Commented glossary for rheumatic spinal diseases.
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Humans↗
Biomedical subjects
J Sieper
Publications and source records attributed to J Sieper.
Third International Workshop on Reactive Arthritis. 23-26 September 1995, Berlin, Germany. Report and abstracts.
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Arthritis, Reactive↗
Computed tomography guided corticosteroid injection of the sacroiliac joint in patients with spondyloarthropathy with sacroiliitis: clinical outcome and followup by dynamic magnetic resonance imaging.
OBJECTIVE: To evaluate computed tomography (CT) guided corticosteroid injections of inflamed sacroiliac (SI) joints in patients with spondyloarthropathies (SpA), and to evaluate dynamic magnetic resonance imaging (DMRI) of the SI joints in serial examinations of these patients, who had different degrees of inflammatory back pain. METHODS: We examined and treated 30 patients with ankylosing spondylitis (n = 9) or undifferentiated SpA (n = 11) (14 women and 16 men, mean age 36.5 +/- 13.4 years, mean disease duration 5.4 +/- 4.0 years) who had severe inflammatory back pain for more than 3 months. All patients had DMRI of the SI joints before and 4-6 months after a CT guided injection of 40 mg triamcinolone acetonide into SI joints (n = 54; 24 patients received injections in both joints). Enhancement of the contrast agent gadolinium-DTPA was quantified by calculating the enhancement of the contrast agent gadolinium-DTPA was quantified by calculating the enhancement gradient Fenh. A subjective index with a visual analog scale (0 = no pain, 10 = very severe pain) was used for assessment of back pain. Followup visits were done every 3 months for a maximum of 18 months. RESULTS: There was significant improvement of inflammatory back pain and sacroiliitis at 5.2 +/- 1.3 months after therapy in 25/30 patients (83.3%). The differences between the Fenh values before (98.2 +/ 56.1) and after (44.3 +/- 31.2) therapy and of the subjective pain index (8.5 +/- 1.5 and 3.0 +/- 2.3, respectively) were statistically significant. Subjective improvement lasted a mean of 8.9 +/- 5.3 months. CONCLUSION: CT guided corticosteroid injection of inflamed SI joints is a useful option in therapy for sacroiliitis in patients with SpA. Different degrees of inflammation in the SI joints can be quantitatively assessed by DMRI.
Adult↗
Use of immunohistologic and in situ hybridization techniques in the examination of sacroiliac joint biopsy specimens from patients with ankylosing spondylitis.
OBJECTIVE: To investigate mechanisms involved in inflammation and new bone formation in the sacroiliac (SI) joints of patients with ankylosing spondylitis (AS). PATIENTS AND METHODS: Computed tomography-assisted biopsy of the SI joint was performed in 5 patients with AS with a mean disease duration of 4.5 years and radiographic stage 2-3 disease. Immunohistologic studies were performed with the alkaline phosphatase-anti-alkaline phosphatase technique, and cytokine messenger RNA (mRNA) was detected by in situ hybridization. RESULTS: Dense cellular infiltrates with varying amounts of CD3+ cells (mean +/- SD 53.3 +/- 24.1%), CD4+ cells (29.7 +/- 17.6%), CD8+ cells (15.8 +/- 11.4%), CD14+ cells (23.6 +/- 16.9%), CD45RO+ cells (48.4 +/- 23.6%), and CD45RA+ cells (4.5 +/- 2.9%) were found in the synovial portion of the SI joints of all 5 patients. In these infiltrates a high amount of tumor necrosis factor alpha (TNF alpha) mRNA and, near the site of new bone formation, a lower amount of transforming growth factor beta (TGF beta) mRNA, were detected, while no message for interleukin-1 was found in the 3 patients examined by this technique. CONCLUSION: The presence of T cells and macrophages was demonstrated in cellular infiltrates in the SI joints of 5 patients with active AS. The finding of abundant TNF alpha message in these joints could have implications regarding potential immunotherapeutic approaches to this disease. TGF beta might be involved in new bone formation in AS.
Adult↗
Pathogenesis of spondylarthropathies. Persistent bacterial antigen, autoimmunity, or both?
We have discussed partially mutually exclusive, partially overlapping models for the pathogenesis of the spondylarthropathies. Not all possibilities have been presented here; others are discussed elsewhere (77, 78). Furthermore, we have not addressed the issue of B27-negative spondylarthropathy. However, in our opinion, the key to understanding the pathogenesis of the spondylarthropathies lies in the interaction between the class I MHC molecule HLA-B27 and the T cell response. Although a T cell response driven by persisting bacterial antigen is still an attractive hypothesis, it does not explain all the known aspects of spondylarthropathy pathogenesis. The possibility of autoimmunity triggered by bacterial infection needs also to be considered, especially the new idea of HLA-B27-derived peptides presented by class II MHC molecules. The predominant involvement of joints is not easily explained in the case of autoimmunity. Cross-reactivity to joint-specific structures such as type II collagen (79) and/or bacteria inside the joint at the beginning of the immune response, with induction of local autoimmunity, might be involved. Most of the issues raised here could be tested by experiment, and we can expect to learn soon whether any of these models will explain the pathogenesis, or if we have to look further. The PCR technique will facilitate the search for bacteria not only in peripheral joints, but also now in sacroiliac biopsy samples from patients with AS and other spondylarthropathies. A prospective study on ReA in an endemic area should teach us more about predisposing factors (for example for Shigella-induced enteritis, which occurs in many parts of the world outside Europe and the US) (80).(ABSTRACT TRUNCATED AT 250 WORDS)
Antigen Presentation↗
Immunology of reactive arthritides.
Reactive arthritis (ReA) and Lyme arthritis together comprise a pair of chronic inflammatory diseases of the joints. Although differing in detail, these relatively rare diseases are related in their immunopathology to the much commoner rheumatoid arthritis (RA), for which they serve as both model and control. The trigger for rheumatoid arthritis is unknown, but for these rarer diseases triggering occurs by certain well-defined bacterial infections. Arthritis is an uncommon outcome of these infections, for reasons unknown, and the development of chronic, as distinct from brief, arthritis is even rarer; again, the reasons are unknown. Not only does knowing the trigger greatly assist us in understanding these diseases, so also does knowing the contrasting pattern of Th1 versus Th2 cytokines observed in RA and ReA. ReA and Lyme arthritis are here considered in the wider setting of infections where chronic morbidity arises first from hypersensitivity, and perhaps finally from autoimmunity, such as occurs in some of the major tropical diseases. The immunology of ReA and Lyme disease is surveyed in detail, concentrating on T cells and including an update on the Lyme vaccine(s). Additional sections deal with the enigma of HLA B27, with epidemiological findings relevant to the chronicity of ReA and to the need for enlarged prospective studies of ReA in the setting of a developing country.
Arthritis, Reactive↗
[Magnetic resonance tomography of finger polyarthritis: morphology and cartilage signals after ademetionine therapy].
This report deals with a prospective study of 21 patients with finger osteoarthritis treated over a period of three months with either Ademetionin (therapy group: 14/21) or without (control group: 7/21). MR-Imaging was carried out before and after treatment using spin-echo and 3D-Flash sequences. Morphological parameters and signal intensity changes of the hyaline cartilage were evaluated. The increase of the cartilage signal intensity was significant in the therapy group, this can be interpreted as an structural improvement. Also a decrease of the cartilage signal intensity with age was found. The morphological parameters showed no significant changes in the therapy and control groups.
Arthritis, Rheumatoid↗
[Sapho syndrome: 2 case reports].
We report on two patients with painful hyperostosis of the mandible and the thoracic skeleton. Other symptoms were arthralgia, arthritis, osteitis, and palmoplantar pustulosis. Radiographic analysis revealed regions of circumscribed hyperostosis which showed in increased uptake in scintiscan. Metastasis, chronic osteomyelitis, Ewing's sarcoma, or Paget's disease were excluded and the diagnosis Sapho syndrome was made. This recently introduced acronym describes a disease with Synovitis, Acne, Pustulosis, Hyperostosis and Osteitis. Because of the possible axial skeleton involvement, an association to the spondylathropathy group is still being discussed. The etiopathogenesis of this rheumatologic disease is not known.
Adult↗
Divergent T-cell cytokine patterns in inflammatory arthritis.
A major immunoregulatory mechanism in inflammatory infections and allergic diseases is the control of the balance of cytokines secreted by Th1/Th2 subsets of T helper (Th) cells. This might also be true in autoimmune diseases; a Th2 pattern that prevents an effective immune response in infections with intracellular bacteria may favor immunosuppression in autoimmune disease. The pattern of cytokine expression was compared in the synovial tissue from patients with a typical autoimmune disease, rheumatoid arthritis, and with a disorder with similar synovial pathology but driven by persisting exogenous antigen, reactive arthritis. We screened 12 rheumatoid and 9 reactive arthritis synovial tissues by PCR and in situ hybridization for their expression of T-cell cytokines. The cytokine pattern differs significantly between the two diseases; rheumatoid arthritis samples express a Th1-like pattern whereas in reactive arthritis interferon gamma expression is accompanied by that of interleukin 4. Studying the expression of cytokines by in situ hybridization confirmed the results found by PCR; they also show an extremely low frequency of cytokine-transcribing cells. In a double-staining experiment, it was demonstrated that interleukin 4 is made by CD4 cells. These experiments favor the possibility of therapeutic intervention in inflammatory rheumatic disease by means of inhibitory cytokines.
Arthritis, Reactive↗
Use of dynamic magnetic resonance imaging with fast imaging in the detection of early and advanced sacroiliitis in spondylarthropathy patients.
OBJECTIVE: To evaluate the new magnetic resonance imaging (MRI) method of dynamic MRI with fast imaging in the diagnosis of sacroiliitis among patients with spondylarthropathy. METHODS: Fifteen patients with a history of inflammatory back pain without radiographic evidence of grade II or greater sacroiliitis (group 1), 25 patients with definite ankylosing spondylitis (group 2), and 12 patients with noninflammatory spinal pain (controls) (group 3) were examined. Dynamic MRI with fast imaging was performed after intravenous bolus injection of the contrast agent gadolinium-diethylenetriamine pentaacetic acid. The degree of enhancement was graded as representing acute sacroiliitis, latent sacroiliitis, or no sacroiliitis. RESULTS: Acute sacroiliitis was detected in 22 of 30 sacroiliac (SI) joints in group 1 patients and in 27 of 50 SI joints in group 2 patients; latent sacroiliitis was seen in 25 of 80 SI joints in patients from groups 1 and 2. No group 3 patient was found to have sacroiliitis. CONCLUSION: Early sacroiliitis can be demonstrated by dynamic MRI in spondylarthropathy patients in whom abnormalities are not revealed by conventional radiography.
Adolescent↗
Chlamydia pneumoniae--a new causative agent of reactive arthritis and undifferentiated oligoarthritis.
OBJECTIVE: To examine whether reactive arthritis (ReA) known to occur after a urogenital infection with Chlamydia trachomatis can also follow an infection with Chlamydia pneumoniae, a recently described species of Chlamydiae that is a common cause of respiratory tract infections. METHODS: Specific antibodies (microimmunofluorescence test) and lymphocyte proliferation to C trachomatis and C pneumoniae in paired samples of peripheral blood and synovial fluid were investigated in 70 patients with either reactive arthritis (ReA) or undifferentiated oligoarthritis (UOA). RESULTS: Five patients with acute ReA after an infection with C pneumoniae are reported. Three had a symptomatic preceding upper respiratory tract infection and two had no such symptoms. In all patients a C pneumoniae-specific lymphocyte proliferation in synovial fluid and a high specific antibody titre suggesting an acute infection was found. CONCLUSION: C pneumoniae needs to be considered a new important cause of reactive arthritis.
Acute Disease↗
The specific antibacterial proliferation of reactive arthritis synovial T cells is not due to their higher proportion of CD45RO+ cells compared to peripheral blood.
OBJECTIVE: To determine the role of synovial fluid (SF) compared to peripheral blood (PB) CD45RO+ T cells in patients with reactive arthritis (ReA) and undifferentiated oligoarthritis. METHODS: We examined SF and PB of 8 patients with a specific lymphocyte proliferation to Yersinia enterocolitica (n = 5) and Chlamydia trachomatis (n = 3). After depletion of the CD45RA+ T cell subset by dynabeads, the remaining T cells (> 95% CD45RO+) from PB and SF of these patients were again stimulated with these bacterial antigens. RESULTS: The mean stimulation index (SI) of these 8 patients with ReA (n = 5) and undifferentiated oligoarthritis (n = 3) was 30.3 +/- 21.86 in SF compared to 1.36 +/- 0.75 in PB. The enrichment of CD45RO+ cells influenced the antigen specific proliferative response of T cells neither in PB (SI = 1.75 +/- 1.35) nor in SF (26.1 +/- 24.05); the initial difference remained unchanged. CONCLUSION: Our findings suggest that the antigen specific lymphocyte proliferation obtained with SF cells is not due to abundance of nonspecific CD45RO+ T cells but can rather be taken as an indication of specific recognition of local bacterial antigens in ReA.
Adult↗
[Principles of therapy in reactive arthritis].
The diagnosis of reactive arthritis relies mainly on the presence of clinical symptoms caused by the initiating infection in the urogenital or enteral tract. An oligoarthritis mainly of the lower limbs occurs 1-6 weeks later. Chlamydia trachomatis and Yersinia enterocolitica are the most frequent triggers of reactive arthritis. Since the infections caused by these microbes are clinically often asymptomatic diagnostic evaluation can be difficult; serology is often nonspecific and cultures are mostly negative. The microscopic detection of bacterial antigens in the joint and the determination of a bacteria specific lymphocyte proliferation in the synovial fluid have changed the pathogenetic concept of reactive arthritis. However, these methods are technically difficult and not suitable for daily routine. There is no indication for short-term antibiotic treatment, as is often prescribed, except in the case of Chlamydia-induced urethritis, which should be treated in any case to prevent the onset or a relapse of reactive arthritis; the sexual partner must also be treated. Long-term therapy with various antibiotic regimens is now being tested in clinical trials. The symptomatic therapy of arthritis comprises physical methods and the use of nonsteroidal anti-inflammatory drugs; intra-articular administration of corticosteroids is of benefit in some cases. If the arthritis takes a chronic course disease modifying drugs such as sulfasalazine are partly successful; in refractory cases arthroscopic synovectomy may become necessary.
Anti-Bacterial Agents↗
The evolutionarily conserved ribosomal protein L23 and the cationic urease beta-subunit of Yersinia enterocolitica O:3 belong to the immunodominant antigens in Yersinia-triggered reactive arthritis: implications for autoimmunity.
BACKGROUND: Reactive arthritis (ReA) is a T cell mediated inflammatory process. The immune response is primarily directed against a triggering organism, although autoimmunity has been invoked in long-lasting, antibiotic-resistant disease. Although a variety of different species are known to trigger Reactive arthritis, the clinical manifestations are strikingly similar as well as closely associated to the HLA-B27 (70%). MATERIALS AND METHODS: Various antigenic fractions and single antigens of Yersinia enterocolitica were prepared, and their immunological activity was assessed by proliferation of synovial fluid mononuclear cells from 10 Reactive arthritis patients. The gene encoding one hitherto unknown antigen has been sequenced. Nonapeptides deduced from sequences of the target antigens were tested in an assembly assay. RESULTS: Two immunodominant proteins of Yersinia enterocolitica were found, one being the urease beta-subunit and the other the 50 S ribosomal protein L23. The latter has been sequenced and belongs to the evolutionarily conserved ribosomal proteins with homology to procaryotes and eucaryotes. One nonapeptide derived from the urease beta-subunit was identified as a possible epitope for HLA-B27-restricted cytotoxic T cells by its high affinity. This epitope is also highly conserved. CONCLUSION: Sharing of conserved immunodominant proteins between different disease triggering microorganisms could provide an explanation of the shared clinical picture in Reactive arthritis. Moreover, autoimmunity in Reactive arthritis might be mediated by antigen mimicry between evolutionarily conserved epitopes of ribosomal proteins and their host analogs.
Adolescent↗
[The diagnosis of reactive arthritis. The possibilities and limits].
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Antibodies, Bacterial↗
Widespread vasculopathy with hemolytic uremic syndrome, perimyocarditis and cystic pancreatitis in a young woman with mixed connective tissue disease. Case report and review of the literature.
A 15-year-old girl had severe Raynaud's phenomenon and arthralgias. A high ANA-IF titer was found and undifferentiated connective tissue disease was diagnosed. After 7 years of moderately flaring disease the patient deteriorated and presented with congestive heart failure, pleuropericardial effusion, hemolytic uremic syndrome, proteinuria and moderate hypertension. Autoantibodies against DNA, Sm-protein, and very high titers against U1RNP were detected. Therapy with high steroid doses, a cyclophosphamide pulse and 4 weeks of plasmaphresis with plasma exchange improved the heart, but not the renal condition. Symptomatic pancreatitis became the dominant problem of a progressively consuming process that resulted in the death of the patient. Post-mortem examination revealed widespread vasculopathy with intima proliferation and only minimal fibrosis involving the kidneys, heart and other main organs, including the pancreas. Taken together, the clinical picture was of an overlap between scleroderma and systemic lupus erythemathosus; the serologic and histopathologic findings suggest a diagnosis of a severe form of mixed connective tissue disease (MCTD).
Adolescent↗
The value of specific antibody detection and culture in the diagnosis of reactive arthritis.
Joint inflammation, predominantly of the lower limbs, occurring some weeks after urogenital or gastrointestinal infection is classified as reactive arthritis (ReA) but there is no general agreement on diagnostic criteria, especially if the preceding infections are asymptomatic. The same is true for Lyme disease (LD) which is caused by Borrelia burgdorferi (BB). Determination of antibody titre or culture of urethral swabs and stools are often used as diagnostic tools. We examined 4 groups of patients: one with undifferentiated arthritis (Group I, n = 55), one with well-defined rheumatic diseases other than ReA (n = 43, Group II), one group without joint disease (n = 50, Group III) and one with ReA or LD (n = 7). Specific antibacterial antibody titres in serum were measured in all patients; stool and urethral cultures were performed in all groups except the last. A calculation of positive predictive value (PPV) was done for each test. Evidence of present or previous infection with the microbes Chlamydia trachomatis (CT), Mycoplasma urethritidis (MU), Yersinia enterocolitica (YE) and BB were found in all groups. In Group I, Group II and Group III respectively, positive serological results were found for CT IgA (20%, 31%, 16%) and IgG (49%, 51%, 34%), YE (7%, 6%, 0%) and BB (17%, 2%, 10%). Positive cultures were found in Group I and Group II respectively for CT (28%, 29%) and MU (14%, 17%). Therefore no test had a significant positive predictive value for ReA in the general population and even in the rheumatology clinic the PPV for most tests was low. We conclude that these methods are of little value in the diagnosis of reactive arthritis when the preceding infection is asymptomatic.
Adolescent↗
Current perspectives in reactive arthritis.
Reactive arthritis (ReA) is an inflammatory arthritis triggered by infection, usually urethritis or gastroenteritis, and is strongly associated with the MHC class I antigen HLA-B27. Two recent observations have excited interest: first, antigen and DNA from the triggering bacteria have been identified in the joint and, second, ReA synovial T cells have been found to respond specifically to the bacterium that caused the initiating infection. Because the trigger of ReA, its onset and the MHC association are all clearly defined, we can investigate hypotheses that are impossible to study in other forms of human arthritis. Here, Gabrielle Kingsley and Jochen Sieper review the topic in the light of a recent workshop.
Animals↗