Seronegative Spondylarthritis Research Articles

Long-term kidney outcome of patients with rheumatological diseases and antineutrophil cytoplasmic antibody-glomerulonephritis: comparison with a primitive ANCA-glomerulonephritis cohort.

Antineutrophil cytoplasmic antibody (ANCA) may appear in the course of rheumatic diseases (RD) but the kidney involvement is very rare and the prognosis poorly defined. We retrospectively identified patients with RD among 153 patients with ANCA glomerulonephritis (ANCA-GN). Their clinical/histological presentation and outcome were compared with that of primitive ANCA-GN patients (1:4) matched for sex, age, ANCA type and follow-up. Nine patients (5.9%) were included: three had rheumatoid arthritis, two systemic sclerosis, two psoriatic arthritis, one ankylosing spondylitis and one seronegative spondylarthritis. Seven patients were MPO positive, two PR3 positive. ANCA-GN developed 74 months after RD with microscopic haematuria and acute kidney dysfunction in all but two patients. After 68-month follow-up, four patients (44.4%) achieved response to therapy defined as eGFR >60/min/1,73 m2 or stable, no microscopic haematuria and negative ANCA. At ANCA-GN diagnosis, serum creatinine and C-reactive protein were significantly lower in RD-ANCA-GN (2.38 vs. 3.34mg/dl, p=0.05 and 2.3mg/dl vs. 7.2mg/dl; p=0.05, respectively) while haemoglobin was higher (12.3g/dl vs. 9.3g/dl p<0.01) than in the 36 primitive ANCA-GN patients of control group. At kidney biopsy, focal forms were more frequent in RD patients (44.45% vs. 18.75%, p=0.11). The treatment between the two groups was not significantly different. At last observation, the percentage of patients with ESKD was lower in RD than in controls (11.1%vs. 30.5%; p=0.23). Patients with RD seem to develop ANCA-GN with less severe clinical/histological kidney involvement, and better long-term kidney survival than primitive ANCA-GN. This is probably due to the strict monitoring of RD patients that allows a prompter ANCA-GN diagnosis and treatment.

Polymyalgia Rheumatica, an Age-Related Rheumatic Disease

Polymyalgia rheumatica (PMR) is an age-related chronic inflammatory disease with rheumatic features at the fore. In addition to the high-grade systemic inflammation, it is characterized by typical “polymyalgic” musculoskeletal symptoms, including diffuse and severe pain and prolonged morning stiffness of the shoulder girdle, pelvic girdle, and neck. PMR is a member of the so-called giant cell arteritis complex; however, in spite of the marked systemic inflammation in PMR, the local vasculitis process aborts. The pathological background is synovitis, with a predominant inflammation of the extra-articular synovial structures. Synovitis of PMR is mild, transient, and non-erosive. Distal musculoskeletal symptoms are also observed but are more variable and less recognizable than the predominant proximal polymyalgic syndrome. PMR often overlaps with elderly-onset seronegative arthritides, elderly-onset rheumatoid arthritis, late-onset seronegative spondylarthritis, and the RS3PE1 syndrome. Although glucocorticoids are the cornerstone of PMR therapy, considerable hope is attached to tocilizumab, an IL-6 receptor inhibitor.

Коронавирус — триггер анкилозирующего спондилита?

SARS-CoV-2 is a rather insidious disease that affects various organs and systems, including the musculoskeletal system. The interest of scientists and doctors is attracted by the condition of patients who have had a coronavirus infection and faced new symptoms. During the pandemic, many medical problems were revealed, which are associated with the relations between the viral infection and immune-inflammatory rheumatic diseases, such as rheumatoid arthritis, sero-negative spondylarthritis, psoriasic and gouty arthritis, systemic diseases of connective tissues. The article describes a clinical case of ankylosing spondylitis that developed after a coronavirus infection in a 59-year-old patient. The infection turns out to be a provoking mechanism for the evolution of immune-inflammatory diseases of the joints, which include Bechterew’s disease.

P1703RESULTS OF RENAL TRANSPLANTATION IN PATIENTS WITH RHEUMATIC DISEASES

Abstract Background and Aims Rheumatic diseases often involve the kidneys and it might lead to chronic kidney disease (CKD). In its final stage it must be treated with renal replacement methods such as dialysis (hemodialysis or peritoneal dialysis) or renal transplantation. Kidney transplantation is the preferred and most cost-effective treatment for the end-stage renal disease, it offers a better quality of life than dialysis. The most common types of renal pathology in rheumatic diseases include glomerular (systemic lupus erythematosus), vascular (ANCA-associated vasculitides) and tubulointerstitial (goat) diseases. According to a research conducted in 2010 at the Minsk Rheumatological Department, 25% of patients had clinical or laboratory features of CKD. The aims were to reveal the most frequent rheumatic diseases affecting the kidneys and evaluate the post-transplant period in these patients. Method 94 medical case were studied retrospectively. All these patients had the end-stage renal disease with GFR of &amp;lt;15 ml/min/1.73m2 and underwent renal transplantation between January 2011 and September 2019. Results A retrospective study of 94 kidney transplant patients was conducted on renal transplantation centers in Belarus. Among the patients that underwent renal transplantation from January 2011 till September 2019, the percentage of recipients with rheumatic diseases was 3.64%. The majority of the recipients (52 %) were females. The mean age was 44.36 years (range, 16-78 years). Of the sample, 90% of kidney allografts were received from brain-dead donors, whereas only 10% of recipients got a new kidney from living-donors. Systemic lupus erythematosus was the most common causative disease in patients with rheumatic diseases (31 cases, 33%) followed by goat (28 cases, 30%) and secondary amyloidosis (17 cases, 18%) that complicated the course of rheumatoid arthritis and seronegative spondylarthritis. The remaining part of patients suffered from ANCA-associated vasculitides (10 cases, 10.6%), anti-glomerular basement membrane disease (6 cases, 6.4%), and single cases were represented by progressive systemic sclerosis and antiphospholipid syndrome (2%). In the post-transplant period, the most common complications were arterial hypertension (38%), anemia (20%), infectious diseases (27%), among them the most frequent were urinary tract infection (20%) and cytomegalovirus infection (7%). The 1-year allograft survival rate was 86%, the 5-year rate was about 82%. The main reasons for failed outcomes were acute renal allograft rejection, postoperative complications and infection. The patient survival rate after 1 and 5 years after transplantation was 93% and 86%, respectively. Infectious diseases (44%) such as nosocomial pneumonia, sepsis and cardiovascular disease (33%) are still the two most important reasons of death. Conclusion 1. The most common rheumatic diseases causing the end-stage renal disease are systemic lupus erythematosus (33%), goat (30%), rheumatoid arthritis, and seronegative spondylarthritis that lead to secondary amyloidosis (18%). 2. The 1-year allograft survival rate was 86%, the 5-year rate was about 82%, the patient survival rate after 1 and 5 years after transplantation was 93% and 86%, respectively. 3. The survival of patients with rheumatic diseases who underwent renal transplantation is comparable to patient survival after transplantation with another kidney pathology. 4. The main causes of death following renal transplantation are infectious and cardiovascular complications. Acute renal allograft rejection, postoperative complications, and infection are the main reasons of allograft failure.

VZV-specific T-cell levels in patients with rheumatic diseases are reduced and differentially influenced by antirheumatic drugs

BackgroundVaricella zoster virus (VZV)-specific cellular immunity is essential for viral control, and the incidence of VZV reactivation is increased in patients with rheumatic diseases. Because knowledge of the influence of antirheumatic drugs on specific cellular immunity is limited, we analyzed VZV-specific T cells in patients with rheumatoid arthritis (RA) and seronegative spondylarthritis (SpA), and we assessed how their levels and functionality were impacted by disease-modifying antirheumatic drugs (DMARDs). A polyclonal stimulation was carried out to analyze effects on general effector T cells.MethodsCD4 T cells in 98 blood samples of patients with RA (n = 78) or SpA (n = 20) were quantified by flow cytometry after stimulation with VZV antigen and the polyclonal stimulus Staphylococcus aureus enterotoxin B (SEB), and they were characterized for expression of cytokines (interferon-γ, tumor necrosis factor [TNF]-α, interleukin [IL]-2) and markers for activation (CD69), differentiation (CD127), or functional anergy programmed death 1 molecule [PD-1], cytotoxic T-lymphocyte antigen 4 [CTLA-4]. Results of patients with RA were stratified into subgroups receiving different antirheumatic drugs and compared with samples of 39 healthy control subjects. Moreover, direct effects of biological DMARDs on cytokine expression and proliferation of specific T cells were analyzed in vitro.ResultsUnlike patients with SpA, patients with RA showed significantly lower percentages of VZV-specific CD4 T cells (median 0.03%, IQR 0.05%) than control subjects (median 0.09%, IQR 0.16%; p < 0.001). Likewise, SEB-reactive CD4 T-cell levels were lower in patients (median 2.35%, IQR 2.85%) than in control subjects (median 3.96%, IQR 4.38%; p < 0.05); however, expression of cytokines and cell surface markers of VZV-specific T cells did not differ in patients and control subjects, whereas SEB-reactive effector T cells of patients showed signs of functional impairment. Among antirheumatic drugs, biological DMARDs had the most pronounced impact on cellular immunity. Specifically, VZV-specific CD4 T-cell levels were significantly reduced in patients receiving TNF-α antagonists or IL-6 receptor-blocking therapy (p < 0.05 and p < 0.01, respectively), whereas SEB-reactive T-cell levels were reduced in patients receiving B-cell-depleting or IL-6 receptor-blocking drugs (both p < 0.05).ConclusionsDespite absence of clinical symptoms, patients with RA showed signs of impaired cellular immunity that affected both VZV-specific and general effector T cells. Strongest effects on cellular immunity were observed in patients treated with biological DMARDs. These findings may contribute to the increased susceptibility of patients with RA to VZV reactivation.

Polymyalgia rheumatica update, 2015

Polymyalgia rheumatica is an inflammatory musculoskeletal disorder of people aged 50 years or over, characterised by pain, aching and morning stiffness in the shoulder girdle and often hip girdle and neck. Marked systemic inflammation and rapid response to corticosteroid therapy are characteristic features. Giant cell arteritis is a well-known association of polymyalgia rheumatica. Recent clinical evidence and scientific results in the field have provided new challenges for rheumatologists. Besides the aspecific - although characteristic - proximal syndrome, less well recognizable and more variable distal musculoskeletal manifestations were observed. Magnetic resonance and ultrasound studies showed mild, remitting and non-erosive synovitis, with dominating inflammation of the extraarticular synovial structures. As no pathognostic sign is known, the diagnosis of polymyalgia rheumatica is based on its differential diagnosis, differentiation from the polymyalgia mimics; particularly from elderly onset inflammatory arthritides, such as elderly onset rheumatoid arthritis and late onset seronegative spondylarthritis. In 2012 the international polymyalgia rheumatica work group under the guidance of the American College of Rheumatology and European League Against Rheumatism elaborated new classification criteria, the scoring algorythm of which is based on clinical symptoms, with ultrasonography increasing the specificity. Corticosteroids remain the cornerstone of the therapy of polymyalgia rheumatica. No effective steroid-sparing drug has been found to date. Corticosteroids are generally needed for 1-1.5 years, though some patients have a chronic-relapsing course and require corticosteroids for several years. Well known corticosteroid-related side effects (diabetes, hypertension, hyperlipidaemia and osteoporosis) cause significant morbidity and economic burden on the society. Novel therapeautic approaches are on trial. Early recognition of the disease, early start of corticosteroids and a well-defined course, prevention and management of side effects are everyday tasks for rheumatologists and family doctors. Knowledge of polymyalgia rheumatica is essential for all medical specialties.

THU0501 Public Awareness of Rheumatic Diseases in Greece is Very Low

BackgroundIt has previously been found that the majority of patients with rheumatoid arthritis or seronegative spondylarthritis consult rheumatologists long after their disease onset; therefore, both correct diagnosis and treatment are...

THU0500 Free Informational Seminars on Rheumatic Diseases for the Public Increase Its Awareness of these Diseases

BackgroundIn previous population based epidemiological studies we have found that most patients with rheumatoid arthritis or seronegative spondylarthritis consult rheumatologists long after their disease onset, resulting in incorrect diagnosis and...

Interleukin-1 associations in inflammatory bowel disease and the enteropathic seronegative spondylarthritis.

PurposeThis study aims to investigate any associations of the proinflammatory cytokine IL-1 in treated patients with inflammatory bowel disease (IBD) and the enteropathic seronegative spondylarthritis (eSpA).MethodsThirty-four patients with Crohn’s disease (CD), 26 with ulcerative colitis (UC) and 14 patients with SpA participated in the study. Valid clinical indexes, CRP values and the endoscopic and histologic examination were used for the determination of disease activity. IL-1α, IL-1β, IL-1 receptor antagonist (IL-1Ra) were measured by ELISA. Nonparametric tests were used for continuous and categorical data.ResultsEnteropathic SpA diagnosed in 29.4 % CD and 30.8 % UC patients. Active disease had 58.8 % CD (aCD), 76.9 % UC and 50 % SpA patients. Active and inactive CD (iCD) significantly differ on IL-1α levels (11.2 vs. 3.9 pg/ml; p = 0.034). Active and inactive UC significantly differ on IL-1β (3.7 vs. 2.3 pg/ml; p = 0.054) and IL-1Ra levels (15.9 vs. 12.7 pg/ml; p = 0.023). Active and inactive SpA (iSpA) significantly differ on IL-1Ra (16.9 vs. 14.8 pg/ml; p = 0.033) and marginally on IL-1α levels (20 vs. 3.9 pg/ml; p = 0.06). Patients with aCD/ieSpA exhibited significant differences on IL-1α (p = 0.022) compared to those with iCD/ieSpA.ConclusionsIL-1α is associated with CD activity, while IL-1β and IL-1Ra are associated with UC activity in treated patients with IBD. Prominent cytokine in SpAs seems to be IL-1α.

Use of aceclofenac (aertal) in back pain

Back pain is a generalized type of locomotor lesion that is caused by soft tissue pathology and degenerative changes in the vertebral column in most cases and by intervertebral disk herniation, spinal stenosis, compression fractures in osteoporosis, by injuries, congenital anomalies, vertebral displacement less frequently, as well as by infections, tumors, inflammatory processes in the vertebral column, and related pain. A number of rheumatic diseases, including seronegative spondylarthritis, Scheuermann-Mau' disease, Forestier's disease, osteoarthrosis, etc., are accompanied by back pain. The cause of back pain syndrome cannot be frequently identified. This abnormality is treated by nonsteroidal antiinflammatory drugs, among which aceclofenac (Aertal) has acquired a reputation as an agent having a good tolerability.

Cyclosporine A area-under-time-concentration-curve in rheumatologic patients after the first dose. Which of the sparse sampling strategies will predict the best?

The aim of the present study was to validate the limited sampling strategies (LSS:s) for prediction of AUC of cyclosporine A (CsA) after the first dose in rheumatologic patients. 22 patients suffering from rheumathoid arthritis, systemic lupus erythematodus, ankylosing spondylitis dermato(poly)myositis or seronegative spondylarthritis were treated with Neoral® (female/male: 11/3, mean ± SD: age 49 ± 14 y, body weight 75 ± 12 kg, height 166 ± 7 cm, dose 71 ± 25 mg, dose per kg 1.0 ± 0.3 mg/kg), or Consupren® (7/1, 78 ± 36, 175 ± 8, 82 ± 22, 1.1 ± 0.3). Two patients whose C12h were missing were excluded from the AUC0-12 calculation. Whole blood levels of CsA were analyzed with HPLC. Blood samples were collected at 0, 0.5, 1, 1.5, 2, 3, 4, 6, 8, and 12 hours after taking the first dose. Altogether 115 LSS:s obtained from the literature were validated. A linear trapezoidal rule was used as a reference method. Mean percentage prediction error (%PE) < ± 15% and maximal one value of absolute %PE > 30% were considered to be acceptable. The root mean squared error (RMSE) was evaluated for equations that passed the criteria. The best performance with all values of the absolute %PE < 30% was found in three LSS:s for AUC0-12 and two for AUC0-8: AUC0-12 = 123.792 + 1.165 × C1h + 3.021 × C3h + 7.33 × C8h; 97.6 + 1.27 × C1h + 3.14 × C3h + 4.06 × C6h; or 124.3 + 1.34 × C1h - 0.16 × C2h + 3.27 × C3h + 3.96 × C6h; AUC0-8 = -19.8 + 1.99 × C2h + 2.38 × C4h + 3.15 × C6h or -22.4 + 2.51 × C2h + 5.49 × C6h. Validation criteria were further fulfilled in AUC0-12 = 24 + 3.66 × C0h + 2.11 × C1.5h + 4.54 × C4h or 0.2 + 2 × C2h + 10.2 × C6h; AUC0-8 = 55.37 + 2.89 × C0h + 1.08 × C1 + 0.9 × C2h + 2.23 × C3h; and AUC0-4 = -41 + 1.17 × C1h + 1.85 × C2h. Only one equation proposed for AUC0-6 did not pass the validation criteria. Equations validated for prediction of AUC0-12, AUC0-8 and AUC0-4 might be used for LSS:s of CsA independently of the length of treatment, indication, dosage or galenic formulation.

Dysregulation of interleukin‐10–dependent gene expression in rheumatoid arthritis synovial macrophages

The inflammatory cytokines tumor necrosis factor alpha (TNFalpha) and interleukin-1 (IL-1) are produced by activated macrophages, are key mediators of pathogenesis, and are validated therapeutic targets in rheumatoid arthritis (RA) and seronegative spondylarthritis (SpA). IL-10 is a potent antiinflammatory cytokine that suppresses macrophage TNFalpha and IL-1 production, yet is not effective in suppressing inflammatory arthritis. To gain insight into IL-10 responses in inflammatory arthritis, we used microarray analysis to determine the patterns of IL-10-inducible gene expression in freshly isolated RA and seronegative SpA synovial macrophages. Macrophages from the synovial fluid of 5 patients with RA and 3 with seronegative SpA (2 with psoriatic arthritis and 1 with ankylosing spondylitis) were isolated by positive selection and stimulated ex vivo with IL-10 or interferon-gamma (IFNgamma). Gene expression was analyzed using Affymetrix microarrays and protocols. Real-time polymerase chain reaction was used to confirm changes in gene expression. The number of genes induced by IL-10 in arthritic macrophages was markedly smaller than that induced in control macrophages, and the strength of induction was lower in arthritic macrophages for most genes. The residual response of arthritic macrophages to IL-10 stimulation was qualitatively altered, such that IL-10 preferentially increased expression of IFNgamma-inducible genes. In contrast, arthritic macrophages expressed many IFNgamma-inducible genes prior to stimulation, and their response to IFNgamma remained mostly intact. These results demonstrate that IL-10 responses are dysregulated in RA synovial macrophages. An altered biologic response to IL-10, with attenuation of its antiinflammatory function and a concomitant retention of IFNgamma-like activating functions, provides a basis for the lack of efficacy of IL-10 in suppressing inflammatory arthritis.

Current evaluation of efficacy of radon baths of various concentrations during rehabilitation of patients with seronegative spondylarthritis

141 patients with seronegative spondylarthritis including ankylosing spondylarthritis (n = 90), reactive arthritis and Reiter's disease (n = 51) took water radon baths (concentration 1.5, 3.0 and 4.5 kB/l). The baths proved similarly effective in patients with seronegative spondylarthritis. They produced analgetic, anti-inflammatory actions, raised quality of life for such patients.

Influence of combined rehabilitation treatment including novel non-pharmacological technologies on immune system of patients with seronegetive spondylarthritis

The immune system was studied in 90 patients with seronegative spondylarthritis (SNSA). Of them, 60 patients had ankylosing spondylarthritis (30 patients with central and 30 patients with peripheral forms) and 30 patients with reactive arthritis. SNSA patients were found to have secondary immunodeficiency. Cellular immunity was characterized by a decreased count of T mu (helper cells), an increased count of T gamma (cytotoxic/suppressors) and suppressed functional activity of lymphocytes, humoral immunity--by a high concentration of circulating immune complexes in an increased concentration of serum immunoglobulins. Integral assessment of the changes in the immune system and clinical data in SNSA patients leads to the conclusion that water radon baths and decimetric wave therapy reach the highest efficacy in ankylosing spondylarthritis while water radon baths and low frequency ultrasound--in reactive arthritis, a complex of water radon baths and ultraphonophoresis of hydrocortisone--in ankylosing spondylarthritis and reactive arthritis.

Combined rehabilitation treatment for seronegative spondylarthritis including novel non-pharmacological technologies

The trial included 90 patients with seronegative spondylarthritis (SA): 60 ones with ankylosing spondylarthritis (30 with central and 30 with peripheral forms) and 30 patients with reactive arthritis (RA). RA patients with affection of the peripheral joints, periarticular tissues and the spine are effectively treated with a complex of water radon baths and low frequency ultrasound but in affection of the peripheral joints and tendon-ligament system water radon baths and ultraphonophoresis of hydrocortisone are recommended. Water radon baths and decimetric therapy are good for patients with central ankylosing spondylarthritis having a dominant lesion of the spine. In involvement of the joints and tendon-ligament system it is recommended to use a complex of water radon baths and ultraphonophoresis of hydrocortisone.

Synovial fluid exoglycosidases are predictors of rheumatoid arthritis and are effective in cartilage glycosaminoglycan depletion.

To analyze enzymes involved in joint damage by simultaneous investigation of glycosidases and matrix metalloproteinases (MMPs) in patients with various joint diseases. Activities of glycosidases (beta-D-glucuronidase, beta-D-N-acetyl-glucosaminidase, beta-D-N-acetyl-galactosaminidase, beta-D-galactosidase, and alpha-D-mannosidase) were tested at an acidic pH as well as at the original pH of the synovial fluid (SF) samples in parallel with activities of MMP-1 and MMP-9. Patients with rheumatoid arthritis (RA) were characterized by significantly elevated activities of beta-D-glucuronidase and beta-D-N-acetyl-glucosaminidase in SF compared with patients with osteoarthritis, seronegative spondylarthritis, or acute sports injury. To select the best predictor for distinguishing among patient groups, a stepwise logistic regression analysis was performed; the strongest association was found to be between RA and beta-D-glucuronidase/beta-D-N-acetyl-glucosaminidase activities (measured at the pH of the SF). Further, a significant correlation was observed between the activity of SF beta-D-N-acetyl-glucosaminidase and the level of rheumatoid factor. In vitro digestion of human hyaline cartilage samples revealed that the dominant glycosidases, alone or in combination with MMPs, proved to be effective in depleting glycosaminoglycans (GAGs) from cartilage. These results suggest that exoglycosidases, which are present in the SF of RA patients, may contribute to the depletion of GAGs from cartilage and thereby facilitate the invasion of synovial cells and their attachment to cartilage in RA.

Malignant lymphoma-associated autoimmune diseases--a descriptive epidemiological study.

Lymphoproliferative disorders and autoimmune diseases have some common aspects in their clinical appearance. We reviewed 940 patient charts with malignant lymphomas to assess the rate of associated autoimmune diseases. Of 421 non-Hodgkin's lymphoma (NHL) patients (230 males, 191 females), 32 (7.6%) had an autoimmune disease (26 females, six males, mean age 48.3 years). The most common diagnosis was Sjögren's syndrome. The other cases were autoimmune skin diseases (5), thyroiditis (3), polymyositis (2), scleroderma (2), other musculoskeletal disorders (2), rheumatoid arthritis (1), vasculitis (1), undifferentiated collagenosis (1), colitis ulcerosa (1), autoimmune hepatitis (1), Addison's disease (1), and autoimmune hemolytic anemia (1). Of 519 Hodgkin's lymphoma patients (308 males, 211 females), an associated autoimmune disease occurred in 45 (8.6%) (25 females, 20 males, mean age 39.2 years). In 31 cases, we found autoimmune thyroid disorders, then came glomerulonephritis (3), immune thrombocytopenia (3), insulin-dependent diabetes mellitus (2), autoimmune hemolytic anemia (1), seronegative spondylarthritis (1), systemic lupus erythematosus (1), mixed connective tissue disease (1), scleroderma (1), and vasculitis (1). We also analyzed histology, choice of treatment, and sequence of appearance of the disease types. We found a difference between NHL and Hodgkin's lymphoma patients, since in NHL autoimmunity - mostly from Sjögren's syndrome - preceded the lymphoma diagnosis (70%), but in Hodgkin's the autoimmunity developed mainly after the treatment of malignancy. The relatively high prevalence of autoimmune diseases in malignant lymphomas has several explanations. Clinicians have to consider autoimmunity when treating lymphoproliferative disorders.

High in vivo expression of interleukin-17 receptor in synovial endothelial cells and chondrocytes from arthritis patients.

To evaluate the presence of interleukin-17 (IL-17) and the expression of IL-17 receptor (IL-17R) in joint tissues from subjects with different arthritides. Immunohistochemistry was used on frozen synovial and cartilage biopsies to identify cells expressing IL-17 and IL-17R. IL-17 staining was present only in synovial biopsies of rheumatoid arthritis (RA) (seven out of nine cases). IL-17R was expressed by all synovial biopsies evaluated except for three cases of post-traumatic arthritis (PTA). Vascular endothelial cells mainly expressed IL-17R. The percentage of IL-17R(+) vessels was the highest in RA synovium and the lowest in PTA. Chondrocytes from all types of arthritides were negative for IL-17 staining, but expressed IL-17R; the highest percentage of positive chondrocytes was found in seronegative spondylarthritis and the lowest in RA. IL-17-positive cells are found exclusively in RA. On the other hand, synovial endothelial cells and chondrocytes expressing IL-17R are found in the majority of patients with different types of arthritis. This finding suggests a role for a second ligand for IL-17R, which could be either a different cytokine or a different isoform of IL-17.

Enteropathic arthritis in the sacroiliac joint. Imaging and differential diagnosis

Objectives: A new high resolution computed tomography (HRCT) scoring system of sacroiliac joint (SIJ) involvement in enteropathic arthritis is introduced. Patients and methods: SIJ’s of 100 patients were studied. A total of 25 patients presented with pain syndrome, 25 with suspicious seronegative spondylarthritis, 25 with inflammatory bowel diseases and 25 without joint or bowel diseases, as a control group. HRCT was carried out in all 100 patients. For comparison, a plain film radiography (PFR), conventional CT (slices of 10 mm) and bone scan were used. Results: Quantitative differences: In the pain syndrome group, there were no erosions identified neither intraarticular calcifications. Disc degeneration was seen in 12/25 cases. In 4/25 patients, vacuum phenomena appeared in the SIJ. In 3/25 patients, ventral capsular calcification occurred in the ventral sacroiliac ligament (anterior capsule complex). In the seronegative spondylarthritis group, 16/25 patients had positive findings, while PFR documented erosions only in 3/25 cases. In the bowel diseases group, erosions were detected in 17/25 cases with HRCT, while the plain film was positive only in three cases and in seven cases the findings were questionable. Intraarticular calcification with erosion was documented in three cases and in seven cases without erosion. The bone scan was positive in 7/25 of this cases, but in 5/7 there was mismatching with HRCT. Important new finding was the HRCT detected erosion which was not detected on BS but was obvious on Anti-Granulocyte–Antibody scintigraphy. In the control group, only degenerative changes were seen in 4/25 cases and no erosions. Conclusion: HRCT is: (1) the reliable imaging of definitive (often ‘cold stage’) sacroileitis; (2) gives optimal detection of erosion; and (3) appears to be the only method in the documentation of calcifications in the posterior ligamental portion of the SIJ.

Three cases of pustulotic arthro-osteitis associated with episcleritis

Three cases of pustulotic arthro-osteitis (PAO) associated with episcleritis were described. In each patient, the episcleritis developed more than 10 years after the onset of PAO. These episcleritis were treated with topical corticosteroids. PAO is classified as a member of the seronegative spondylarthritis group of diseases. Though complications of seronegative spondylarthritis include uveitis and episcleritis. PAO associated with episcleritis was not reported. Episcleritis should be considered as a complication of PAO. (J Am Acad Dermatol 1999;41:845-6.)