Spectrum Of Rheumatic Diseases Research Articles

Air pollution exposure and auto-inflammatory and autoimmune diseases of the musculoskeletal system: a review of epidemiologic and mechanistic evidence.

Auto-inflammatory and autoimmune diseases of the musculoskeletal system can be perceived as a spectrum of rheumatic diseases, with the joints and connective tissues are eroded severely that progressively develop chronic inflammation and lesion. A wide range of risk factors represented by genetic and environmental factors have been uncovered by population-based surveys and experimental studies. Lately, the exposure to air pollution has been found to be potentially involved in the mechanisms of occurrence or development of such diseases, principally manifest in oxidative stress, local and systemic inflammation, and epigenetic modifications, as well as the mitochondrial dysfunction, which has been reported to participate in the intermediate links. The lungs might serve as a starting area of air pollutants, which would cause oxidative stress-induced bronchial-associated lymphoid tissue (iBALT) to further to influence T, B cells, and the secretion of pro-inflammatory cytokines. The binding of aromatic hydrocarbon receptor (AhR) to the corresponding contaminant ligands tends to regulate the reaction of Th17 and Tregs. Furthermore, air pollution components might spur on immune and inflammatory responses by damaging mitochondria that could interact with and exacerbate oxidative stress and pro-inflammatory cytokines. In this review, we focused on the association between air pollution and typical auto-inflammatory and autoimmune diseases of the musculoskeletal system, mainly including osteoarthritis (OA), rheumatoid arthritis (RA), spondyloarthritis (SpA) and juvenile idiopathic arthritis (JIA), and aim to collate the mechanisms involved and the potential channels. A complete summary and in-depth understanding of the autoimmune and inflammatory effects of air pollution exposure should hopefully contribute new perspectives on how to formulate better public health policies to alleviate the adverse health effects of air pollutants.

Canadian Rheumatology Association Annual Meeting, February 2-5, 2022.

The 76th Annual Meeting of the Canadian Rheumatology Association was held virtually on February 2-5, 2022. The program consisted of presentations covering original research, symposia, awards, and lectures. Highlights of the meeting include the following 2022 Award Winners: Distinguished Rheumatologist, John G. Hanly and Lori B. Tucker; Distinguished Teacher-Educator, Stephen Aaron; Emerging Investigator, Jessica Widdifield; Ian Watson Award for the Best Abstract on SLE Research by a Trainee, Maher Banjari; Phil Rosen Award for the Best Abstract on Clinical or Epidemiology Research by a Trainee, Molly Dushnicky; Best Abstract by a Rheumatology Resident, Wen Qi; Best Abstract on Basic Science Research by a Trainee, Omar Cruz Correa; Best Abstract by a Post-Graduate Research Trainee, Holly Philpott; Best Abstract on Quality Care Initiatives in Rheumatology, Michael Zeeman; Best Abstract by a Medical Student, Samir Magdy Iskander; Best Abstract by an Undergraduate Student, Daniel Onwuka; Best Abstract by a Rheumatology Post-Graduate Research Trainee, Jennifer Lee; Best Abstract on Research by Young Faculty, Nancy Maltez; Best Abstract on Pediatric Research by Young Faculty, Chelsea DeCoste; Best Abstract on Spondyloarthritis Research, Vanessa Ocampo; Practice Reflection Award, Gold, Bailey Dyck. Lectures and other events included: Keynote Lecture by Grace Wright: Towards Equity: Is Everyone in the Rheum Paving the Path to Equity with Diversity?; State of the Art Lecture by Tuhina Neogi: Pain Across the Spectrum of Rheumatic Diseases; Dunlop-Dottridge Lecture by Simon Carette: Vasculitis: What Have We Learned in the Past 50 Years?; and the Great Debate: Be it Resolved that the Rheumatology Healthcare Provider Is Responsible for Prescribing and Monitoring Physical Activity. Arguing for: Claire LeBlanc and Laura Passalent, and against: Arthur Bookman and Marie Clements-Baker. Topics including rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, Sjögren syndrome, psoriatic arthritis, spondyloarthritis, vasculitis, osteoarthritis, fibromyalgia, and their respective diagnoses, treatments, and outcomes are reflected in the abstracts, which we are pleased to publish in this issue of The Journal of Rheumatology.

Molecular Genetics of Rheumatoid Arthritis and Future Prospectus in Pakistan

The spectrum of rheumatic disease is wide and includes conditions with diverse pathology, although most have in common a heritable risk with a complex genetic basis. Over the past decade intense efforts have been done to understand the contribution of genotype to the expression of disease in terms of both basic pathogenesis and clinical characteristics. The dramatic improvement in technology and methodology has accelerated the pace of gene discovery in complex disorders in an exponential fashion. This review focuses on rheumatoid arthritis and describes some of the recently described genes that underlie this condition and the extent to which they overlap.

Rheumatology in Egypt: back to the future.

Medical knowledge in ancient Egypt had a remarkable reputation since rulers of other empires used to request the pharaoh to send them their best physician to treat their beloved ones. Many rheumatologic conditions as giant-cell arteritis, reactive arthritis and other forms of spondyloarthritis have been identified in ancient Egyptian materials. Rheumatologists in Egypt are enormously expanding and mastering the tools that aid them in enhancing the management of rheumatic diseases. More Egyptian rheumatologists are actively participating in the annual European League Against Rheumatism (EULAR) and American College of Rheumatology conferences and those attached to well known state of the art centers are increasing. EULAR certified Egyptian MSUS trainers are effectively performing regionally. This review throws light on the rheumatology practice in Egypt, its progress from ancient times passing through Egyptian medical healthcare services, education systems for rheumatologists, rheumatology associations, an overview on the spectrum of rheumatic diseases through publications in the field till future perspectives. Rheumatology in Egypt is an actively growing and dynamic specialty of medicine with considerable contributions to the world's literature. These days, persistent efforts are mandatory to raise the standard of clinical and basic research, to optimize clinical practice with regard to new biologics, to develop tailored and targeted therapies for the rheumatic diseases, and to meet the medical demands of the exponentially increasing Egyptian population. Opportunities and challenges discussed high-lighten future perspectives needed to boost the rheumatology practice in Egypt.

Nature versus nurture in the spectrum of rheumatic diseases: Classification of spondyloarthritis as autoimmune or autoinflammatory.

Spondyloarthritides (SpA) include inflammatory joint diseases with various clinical phenotypes that may also include the axial skeleton and/or entheses. SpA include psoriatic arthritis, reactive arthritis, enteropathic arthritis and ankylosing spondylitis; the latter is frequently associated with extra-articular manifestations, such as uveitis, psoriasis, and inflammatory bowel disease. SpA are associated with the HLA-B27 allele and recognize T cells as key pathogenetic players. In contrast to other rheumatic diseases, SpA affect women and men equally and are not associated with detectable serum autoantibodies. In addition, but opposite to rheumatoid arthritis, SpA are responsive to treatment regimens including IL-23 or IL-17-targeting biologics, yet are virtually unresponsive to steroid treatment. Based on these differences with prototypical autoimmune diseases, such as rheumatoid arthritis or connective tissue diseases, SpA may be better classified among autoinflammatory diseases, with a predominant innate immunity involvement. This would rank SpA closer to gouty arthritis and periodic fevers in the spectrum of rheumatic diseases, as opposed to autoimmune-predominant diseases. We herein provide available literature on risk factors associated with SpA in support of this hypothesis with a specific focus on genetic and environmental factors.

Effect of CD4 T-lymphocyte count and human immunodeficiency virus (HIV) infection stage on the prevalence and pattern of rheumatologic disease in HIV-infected patients in Zaria, North-Western Nigeria

Introduction Human immunodeficiency virus (HIV) infection is a scourge of the modern time. Occurring with high frequency in patients of all ages and both genders, and across all strata of the society, HIV being a systemic disease can affect the musculoskeletal system, and therefore, musculoskeletal disease maybe a presenting symptom of HIV infection. There is paucity of research on the effect of different stages of HIV and CD4 T-lymphocyte count on HIV rheumatological manifestations among Nigerian patients. This study aims at evaluating the effect of CD4 T-lymphocyte count and the stages of HIV on the prevalence and pattern of rheumatological disease in Nigerian patients with HIV infection. Objective To determine the effect of CD4 T-lymphocyte count and HIV stage on the occurrence and pattern of rheumatologic diseases among patients attending HIV clinic at Ahmadu Bello University Teaching Hospital, Zaria. Materials and Methods Between February 2011 and March 2012, 200 HIV-seropositive patients [consisting of 100 patients on combined antiretroviral therapy (cART) and 100 cART naive patients] and 200 age and gender-matched HIV-negative controls were screened for the presence of rheumatologic disease, using a validated interviewer administered questionnaire. Information gathered on patients included sociodemographic characteristics, risk factors for HIV infection, clinical and laboratory parameters. CD4 T-lymphocyte of HIV patients and controls were quantified using flow cytometry method. CD4 categorization of patients was performed using the Centre for Disease Control Criteria, and HIV staging was done using World Health Organization criteria. Those with rheumatologic diseases were diagnosed using the American College of Rheumatology classification criteria or, where not available, other well validated rheumatological classification criteria. Data obtained were analyzed using Statistical Package for Social Sciences window software version 17.0. A P value of Results Rheumatological disease was diagnosed in 56 (28%) of HIV-positive patients and 15 (7.5%) of HIV-negative control. The odd ratio for occurrence of rheumatologic disease in HIV-positive patients compared to control was 4.8 [95% confidence interval (CI) = 2.61–8.82, P = 0.001]. In 3% of HIV infected patients, rheumatologic disease was the reason for their 1st presentation. The spectrum of rheumatic disease seen in HIV-positive patients is as follows: HIV-associated polyarthritis in 13 (16.5%) patients, polyarthralgia in 10 (5%) patients, undifferentiated spondyloarthropathy and reactive arthritis in nine (4.5%) patients each, septic arthritis in five (2.5%), and Tuberculosis (TB) of the spine and pyomyositis in three (1.5%) patients each. CD4 T-lymphocyte count and HIV stages were independent determinants of HIV-associated rheumatologic disease. Conclusion Rheumatologic diseases occur more frequently in HIV-seropositive patients compared to HIV-negative controls, and low CD4 T-lymphocyte counts and advanced HIV stage are associated with higher prevalence of rheumatologic diseases.

Genetic epidemiology: disease susceptibility and severity.

Genetic factors are increasingly recognized to have an important contribution to the occurrence of both inflammatory and noninflammatory rheumatic disease. Although identifying the specific genetic mechanisms involved in the rheumatic diseases continues to present considerable challenges, the prospect of identifying individual gene action has been brought closer by a number of recent developments. These include newer approaches to phenotype definition, refinements in statistical tools for analysis, and the advent of newer technologies, including the use of microarrays. In this article, we review some of these developments together with the recent literature on the contribution of both broad and specific genetic factors to the spectrum of rheumatic disease. We also consider contemporary opinions on the potential impact of genetic discoveries to human health.

The characterisation and regulation of type 1 immune responses in psoriatic arthritis

Psoriatic arthritis (PsA) is a chronic inflammatory arthritis. It affects approximately 0.05% of the general population presenting as peripheral arthritis, axial disease or a combination of both. About 10% of patients with psoriasis suffer from PsA. Currently available therapies have limited efficacy with associated toxicity. PsA is therefore a common arthropathy for which novel therapies are urgently required. Our understanding of the role of the immune system in the pathogenesis of rheumatic disease has led to the development of specific targeted therapies. The identification of tumour necrosis factor alpha (TNFα) as a key player in the inflammatory response has been a major advance in the field of rheumatology. The effects of blocking this pro inflammatory molecule have resulted in dramatic clinical effects across the spectrum of rheumatic diseases. Unfortunately however there remain a proportion of non-responders and concerns have been raised surrounding the adverse effects of these therapies (Furst, Keystone et al. 2001). It is therefore important to continue to elucidate other key players in the inflammatory cascade that can be modified to achieve clinical response. A critical advance in understanding the immune system's role in driving inflammation has been the recognition of different functional subsets of T helper (Th) cells according to their cytokine profile. Techniques have evolved that enable us to achieve clarification of a true in vivo Th1 response by identifying cells in SF that spontaneously secrete IFNγ. In this thesis, spontaneously secreting cells were identified in SF of patients with active PsA. That such IFNγ expressing cells may have a pathogenic role in PsA is supported by the following observations: IFNγ is the prototype macrophage activator of TNFα that drives inflammation in psoriasis and PsA. IFNγ when tested as a potential treatment for psoriasis induced synovitis in a subset of patients. (O'Connell, Gerber et al. 1992). The injection of IFNγ into the skin induces hyperkeratosis (Fierlbeck, Rassner et al. 1990). Autologous Natural Killer T (NKT) cells, potent producers of IL-4 and IFNγ, are able to induce psoriasis in 'normal skin' grafted onto a SCID mouse (Nickoloff, Wrone- Smithetal. 1999). Those factors regulating the expression of IFNγ may therefore be of considerable interest as they may offer potential targets to modify Th1 responses in PsA. Cytokines such as interleukin 18 (IL-18) and interleukin 12 (IL-12) have been shown to regulate Th1 responses in animal models of arthritis (Leung, McInnes et al. 2000). Whether such cytokines are present and indeed induce inflammation in PsA is unknown. The first part of this thesis focuses on the characterisation of the predominant Th response in PsA and the identification of key regulatory cytokines such as IL-12 and IL-18 that may drive TNFα production and as such lead to inflammation. The presence of other regulatory cells capable of driving the inflammatory response was explored briefly. NKT cells are a subset of T cell, which secrete IFNγ and IL-4 depending on the predominant cytokine milieu (Hafner, Falk et al. 1999). A pathogenic role for NKT cells in psoriasis has been suggested. (Bonish, Jullien et al. 2000). The ability of synovial fluid mononuclear cells (SF MC) to proliferate and secrete TNFα in response to glycolipid presented to NK T cells was investigated. Although TNFα contributes directly to synovial inflammation, the blockade of TNFα does not protect completely against cartilage damage (Joosten, Helsen et al. 1999). IFNγ and IL- 17 have opposing effects on bone resorption. IFNγ inhibits bone resorption whereas IL-17 enhances resorption through the degradation or enhancement of TNF receptor associated factor 6 (TRAF6) respectively (Chabaud, Lubberts et al. 2001). The expression of IL-17 and the functional effects of this cytokine on MMP3 expression by fibroblasts were therefore studied as a final section in this thesis.

The spectrum of rheumatic diseases in Saudi Arabia.

The spectrum of rheumatic diseases seen in Saudi Arabia appeared to be broadly similar to that seen in the West although interesting differences were noted. Rheumatoid arthritis was the predominant inflammatory joint disease, but was less severe. Ankylosing spondylitis is probably rare among the Saudis. Brucellosis was an important cause of acute back pain. Osteoarthritis was characterized by frequent involvement of the knee while the hip was rarely involved. Environmental factors may be responsible for this disease pattern. Regional pain syndromes, associated with obesity, bad posture, and poor physical fitness were also frequent problems.

Study of Spectrum of Rheumatic Diseases in the Department of Physical Medicine & Rehabilitation, Chittagong Medical College Hospital, Bangladesh

Key words: rheumatic disorder; spectrum; teaching hospitalDOI: 10.3329/jcmcta.v20i1.4927 Journal of Chittagong Medical College Teachers' Association 2009: 20(1):6-11