine critical for the acute defence against extracellular bacterial and fungal infections. Excess production during chronic inflammation has been associated with many inflammatory and autoimmune disorders. The present review describes the key molecules of the IL-17 pathway, which are or could be targeted for treatment. Since targeting of IL-17A may affect defence mechanisms, the pathogenesis of such possible adverse events is analysed. Then the contributions of IL-17 to bone changes in various forms of arthritis are discussed. Finally, the results of current inhibitors of the IL-17 pathway in clinical trials are detailed. IL-17A inhibition has been first registered for the treatment of psoriasis, psoriatic arthritis and ankylosing spondylitis. Other therapeutic options are now tested in a long list of diseases.
Reactive (inflammatory) arthritis has been known for many years to follow genital infection with the intracellular bacterial pathogen Chlamydia trachomatis in some individuals. Recent studies from several groups have demonstrated that a related bacterium, the respiratory pathogen Chlamydia pneumoniae, can elicit a similar arthritis. Studies of these organisms, and of a set of gastrointestinal pathogens also associated with engendering inflammatory arthritis, have been relatively extensive. However, reports focusing on coinfections with these and/or other organisms, and the effects of such coinfections on the host immune and other systems, have been rare. In this article, we review the extant data regarding infections by multiple pathogens in the joint as they relate to engendering arthritis, and we suggest a number of research areas that must be given a high priority if we are to understand, and therefore to treat in an effective manner, such arthritides.
The objective of the study is to determine the risk factors for the development of reactive arthritis (ReA) and examine the factors associated with the persistence of symptoms. Patients with a new diagnosis of ReA and controls with a gastrointestinal (GI), urogenital, or sexually transmitted infection in the 3–6 months prior to study entry were prospectively enrolled in Guatemala City. ReA patients fulfilled the Assessment in Spondyloarthritis International Society criteria for peripheral spondyloarthropathy (SpA). Patients underwent history, examination, Achilles tendon ultrasound, and blood draw. Human leukocyte antigen (HLA) type and serum biomarkers were measured. t tests and nonparametric equivalents were used to examine the association of clinical, laboratory, and imaging factors with ReA. Patients were contacted 2 years later to assess for persistence of symptoms. Study subjects included patients with ReA (N = 32) and controls (N = 32). ReA patients were most frequently infected in April whereas controls were most frequently infected in August. Two ReA patients and two controls were HLA-B27-positive. Serum cathepsin K and C-reactive protein were higher in ReA patients compared to controls (p = 0.03 for both), while total cholesterol and low-density lipoprotein were lower (p = 0.008 and 0.045, respectively). Among those with ReA, 15 (47%) patients had continued symptoms at 2 years. These patients had a lower matrix metalloproteinase-3 level at diagnosis than patients for whom ReA resolved (p = 0.004). HLA-B27 was not associated with development of ReA in Guatemala; however, the month of infection was associated with ReA. The most striking finding was the persistence of arthritis at 2 years in nearly half of the patients.
Microbes have coevolved with their human hosts for millions of years and are vital to their normal development and homoeostasis. It is now clear that there is direct and indirect cross talk between the microbiome and host immune responses. However, the exact mechanisms for this microbial influence in disease pathogenesis remain elusive and are now a major research focus.
Objective:
Reactive arthritis (ReA) is an inflammatory disorder occurring several weeks after gastrointestinal or genitourinary tract infections. HLA-B27 positivity is considered a risk factor, although it is not necessarily predictive of disease incidence. Among nongenetic factors, the intestinal microbiome may play a role in disease susceptibility. The objective of this study was to characterize the gut microbiota and host gene interactions in ReA and postinfectious spondyloarthritis.
Methods:
Adult subjects with peripheral spondyloarthritis and control subjects with preceding infections who did not develop arthritis were prospectively recruited from a geographic region with a high prevalence of ReA. Clinical variables, HLA status, and 16S ribosomal RNA gene sequencing of intestinal microbiota were analyzed.
Results:
Subjects with ReA showed no significant differences from controls in gut bacterial richness or diversity. However, there was a significantly higher abundance of Erwinia and Pseudomonas and an increased prevalence of typical enteropathogens associated with ReA. Subjects with ultrasound evidence of enthesitis were enriched in Campylobacter, while subjects with uveitis and radiographic sacroiliitis were enriched in Erwinia and unclassified Ruminococcaceae, respectively; both were enriched in Dialister. Host genetics, particularly HLA-A24, were associated with differences in gut microbiota diversity irrespective of disease status. We identified several co-occurring taxa that were also predictive of HLA-A24 status.
Conclusion:
This is the first culture-independent study characterizing the gut microbial community in postinfectious arthritis. Although bacterial factors correlated with disease presence and clinical features of ReA, host genetics also appeared to be a major independent driver of intestinal community composition. Understanding of these gut microbiota-host genetic relationships may further clarify the pathogenesis of postinfectious spondyloarthritides.
Reactive arthritis (ReA) is an inflammatory spondyloarthritis occurring after infection at a distant site. Chlamydia trachomatis is proposed to be the most common cause of ReA, yet the incidence of sexually acquired ReA (SARA) has not been well established. We therefore carried out a systematic literature review to collate and critically evaluate the published evidence regarding the incidence of SARA. MEDLINE and EMBASE databases were searched using free-text and MeSH terms relating to infection and ReA. The title and abstract of articles returned were screened independently by two reviewers and potentially relevant articles assessed in full. Data was extracted from relevant articles and a risk of bias assessment carried out using a validated tool. Heterogeneity of study methodology and results precluded meta-analysis. The search yielded a total of 11,680 articles, and a further 17 were identified from review articles. After screening, 55 papers were assessed in full, from which 3 met the relevant inclusion criteria for the review. The studies reported an incidence of SARA of 3.0–8.1 % and were found to be of low to moderate quality. More studies are required to address the lack of data regarding the incidence of SARA. Specific and sensitive classification criteria must be developed in order for consistent classification and valid conclusions to be drawn. In clinical practice, it is recommended clinicians discuss the possibility of ReA developing at the time of STI diagnosis and to encourage patients to return if they experience any relevant symptoms.
The human gut harbours a tremendously diverse and abundant microbial community that correlates with, and even modulates, many health-related processes. The mucosal interfaces are particularly active sites of microorganism-host interplay. Growing insight into the characteristic composition and functionality of the mucosal microbiota has revealed that the microbiota is involved in mucosal barrier integrity and immune function. This involvement affects proinflammatory and anti-inflammatory processes not only at the epithelial level, but also at remote sites such as the joints. Here, we review the role of the gut microbiota in shaping local and systemic immune responses and how disturbances in the host-microorganism interplay can potentially affect the development and progression of rheumatic diseases. Increasing our understanding of how to promote host-microorganism homeostasis could therefore reveal novel strategies for the prevention or alleviation of rheumatic disease.
