Reactive Arthritis

2/20/2005

Question:  How is reactive arthritis differentiated from other similar diseases?

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16206358.ui or 16195157.ui or 15956835.ui or 15942084.ui or 15918996.ui or 15454127.ui or 15150434.ui or 15124937.ui or 15084505.ui or 15016341.ui or 14680436.ui or 12819467.ui or 12810429.ui or 12635499.ui or 12635498.ui or 12610801.ui or 12406424.ui or 12209542.ui or 12192255.ui or 12079895.ui

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16206358[PMID] OR 16195157[PMID] OR 15956835[PMID] OR 15942084[PMID] OR 15918996[PMID] OR 15454127[PMID] OR 15150434[PMID] OR 15124937[PMID] OR 15084505[PMID] OR 15016341[PMID] OR 14680436[PMID] OR 12819467[PMID] OR 12810429[PMID] OR 12635499[PMID] OR 12635498[PMID] OR 12610801[PMID] OR 12406424[PMID] OR 12209542[PMID] OR 12192255[PMID] OR 12079895[PMID]

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<1>

Unique Identifier [PMID]: 16206358

Authors: Alexopoulou A. Dourakis SP. Stamoulis ND. Vassilopoulos D. Archimandritis AJ.

Institution: 2nd Department of Medicine, University of Athens Medical School, Hippokration General Hospital, 20 N. Politi Street, 16346 Athens, Greece. alexopou@ath.forthnet.gr

Title: Poststreptococcal reactive arthritis with thoracic spine involvement in an adult.

Source: Journal of Rheumatology. 32(10):2002-5, 2005 Oct.

Abstract: It is controversial whether poststreptococcal reactive arthritis (PSReA) is an entity separate from acute rheumatic fever (ARF) or is a forme fruste of ARF. Although there are many case series of PSReA in children, this entity is not common in adults. We describe an adult patient with polyarthritis and thoracic spine involvement attributed to PSReA.

Publication Type: Case Reports. Journal Article.

<2>

Unique Identifier [PMID]: 16195157

Authors: Leirisalo-Repo M.

Institution: Division of Rheumatology, Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland. marjatta.leirisalo-repo@hus.fi

Title: Reactive arthritis. [Review] [83 refs]

Source: Scandinavian Journal of Rheumatology. 34(4):251-9, 2005 Jul-Aug.

Abstract: Reactive arthritis (ReA) was known as Reiter's disease or Fiessinger-Leroy disease for nearly 100 years. However, during the past 30 years the disease has been known as reactive arthritis, a member of the spondyloarthritis family. Despite knowing the initiating event (infection) and genetic constitution (many patients have HLA-B27) of ReA, a model of interplay between environment and genetics, its pathogenesis is still incompletely known. This review covers the epidemiology, clinical features, treatment, and prognosis of ReA. [References: 83]

Publication Type: Journal Article. Review.

<3>

Unique Identifier [PMID]: 15956835

Authors: Kim TH. Uhm WS. Inman RD.

Institution: The Hospital for Rheumatic Diseases, Hanyang University, Seoul, Korea.

Title: Pathogenesis of ankylosing spondylitis and reactive arthritis. [Review] [73 refs]

Source: Current Opinion in Rheumatology. 17(4):400-5, 2005 Jul.

Abstract: PURPOSE OF REVIEW: The hallmark of ankylosing spondylitis is acute and chronic spinal inflammation initiating in the sacroiliac joints, often coupled with enthesitis, presenting as chronic inflammation at the sites of ligamentous and tendinous insertions into bone. Peripheral joint synovitis can be a prominent feature as well. Reactive arthritis is a sterile synovitis arising after an extra-articular infection of enteric or urogenital tracts. HLA-B27 has been known for about the past 30 years to be associated with ankylosing spondylitis and reactive arthritis, but the pathogenesis of ankylosing spondylitis and reactive arthritis is still not well defined. Although the clinical manifestations of ankylosing spondylitis and reactive arthritis may differ, this update discusses the two diseases together and focuses on recent evidence in both. RECENT FINDINGS: With respect to HLA-B27 several recent studies address arthritogenic peptides, molecular mimicry, and aberrant forms of B27. Several candidate genes in addition to B27 have been implicated in recent genetic studies. With respect to bacterial infection, recent findings in bacterial antigenicity, host response through interactions of antigen-presenting cells, T cells, and cytokines are providing new understanding of host-pathogen interactions and the pathogenesis of arthritis. Endogenous host factors such as proteoglycans may play a role as autoantigens and contribute to chronic inflammation on that basis. SUMMARY: Recent advances provide additional new insights into distinct pathogenetic mechanisms in AS and ReA that arise from a complex interplay between genetic factors including HLA-B27 and environmental factors. [References: 73]

Publication Type: Journal Article. Review.

<4>

Unique Identifier [PMID]: 15942084

Authors: Kobayashi S. Kida I.

Title: Reactive arthritis: recent advances and clinical manifestations.[comment].

Comments Comment on: Intern Med. 2005 May;44(5):509-10; PMID: 15942107

Source: Internal Medicine. 44(5):408-12, 2005 May.

Publication Type: Comment. Editorial.

<5>

Unique Identifier [PMID]: 15918996

Authors: Colmegna I. Espinoza LR.

Title: Recent advances in reactive arthritis. [Review] [49 refs]

Source: Current Rheumatology Reports. 7(3):201-7, 2005 Jun.

Abstract: Reactive arthritis (ReA), one of the spondyloarthropathies, is an infectious related disease that occurs in a genetically predisposed individual, characterized by an immune-mediated synovitis with intra-articular persistence of viable nonculturable bacteria and/or immunogenic bacterial antigens. ReA long term prognosis is not as good as it was earlier believed. Two-thirds of patients develop prolonged joint discomfort, low back pain, or enthesopathies after acute ReA, and 15% to 30% of them develop chronic symptoms. The therapeutic options for patients with the more severe forms of the disease have been rather limited. The efficacy of tumor necrosis factor antagonists in other spondyloarthritis suggested that anticytokine therapy could also be effective for ReA. This paper reviews the latest concepts in urogenital and postenteric human leukocyte antigen-B27-associated ReA. [References: 49]

Publication Type: Journal Article. Review.

<6>

Unique Identifier [PMID]: 15454127

Authors: Toivanen A. Toivanen P.

Institution: Department of Medicine, Turku University, FIN-20520 Turku, Finland. auli.toivanen@utu.fi

Title: Reactive arthritis. [Review] [76 refs]

Source: Best Practice & Research in Clinical Rheumatology. 18(5):689-703, 2004 Oct.

Abstract: Reactive arthritis is an infectious disease which may be initiated by several microbes in genetically susceptible hosts. The best known predisposing genetic factor is HLA-B27, but the mechanisms behind its action are still elusive. Worldwide agreement exists regarding the general guidelines in the diagnosis, differential diagnosis and management, even though official diagnostic criteria are not yet available. Several studies indicate that antibiotics are effective only if started before the immunological mechanisms of pathogenesis have been turned on. However, recent observations suggest that a 3-month course of antibiotics may diminish the late risk of chronic sequelae, especially in HLA-B27-positive patients with reactive arthritis. [References: 76]

Publication Type: Journal Article. Review.

<7>

Unique Identifier [PMID]: 15150434

Authors: Mackie SL. Keat A.

Institution: Department of Rheumatology, Northwick Park Hospital, Harrow, Middlesex, UK. sarah.mackie@doctors.org.uk

Title: Poststreptococcal reactive arthritis: what is it and how do we know?[see comment]. [Review] [48 refs]

Comments Comment in: Rheumatology (Oxford). 2005 Jan;44(1):136; author reply 136-7; PMID: 15611313

Source: Rheumatology. 43(8):949-54, 2004 Aug.

Abstract: OBJECTIVE: To find out whether poststreptococcal reactive arthritis (PSRA) is a discrete, homogeneous clinical syndrome. METHOD: Literature review from case reports and case series. RESULTS: One hundred and eighty-eight cases were identified. The age distribution was bimodal, with one peak in childhood and one peak in adulthood. Eighty-three percent of streptococcal isolates were group A. The clinical presentation was heterogeneous but appeared different both from that of acute rheumatic fever (ARF) and from that of HLA B27-associated reactive arthritis. Carditis was rare. CONCLUSIONS: The term PSRA encompasses significant heterogeneity. The link between the arthritis and the streptococcal infection is unproven. [References: 48]

Publication Type: Journal Article. Review.

<8>

Unique Identifier [PMID]: 15124937

Authors: Kuuliala A. Takala A. Siitonen S. Leirisalo-Repo M. Repo H.

Institution: Department of Bacteriology and Immunology, Haartman Institute, University of Helsinki, Finland. antti.kuuliala@helsinki.fi

Title: Cellular and humoral markers of systemic inflammation in acute reactive arthritis and early rheumatoid arthritis.

Source: Scandinavian Journal of Rheumatology. 33(1):13-8, 2004.

Abstract: OBJECTIVE: To compare systemic inflammation in reactive arthritis (ReA), rheumatoid arthritis (RA), and sepsis using novel markers of systemic inflammation, and to study whether they are helpful in distinguishing between ReA and RA. METHODS: In 28 patients with acute ReA, 16 patients with early untreated RA, and 25 patients with blood culture-positive sepsis, phagocyte CD 11b expression was measured by flow cytometry, serum procalcitonin (PCT) levels by immunoluminometric assay, and soluble E-selectin (sE-selectin) levels by enzyme-linked immunosorbent assay (ELISA). RESULTS: Neutrophil and monocyte CD11b expression and serum levels of PCT and sE-selectin were higher in patients with sepsis than patients with ReA or RA, or in healthy subjects (all p < 0.01). They were comparable in healthy subjects, ReA, and RA. CONCLUSION: Patients with acute ReA and early RA have normal CD11b expression levels on phagocytes and normal PCT and sE-selectin levels in serum. Elevated levels suggest possible sepsis.

Publication Type: Journal Article.

<9>

Unique Identifier [PMID]: 15084505

Authors: Colmegna I. Cuchacovich R. Espinoza LR.

Institution: Section of Rheumatology, Department of Medicine, LSU Health Science Center, New Orleans, Louisiana 70112, USA.

Title: HLA-B27-associated reactive arthritis: pathogenetic and clinical considerations. [Review] [234 refs]

Source: Clinical Microbiology Reviews. 17(2):348-69, 2004 Apr.

Abstract: Current evidence supports the concept that reactive arthritis (ReA) is an immune-mediated synovitis resulting from slow bacterial infections and showing intra-articular persistence of viable, non-culturable bacteria and/or immunogenetic bacterial antigens synthesized by metabolically active bacteria residing in the joint and/or elsewhere in the body. The mechanisms that lead to the development of ReA are complex and basically involve an interaction between an arthritogenic agent and a predisposed host. The way in which a host accommodates to invasive facultative intracellular bacteria is the key to the development of ReA. The details of the molecular pathways that explain the articular and extra-articular manifestations of the disease are still under investigation. Several studies have been done to gain a better understanding of the pathogenesis of ReA; these constitute the basis for a more rational therapeutic approach to this disease. [References: 234]

Publication Type: Journal Article. Review.

<10>

Unique Identifier [PMID]: 15016341

Authors: Sieper J.

Institution: Medical Department I, Rheumatology, Charite, Campus Benjamin Franklin, Hindenburgdamm 30, 12200 Berlin, Germany. joachim.sieper@charite.de

Title: Disease mechanisms in reactive arthritis. [Review] [42 refs]

Source: Current Rheumatology Reports. 6(2):110-6, 2004 Apr.

Abstract: Reactive arthritis (ReA) occurs after a preceding bacterial infection of the urogenital or gastroenteral tract. The bacteria triggering ReA persist in vivo and seem to be responsible for triggering an immune response. A cytokine imbalance with a relative lack of T-helper 1 cytokines may play an important role allowing these bacteria to survive. This seems to be relevant for manifestation and chronicity of the arthritis. For the chronic cases and cases evolving into ankylosing spondylitis, the interaction between bacteria and human leukocyte antigen B27 plays an additional crucial role. Among others, the arthritogenic peptide hypothesis is one way to explain this association. Human leukocyte antigen B27-restricted peptides from Yersinia and Chlamydia, which are stimulatory for CD8+ T cells derived from patients with ReA, have been identified. The exact role of such peptides for the pathogenesis of ReA and other spondyloarthritides still has to be defined. [References: 42]

Publication Type: Journal Article. Review.

<11>

Unique Identifier [PMID]: 14680436

Authors: Palazzi C. Olivieri I. D'Amico E. Pennese E. Petricca A.

Institution: Unita Operativa Reumatologia, Casa di Cura, Villa Pini d'Abruzzo, Via Dei Frentani, 228, Chieti, Italy. kaps57@virgilio.it

Title: Management of reactive arthritis. [Review] [86 refs]

Source: Expert Opinion on Pharmacotherapy. 5(1):61-70, 2004 Jan.

Abstract: Reactive arthritis (ReA) is an aseptic form of articular inflammation induced by infections mainly localised in the gastrointestinal (enteroarthritis) or urogenital (uroarthritis) tracts. The bacteria principally involved as causative agents are Chlamydia, Salmonella, Shigella, Campylobacter and Yersinia. The clinical picture is usually characterised by a mono-oligoarthritis of the lower limbs. Axial involvement is possible and extra-articular manifestations such as enthesitis, tenosynovitis, bursitis and dactylitis are frequent. NSAIDs and sulfasalazine are still the drugs most commonly used in the treatment of ReA. Steroids are administered when inflammatory symptoms are resistant to NSAIDs. Experiences with other DMARDs (disease modifying antirheumatic drugs) such as azathioprine, methotrexate and cyclosporin, have been sporadically reported and they can be employed in patients that are unresponsive to the more usual medicaments. The intake of antibacterials (tetracyclines) may be useful in uroarthritis but have not been so successful in enteroarthrits. In more aggressive cases, or when ReA evolves towards ankylosing spondylitis, TNF-alpha blockers could represent an effective choice. [References: 86]

Publication Type: Journal Article. Review.

<12>

Unique Identifier [PMID]: 12819467

Authors: Leirisalo-Repo M. Hannu T. Mattila L.

Institution: Division of Rheumatology, Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland. marjatta.leirisalo-repo@hus.fr

Title: Microbial factors in spondyloarthropathies: insights from population studies. [Review] [66 refs]

Source: Current Opinion in Rheumatology. 15(4):408-12, 2003 Jul.

Abstract: Infections and genetics play a role in the development of reactive arthritis. The clinical manifestations and severity of the features depend on the triggering infections and the epidemiologic setting. Reports from hospital-based series show the lowest frequency of reactive arthritis, but often, patients have severe arthritis associated with a high frequency of HLA-B27. At the population level, reactive arthritis occur in 7 to 15% of the infected subjects. The disease is usually mild, affects small joints, can be polyarticular, often rapidly disappears, and has a low association with HLA-B27. There also seems to be a change in the spectrum of triggering infections. Reports of Yersinia arthritis are less common, whereas arthritis in association with Campylobacter or Salmonella infections seems to be increasing. The role of early antimicrobial chemotherapy for the prevention of reactive arthritis needs to be studied. [References: 66]

Publication Type: Journal Article. Review.

<13>

Unique Identifier [PMID]: 12810429

Authors: Laasila K. Laasonen L. Leirisalo-Repo M.

Institution: Division of Rheumatology, Department of Medicine, Helsinki University Central Hospital, Helsinki, Finland.

Title: Antibiotic treatment and long term prognosis of reactive arthritis.

Source: Annals of the Rheumatic Diseases. 62(7):655-8, 2003 Jul.

Abstract: OBJECTIVE: To evaluate whether a three month course of lymecycline has an effect on the long term prognosis of reactive arthritis (ReA). METHODS: In 1987-88 a double-blind controlled study with three month course of lymecycline/placebo was conducted. 17 of 23 patients treated at the outpatient department of Helsinki University Central Hospital volunteered to take part in a follow up study, where a physical examination were performed, and erythrocyte sedimentation rate, C reactive protein, rheumatoid factor, and radiographs of the lumbosacral spine and sacroiliac joints and of symptomatic peripheral joints were examined. RESULTS: 16/17 (94%) patients reported some kind of back pain and 10/17 (59%) peripheral joint symptoms during the follow up. Two patients had unilateral grade 1 sacroiliitis, one patient grade 4 sacroiliitis, and one patient bilateral grade 2 sacroiliitis. In one patient the disease had progressed to ankylosing spondylitis (AS), and in another to chronic spondyloarthropathy. In addition, two patients had small erosions in radiocarpal joints. No statistically significant differences were found between placebo and lymecycline groups in the development of chronic arthritis, sacroiliitis, or AS. CONCLUSION: The results of the initial study showed that long term treatment with lymecycline in patients with acute ReA decreased the duration of arthritis in those with Chlamydia trachomatis triggered ReA, but not in other patients with ReA. Ten years after the acute arthritis one patient had developed AS, and three had radiological sacroiliitis, three patients had radiological changes at peripheral joints. Long term lymecycline treatment did not change the natural history of the disease.

Publication Type: Clinical Trial. Journal Article. Randomized Controlled Trial.

<14>

Unique Identifier [PMID]: 12635499

Authors: Flores D. Marquez J. Garza M. Espinoza LR.

Institution: Section of Rheumatology, Department of Medicine, Louisiana State University Health Sciences Center, 1542 Tulane Avenue, New Orleans, LA 70112-2822, USA.

Title: Reactive arthritis: newer developments. [Review] [139 refs]

Source: Rheumatic Diseases Clinics of North America. 29(1):37-59, vi, 2003 Feb.

Abstract: Reactive arthritis (ReA) is characterized by an aseptic inflammatory articular involvement occurring in a genetically predisposed individual secondary to an infectious process localized outside the joint. ReA usually refers to an acute or insidious oligoarthritis process after enteric (enteroarthritis) or urogenital (uroarthritis) infection. Conventional antirheumatic therapeutic modalities based on nonsteroid anti-inflammatory drugs, sulfasalazine, and steroids are effective in the majority of patients. In more refractory cases, the use of second-line agents including methotrexate and more recently biological agents such as etanercept and infliximab has been found highly effective. The role of antibiotics remains not well established, although they appear to be effective in acute ReA of urogenital origin. [References: 139]

Publication Type: Journal Article. Review.

<15>

Unique Identifier [PMID]: 12635498

Authors: Yu D. Kuipers JG.

Institution: Division of Rheumatology, University of California at Los Angeles, 35-40 Rehab Center, 1000 Veterans Avenue, Los Angeles, CA 90095, USA. dtyyu@ucla.edu

Title: Role of bacteria and HLA-B27 in the pathogenesis of reactive arthritis. [Review] [41 refs]

Source: Rheumatic Diseases Clinics of North America. 29(1):21-36, v-vi, 2003 Feb.

Abstract: Strictly speaking, "reactive arthritis" is a conventional term with no study-verified definition. This review will focus on the type of arthritis that is induced by the following species: Chlamydia, Shigella, Salmonella, Yersinia, and Campylobacter. The types of arthritis caused by these pathogens share a clinical pattern that is common in the spondyloarthropathies, especially undifferentiated spondyloarthropathy and Reiter's syndrome. All these diseases, including ankylosing spondylitis, must also share major pathogenetic pathways. [References: 41]

Publication Type: Journal Article. Review.

<16>

Unique Identifier [PMID]: 12610801

Authors: Soderlin MK. Kautiainen H. Puolakkainen M. Hedman K. Soderlund-Venermo M. Skogh T. Leirisalo-Repo M.

Institution: Department of Internal Medicine, Vaxjo Central Hospital, Vaxjo, Sweden. maria.soderlin@ltkronoberg.se

Title: Infections preceding early arthritis in southern Sweden: a prospective population-based study.[see comment].

Comments Comment in: J Rheumatol. 2003 Mar;30(3):425-9; PMID: 12610794

Source: Journal of Rheumatology. 30(3):459-64, 2003 Mar.

Abstract: OBJECTIVE: To detect evidence of infections preceding early arthritis in Southern Sweden and to compare the clinical outcome of remission during a 6-month followup for patients with and without signs of prior infection. METHODS: Adult patients with arthritis of less than 3 months' duration were referred from primary health care centers to rheumatologists. All patients were systematically screened for infections caused by Salmonella typhimurium and Salmonella enteritidis, Yersinia enterocolitica, Campylobacter jejuni, Borrelia burgdorferi, Chlamydia trachomatis, Chlamydia pneumoniae, and parvovirus B19. RESULTS: Seventy-one patients were included in this study. Twenty-seven (38%) patients had reactive arthritis (ReA), 17 (24%) undifferentiated arthritis, 15 (21%) rheumatoid arthritis (RA), 4 (6%) psoriatic arthritis, and the rest (11%) other diagnoses. Of all the patients, 45% had evidence of a recent infection preceding the arthritis, as indicated by laboratory tests and/or disease history. C. jejuni dominated the ReA group. The occurrence of recent C. trachomatis, B. burgdorferi, C. pneumoniae, and parvovirus B19 infections was low. Overall, 58% of the patients went into remission during the 6-month followup. Of the patients with a preceding infection, 69% went into remission as compared to 38% of the patients without a preceding infection (p = 0.011). Thirty-three percent of the patients with RA were in remission after 6 months. CONCLUSION: In this population-based cohort, 45% of the patients presenting with a new-onset arthritis had had a prior infection. Campylobacter ReA dominated the ReA group. There were only a few cases preceded by infections by C. trachomatis, B. burgdorferi, C. pneumoniae, and parvovirus B19 infections. Remission during the first 6 months was especially frequent in the group of patients with a prior infection, but the remission rate was relatively high even for arthritis without prior infection.

Publication Type: Journal Article.

<17>

Unique Identifier [PMID]: 12406424

Authors: Keat A.

Institution: Department of Rheumatology, Northwick Park Hospital, Harrow, Middlesex, HA1 3UJ, UK.

Title: Reactive arthritis or post-infective arthritis?. [Review] [95 refs]

Source: Best Practice & Research in Clinical Rheumatology. 16(4):507-22, 2002 Sep.

Abstract: Infective mechanisms probably underlie a wide range of inflammatory arthropathies. There appears to be a spectrum of mechanisms ranging from the frankly septic, through low-grade infection with very small numbers of microorganisms in the joint to arthritides in which no hard evidence for an infective cause exists. In the midst of the spectrum lie 'post-infective' and 'reactive' arthritides, characterized clinically, genetically and by epidemiological links with infection. Identification of bacterial components within joint material from such patients suggested that the causes of the arthritis had been found. It is now clear that many bacteria are present in inflamed joints; establishing their significance will be of crucial importance, but not easy. [References: 95]

Publication Type: Journal Article. Review.

<18>

Unique Identifier [PMID]: 12209542

Authors: Ford DK.

Title: Synovial lymphocyte responses to microbiologic antigen stimulation indicate the etiology of undifferentiated and reactive arthritis, and possibly of rheumatoid arthritis: Comment on the article by Schnarr et al.[comment].

Comments Comment on: Arthritis Rheum. 2001 Nov;44(11):2679-85; PMID: 11710723

Source: Arthritis & Rheumatism. 46(8):2259-60; author reply 2260, 2002 Aug.

Publication Type: Comment. Letter.

<19>

Unique Identifier [PMID]: 12192255

Authors: Shulman ST. Ayoub EM.

Institution: Department of Pediatrics, Northwestern University, Feinberg School of Medicine, The Children's Memorial Hospital, Chicago, Illinois 60614-3394, USA. sshulman@northwestern.edu

Title: Poststreptococcal reactive arthritis. [Review] [15 refs]

Source: Current Opinion in Rheumatology. 14(5):562-5, 2002 Sep.

Abstract: Poststreptococcal reactive arthritis (PSRA) refers to a poststreptococcal arthritic condition that does not fulfill the Jones Criteria for diagnosis of acute rheumatic fever. Clinical features include additive rather than migratory arthritis that responds relatively poorly to salicylates and nonsteroidals; persistence for mean of 2 months; elevated acute phase reactants; and laboratory (usually serologic) evidence of recent group A streptococcal infection. PSRA is not associated with HLA-B27 but rather with HLA-DRB1*01. Because up to 6% of PSRA patients develop mitral valve disease, it is recommended that antistreptococcal prophylaxis be administered for 1 year and then discontinued if there is no evidence of cardiac involvement. [References: 15]

Publication Type: Journal Article. Review.

<20>

Unique Identifier [PMID]: 12079895

Authors: Sibilia J. Limbach FX.

Institution: Rheumatology Department, University Hospital of Strasbourg, France. jean.sibilia@wanadoo.fr

Title: Reactive arthritis or chronic infectious arthritis?[see comment]. [Review] [108 refs]

Comments Comment in: Ann Rheum Dis. 2003 Oct;62(10):1027-8; PMID: 12972495

Source: Annals of the Rheumatic Diseases. 61(7):580-7, 2002 Jul.

Abstract: Microbes reach the synovial cavity either directly during bacteraemia or by transport within lymphoid cells or monocytes. This may stimulate the immune system excessively, triggering arthritis. Some forms of ReA correspond to slow infectious arthritis due to the persistence of microbes and some to an infection triggered arthritis linked to an extra-articular site of infection. [References: 108]

Publication Type: Journal Article. Review.