Analysis of childhood reactive arthritis and comparison with juvenile idiopathic arthritis

There is currently no agreement on how to classify and diagnose reactive arthritis (ReA) and what kind of clinical and laboratory findings are specific for the diagnosis. This study retrospectively analyzed the initial clinical manifestations and laboratory findings in children diagnosed with ReA and juvenile idiopathic arthritis (JIA). A comparison was also made between these two groups to see if there were differences. A retrospective chart review was performed and 44 patients diagnosed with ReA and 80 patients with JIA were enrolled in this study. Their initial clinical manifestations and laboratory findings were also analyzed and compared. The initial clinical manifestations in ReA were analyzed including the demographic data, the preceding infection history, the duration of the infectious episode to the onset of arthritis, the duration of arthritic symptoms, and the involved joint pattern. Comparison of the initial laboratory findings between patients with ReA and JIA showed significant differences between erythrocyte sedimentation rates (ESR) in the first hour, platelet counts (p<0.05), and ESR in the second hour (p=0.052). Further, comparing ReA with the subtypes of JIA, significant differences were noted between ReA and the systemic type in terms of hemoglobin level, platelet counts, C-reactive protein, and first and second hour ESR (p<0.05). However, if compared with the polyarticular or pauciarticular type, only the platelet counts showed any significant statistical difference (p<0.05). This study summarizes clinical experiences in ReA. The differences in laboratory findings of ReA and JIA may provide a clue in making a differential diagnosis.     

Clinical features and disease outcomes of undifferentiated arthritis in Thailand

Background: Undifferentiated arthritis (UA) comprises arthritis not yet identifiable as a specific rheumatic disease. Few reports exist on the natural course of UA in Thai patients. Objective: To study the clinical features and natural course of UA in Thai patients. Method: A retrospective, analytical study was performed among Thai patients diagnosed with UA seen at Srinagarind Hospital, Khon Kaen, Thailand, between January 2002 and December 2007. Results: The medical records of 95 UA patients were reviewed. The mean age at onset was 40.7 ± 14.7 years (range, 15–78). The female:male ratio was 1.25 : 1.00. Common presentations included asymmetrical oligoarthritis followed by polyarthritis. The knee was the most commonly affected joint, followed by the wrist and ankle. Complete remission occurred within 6 months of onset in 4.2% of cases. A diagnosis was specified in 29 patients (30.5%) during the follow‐up period (which averaged 17.1 ± 24.0 months [range, 6–84]), including reactive arthritis (in 9 patients), undifferentiated spondyloarthropathy (7), rheumatoid arthritis (6), psoriatic arthritis (4), ankylosing spondylitis (1), gout (1) and unclassified connective tissue disease (1). UA was the default diagnosis for 66 patients (69.5%) after 24 months of follow‐up. Hyperglobulinemia was correlated with persistent arthritis (i.e., > 6 months, P = 0.045). The only predictive factor for RA development was old‐age at onset (P = 0.038). Conclusion: The most common presentation of Thai UA was asymmetrical oligoarthritis and most patients had persistent arthritis correlated with hyperglobulinemia. Elderly‐onset, without any radiographic changes or rheumatoid factor, was predictive of RA development during follow‐up.     

Apsoriatic psoriatic arthritis

Numerous features distinguish psoriatic arthritis (PsA) from other arthropathies, including the presence of psoriasis, distal interphalangeal (DIP) joint involvement, nail dystrophy, enthesitis, dactylitis and spinal involvement. Two decades ago, the presence of psoriasis was mandatory in the diagnosis of PsA. Up to 15% of patients had joint disease preceding psoriasis. In this group of patients, it may have been years after the onset of arthritis before the definitive diagnosis of PsA could be made. With advancements in treatment modalities, an accurate and proper diagnosis is relevant to the management of PsA. In their case report appearing in this issue, Taniguchi and Kamatani present a case with classical PsA without skin and nail lesions for 21 years. It may not be that unusual to encounter this in clinical practice, but we think it an opportune time to review the classification criteria and illustrate how the diagnosis of PsA can be made earlier.     

The importance of the disease process and disease‐modifying antirheumatic drug treatment in the development of septic arthritis in patients with rheumatoid arthritis

Objective

To evaluate the effect of disease‐modifying antirheumatic drugs (DMARDs) on the likelihood of patients with rheumatoid arthritis (RA) developing septic arthritis (SA).

Methods

The United Kingdom General Practice Research Database (GPRD) was used to identify adults with RA, and age‐, sex‐, and practice‐matched control subjects. Subjects were studied between 1987 and 2002. The risk of developing SA (excluding infected joint replacements) for individuals with RA was calculated and the effect of DMARD use determined.

Results

A total of 136,977 subjects (34,250 patients with RA, 102,747 controls) were identified. SA was identified in 345 subjects, of which 321 (236 in patients with RA, 85 in controls) cases occurred during the study period. The incidence rate of SA was 12.9 times higher in subjects with RA than in those without (95% confidence interval [95% CI] 10.1–16.5, P < 0.001). The incident rate ratios (IRRs) for developing SA while receiving DMARDs compared with receiving no DMARDs were different for different medications. Penicillamine (adjusted IRR 2.51, 95% CI 1.29–4.89, P = 0.004), sulfasalazine (adjusted IRR 1.74, 95% CI 1.04–2.91, P = 0.03), and prednisolone (adjusted IRR 2.94, 95% CI 1.93–4.46, P < 0.001) were associated with an increased incidence of SA when compared with not receiving any DMARD. The use of other DMARDs including methotrexate showed no such effect.

Conclusion

Individuals with RA have an increased risk of developing SA. This increased risk can be attributed to both the disease process and the use of DMARDs.     

Assessment of mutilans-like hand deformities in chronic inflammatory joint diseases. A radiographic study of 52 patients

OBJECTIVES: To evaluate patients with mutilans-like hand deformities in chronic inflammatory joint diseases and to determine radiographic scoring systems for arthritis mutilans (AM). METHODS: A total of 52 patients with severe hand deformities were collected during 1997. A Larsen hand score of 0-110 was formed to describe destruction of the hand joints. Secondly, each ray of the hand was assessed individually by summing the Larsen grade of the wrist and the grades of the MCP and PIP joints. When the sum of these grades was > or = 13, the finger was considered to be mutilated. A mutilans hand score of 0-10 was formed according to the number of mutilans fingers. Surgical treatment and spontaneous fusions were recorded. RESULTS: The study consisted of 22 patients with juvenile rheumatoid arthritis (JRA), nine with rheumatoid factor (RF) positive and 13 with RF negative arthritis, 27 patients with RF positive RA, and three adult patients with other diagnoses. The mean age of patients with adult rheumatic diseases was 27 years at the onset of arthritis. The mean disease duration in all patients was 30 years. The mean Larsen hand score was 93. Four patients had no mutilans fingers and in 15 patients all 10 fingers were mutilated. The Larsen hand score of 0-110 and the mutilans hand score of 0-10 correlated well (rs = 0.90). Fourteen patients showed spontaneous fusions in the peripheral joints. A total of 457 operations were performed on 48 patients. CONCLUSION: Both the Larsen hand score of 0-110 and the mutilans hand score of 0-10 improve accuracy in evaluating mutilans-like hand deformities, but in unevenly distributed hand deformities the mutilans hand score is better in describing deformation of individual fingers.     

The effectiveness of a traditional therapeutical approach in early psoriatic arthritis: results of a pilot randomised 6-month trial with methotrexate

Thirty-five patients with Early Psoriatic Arthritis (EPA) (17 female and 18 male; mean age 25.6 years) entered this randomised 6-month study. At the enrolment, all patients were on non-steroidal anti-inflammatory drug (NSAID) therapy on demand and were divided in two matched groups (A and B). Group A continued NSAID therapy at full dosage in the following 3 months and then added methotrexate (MTX) for another 3 months. Group B was under the combination of NSAID and MTX for the entire 6-month period. Clinical and laboratory assessment included the count of tender joints and/or entheses (TJC), the count of swollen joints and/or entheses (SJC), patient's global assessment (PGA), physician's global assessment (PhGA), patient's assessment of pain (VAS), erythrocyte sedimentation rate (ESR) and serum concentration of C-reactive protein (CRP). All variables were done at baseline (T0), at 3 (T3) and at 6 months (T6). In both group A and in group B, there was a significant improvement of all variables at T3 and T6. However, in comparison to the patients of group A, patients included in group B showed a more rapid and marked improvement of TJC and SJC, which was statistically significant at T3 (p < 0.05). In contrast, the improvement of PGA, PhGA, VAS, ESR and CRP was not significantly different between groups. The early use of MTX in EPA patients markedly improves TJC and SJC. In fact, at T3, other markers used to quantify EPA disease activity, in particular PGA, PhGA, VAS, ESR and CRP, did not show significant differences in EPA patients treated with either NSAIDs or MTX. This finding suggests an incomplete control under MTX of the pathogenetic process and stimulates further interest on early use of other therapeutical approaches capable of modifying the course of disease.     

Symptoms in individuals at risk of rheumatoid arthritis

An increasing interest in treating individuals at risk of rheumatoid arthritis (RA) to prevent the development of this chronic condition has focussed attention on the identification of risk factors of this disease. Most patients who develop RA progress through a preceding symptomatic phase that may take the form of arthralgia, palindromic rheumatism or unclassified arthritis before a disease currently classifiable as RA is established. An understanding of symptoms that identify individuals as being at risk of RA is a critical issue. Constellations of relevant symptoms could (1) form the basis of public health campaigns to encourage rapid consultation, (2) inform primary health care providers regarding which patients to perform additional tests in or whom to refer to a rheumatologist and (3) be included in algorithms to predict RA development. In this review, we present qualitative and quantitative data summarising current understanding of the symptoms experienced by individuals at risk of RA.     

Primary cultured T cell vaccine for adjuvant arthritis (AA), collagen-induced arthritis (CA) and arthritis in HTLV-1 pX-transgenic mice as models of rheumatoid-like arthritis: dominancy of the roles of T cells or humoral factors in the pathogenesis of CA and pX-transgenic arthritis

Abstract

It has been reported that a T cell vaccine is capable of regulating auto-reactive T cells, and may be used for protection against and treatment of adjuvant arthritis (AA), but no reports have appeared regarding other forms of autoimmune arthritis. In this paper, we aimed for protection against and treatment of collagen-induced arthritis (CA) and arthritis induced in HTLV-1 pX-transgenic mice (pX-A) with a T cell vaccine as another model of autoimmune arthritis, in addition to a parallel study on AA. Drained lymph node lymphocytes were cultured in either Mycobacterium tuberculosis, type II collagen or in an anti-CD3 antibody immobilized dishes for a total of 7 days. These cells were then fixed with 0.5% glutaraldehyde and used as a T cell vaccine. This was applied in the following five groups: protection and treatment of AA, protection (tolerance induction) and treatment of CA, and treatment of pX-a. The effects of a T cell vaccine were examined as: (i) an arthritis score, (ii) a histopathological examination of joint lesions, (iii) serum titers of anti-type II collagen antibodies and (iv) serum levels of several cytokines. In terms of the arthritis score, although the T cell vaccine was effective both in the protection of and treatment against AA, it was not effective for either CA or pX-A. The serum titers of anti-collagen antibodies were unchanged in the four groups examined. The serum levels of interleukin-1 β showed almost no differences in the four groups. Serum levels of tumor necrosis factor-α and interferon-γ were significantly higher in the pX-A treatment group. The T cell vaccine was effective in both protecting against and treating AA; however, it was not effective with regard to CA and pX-A. The possible dominancy of T cells in the pathogenesis of each autoimmune arthritis was discussed.     

Primary cultured T cell vaccine for adjuvant arthritis (AA), collagen-induced arthritis (CA) and arthritis in HTLV-1 pX-transgenic mice as models of rheumatoid-like arthritis: dominancy of the roles of T cells or humoral factors in the pathogenesis of CA and pX-transgenic arthritis

It has been reported that a T cell vaccine is capable of regulating auto-reactive T cells, and may be used for protection against and treatment of adjuvant arthritis (AA), but no reports have appeared regarding other forms of autoimmune arthritis. In this paper, we aimed for protection against and treatment of collagen-induced arthritis (CA) and arthritis induced in HTLV-1 pX-transgenic mice (pX-A) with a T cell vaccine as another model of autoimmune arthritis, in addition to a parallel study on AA. Drained lymph node lymphocytes were cultured in eitherMycobacterium tuberculosis, type II collagen or in an anti-CD3 antibody immobilized dishes for a total of 7 days. These cells were then fixed with 0.5% glutaraldehyde and used as a T cell vaccine. This was applied in the following five groups: protection and treatment of AA, protection (tolerance induction) and treatment of CA, and treatment of pX-a. The effects of a T cell vaccine were examined as: (i) an arthritis score, (ii) a histopathological examination of joint lesions, (iii) serum titers of anti-type II collagen antibodies and (iv) serum levels of several cytokines. In terms of the arthritis score, although the T cell vaccine was effective both in the protection of and treatment against AA, it was not effective for either CA or pX-A. The serum titers of anti-collagen antibodies were unchanged in the four groups examined. The serum levels of interleukin-1 β showed almost no differences in the four groups. Serum levels of tumor necrosis factor-α and interferon-γ were significantly higher in the pX-A treatment group. The T cell vaccine was effective in both protecting against and treating AA; however, it was not effective with regard to CA and pX-A. The possible dominancy of T cells in the pathogenesis of each autoimmune arthritis was discussed.     

Clinical presentations of chlamydial and non-chlamydial reactive arthritis

The aim of this study was to investigate the triggering micro-organisms and the clinical as well as laboratory differences between Chlamydial and non-chlamydial reactive arthritis (ReA) in a prospective study on 98 patients with acute/subacute arthritis. An inciting organism was found in 42 patients. Eighteen of these were chlamydial. Fifty-seven percent of all ReA patients were carriers for HLA-B27, which increased to 67% in the chlamydial group. Chlamydial ReA patients had more urethritis (P<0.05) with a longer period between arthritis and inciting infection, significantly lower CRP levels, and involved joint counts (P<0.05). Additionally, sacroiliitis was more frequent besides extra-articular manifestations in chlamydial ReA group. This study shows that chlamydial ReA differs in some points from non-chlamydial ReA, which in turn may affect the evaluation of an arthritic patient. ReA due to chlamydia more frequently encompasses a monoarticular or oligoarticular clinical picture with predominant distal extremity involvement. Non-chlamydial ReA presents higher joint counts and may involve upper extremity joints.     

Spondyloarthropathies: an overview

Abstract
Spondyloarthropathies are important and common inflammatory arthropathies that occur in approximately 2% of the population. They are often underrecognized. The diagnosis features the presence of asymmetrical, predominately lower limb arthritis and/or inflammatory back pain. The spondyloarthropathies can be subdivided into several disease subcategories, including ankylosing spondylitis, Reiter's/reactive arthritis, psoriatic arthritis, inflammatory bowel disease-associated arthritis and a large group of undifferentiated spondyloarthritis. The interactions between infectious agents and the individual's genetic background are important aetiological factors. Therapies for these conditions include physical therapy, non-steroidal anti-inflammatories and disease-modifying drugs. (Intern Med J 2002; 32: 40–46)     

Somatostatin analogue treatment attenuates histological findings of inflammation and increases mRNA expression of interleukin-1 beta in the articular tissues of rats with ongoing adjuvant-induced arthritis

Objective Somatostatin is a neuropeptide with modulatory effects on the immune system and the function of synovial cells; it has antiangiogenic and antiproliferative properties. This study aimed to evaluate the clinical, histological, and articular tissue cytokine mRNA response to somostatin treatment in rat adjuvant-induced arthritis (AIA).Methods Adjuvant-induced arthritis was induced in a total of 68 Lewis rats by immunization with complete Freunds adjuvant. Twenty-four rats were treated with a long-acting somostatin analogue 14 days after disease induction. Twenty-four untreated rats served as controls. The severity of arthritis was scored weekly for 42 days. In a second experiment, 20 rats (ten treated, ten controls) were killed 21 days after treatment for assessment of joint histopathology and articular tissue cytokine mRNA expression.Results Somatostatin analogue treatment significantly reduced histological scores of early inflammatory changes and increased articular tissue mRNA expression of interleukin-1 beta (IL-1). A trend toward improvement in physical scores of joint inflammation was seen in the treated group. Late destructive changes were not significantly different.Conclusion Treatment with a somostatin analogue attenuated early inflammatory changes in AIA joints and increased mRNA expression of IL-1 in the articular tissues of rats with ongoing arthritis. Improvement in the physical findings of joint inflammation was mild.     

A case report of monoarthritis in a COVID-19 patient and literature review: Simple actions for complex times

Rationale:COVID-19 presentation is multifaceted and up to 44% of patients affected by COVID-19 experience musculoskeletal complaints, mostly in the form of diffuse aspecific arthromyalgias. Nevertheless, only a few cases of arthritis following SARS-CoV2 infection are reported.Patient concerns:A 27-year-old man affected by nail psoriasis presented with monoarthritis 2 weeks after being diagnosed with COVID-19.Diagnoses:Diagnostic work-up and differential diagnosis were made difficult by patient isolation, absence of lab tests, and his visit via telemedicine, even though signs of first metacarpophalangeal joint involvement were clear.Interventions:Due to the inefficacy of acetaminophen and nonsteroidal anti-inflammatory drugs, the patient was prescribed oral steroids with a rapid benefit.Outcomes:The patient''s response to oral steroid was prompt and maintained even after therapy tapering. Even so, a formal diagnosis was not possible due to a difficult diagnostic work-up and lack of a long-term follow-up.Lessons:Like many other viral diseases, SARS-CoV2 can play as a causative agent or as a trigger for inflammatory arthritis development in predisposed individuals.     

Predictive factors in early arthritis: long-term follow-up

BACKGROUND: Because recent-onset inflammatory arthritis exhibits considerable clinical and prognostic variability, it is important to attempt to predict which patients are likely to have a poor prognosis as early as possible. Most prognostic studies have looked at patients who fulfilled proposed criteria for a definite diagnosis of rheumatoid arthritis (RA) or other well-defined conditions; less information exists concerning predictive factors for other types of early arthritis. OBJECTIVES: To examine prognosis in early arthritis, the authors assessed the long-term outcome in a cohort of patients who presented with inflammatory arthritis of short duration. Associations between outcome and patient clinical characteristics were analyzed to determine possible prognostic factors. METHODS: Since 1968, patients were selected to be followed up in 2 early-arthritis clinics if they had evidence of inflammatory joint disease and symptom duration was <1 year. Length of follow-up was variable, but was at least 1 year. At last follow-up, patients were classified as being in remission or as having persistent disease. Factors associated with a poor outcome were identified by using formal statistical methods. RESULTS: A total of 121 patients were included in this analysis. Mean disease duration to the first evaluation was 3 months, and median follow-up was 5 years (range, 1 to 30 months). Twenty-one patients (17%) had transient disease defined as total duration of <6 weeks. Sixty-three patients (52%) were in remission at final follow-up, with unclassified patients doing the best. Patients meeting criteria for RA or spondylarthropathies had more persistent disease. Polyarticular disease predicted more persistent disease (P <.05). In multivariable analyses, patients with initial hand involvement were much less likely to achieve remission of their disease (odds ratio, 0.18; 95% confidence interval, 0.05 to 0.66). Only 4 patients had either class 4 function or joint replacement. CONCLUSIONS: Our findings indicate that prognosis in early inflammatory arthritis is generally good, with more than half of all patients achieving remission in our cohort. Patients with unclassified arthritis fared better than those meeting criteria for RA or spondylarthropathy. Of the many clinical variables examined as possible prognostic factors, hand involvement was the strongest predictor of a poor outcome. RELEVANCE: The long follow-up of these patients with early arthritis provides clues for the clinician to the likely course and shows that many patients will do well.     

Rheumatoid arthritis: Evolving recognition of a common disease

Rheumatoid arthritis (RA) is a highly prevalent autoimmune disease and the most common form of autoimmune inflammatory arthritis. Studies of RA pathogenesis have contributed significantly to understanding the basis for complex immune-mediated disease, identified key steps in the development of autoimmune activation and joint damage in RA, and led to the development of targeted therapies that opened up the era biologic therapy. Current studies are linking differences in gene expression to abnormalities in cellular function that will help optimize therapy for individual patients and advance the goal of personalized medicine. Our evolving understanding and current important issues in RA are highlighted.