Inflammatory arthritis in HIV positive patients: A practical guide

Background: Musculoskeletal manifestations of the human immunodeficiency virus (HIV) have been described since the outset of the global HIV epidemic. Articular syndromes that have been described in association with HIV include HIV-associated arthropathy, seronegative spondyloarthropathies (SPA) (reactive arthritis, psoriatic arthritis (PsA) and undifferentiated SPA), rheumatoid arthritis (RA) and painful articular syndrome. Methods: We carried out a computer-assisted search of PubMed for the medical literature from January 1981 to January 2015 using the keywords HIV, acquired immune-deficiency syndrome, rheumatic manifestations, arthritis, spondyloarthropathy, anti-TNF and disease modifying antirheumatic drugs. Only English language literature was included and only studies involving adult human subjects were assessed. Results: There are challenges in the management of inflammatory arthritis in patients who are HIV-positive, including difficulties in the assessment of disease activity and limited information on the safety of immunosuppressive drugs in these individuals. Conclusions: This review focuses on the clinical characteristics of the inflammatory articular syndromes that have been described in association with HIV infection and discusses the therapeutic options for these patients

Basic science232. Certolizumab pegol prevents pro-inflammatory alterations in endothelial cell function

Background: Cardiovascular disease is a major comorbidity of rheumatoid arthritis (RA) and a leading cause of death. Chronic systemic inflammation involving tumour necrosis factor alpha (TNF) could contribute to endothelial activation and atherogenesis. A number of anti-TNF therapies are in current use for the treatment of RA, including certolizumab pegol (CZP), (Cimzia ®; UCB, Belgium). Anti-TNF therapy has been associated with reduced clinical cardiovascular disease risk and ameliorated vascular function in RA patients. However, the specific effects of TNF inhibitors on endothelial cell function are largely unknown. Our aim was to investigate the mechanisms underpinning CZP effects on TNF-activated human endothelial cells. Methods: Human aortic endothelial cells (HAoECs) were cultured in vitro and exposed to a) TNF alone, b) TNF plus CZP, or c) neither agent. Microarray analysis was used to examine the transcriptional profile of cells treated for 6 hrs and quantitative polymerase chain reaction (qPCR) analysed gene expression at 1, 3, 6 and 24 hrs. NF-κB localization and IκB degradation were investigated using immunocytochemistry, high content analysis and western blotting. Flow cytometry was conducted to detect microparticle release from HAoECs. Results: Transcriptional profiling revealed that while TNF alone had strong effects on endothelial gene expression, TNF and CZP in combination produced a global gene expression pattern similar to untreated control. The two most highly up-regulated genes in response to TNF treatment were adhesion molecules E-selectin and VCAM-1 (q 0.2 compared to control; p > 0.05 compared to TNF alone). The NF-κB pathway was confirmed as a downstream target of TNF-induced HAoEC activation, via nuclear translocation of NF-κB and degradation of IκB, effects which were abolished by treatment with CZP. In addition, flow cytometry detected an increased production of endothelial microparticles in TNF-activated HAoECs, which was prevented by treatment with CZP. Conclusions: We have found at a cellular level that a clinically available TNF inhibitor, CZP reduces the expression of adhesion molecule expression, and prevents TNF-induced activation of the NF-κB pathway. Furthermore, CZP prevents the production of microparticles by activated endothelial cells. This could be central to the prevention of inflammatory environments underlying these conditions and measurement of microparticles has potential as a novel prognostic marker for future cardiovascular events in this patient group. Disclosure statement: Y.A. received a research grant from UCB. I.B. received a research grant from UCB. S.H. received a research grant from UCB. All other authors have declared no conflicts of interes

Psoriatic Arthritis in HIV infected patients : a review

Fil: Adizie, T. Solihull Hospital. Rheumatology Department; United KingdomFil: Hodkinson, B. University of Cape Town. Groote Schuur Hospital. Department of Medicine; South AfricaFil: Espinoza, L. LSU Health Sciences Center. Department of Medicine. Section of Rheumatology; United StatesFil: Adebajo, A. University of Sheffield. Faculty of Medicine. Academic Rheumatology Group; United KingdomThe pathogenesis of psoriasis and psoriatic arthritis(PsA) in the setting of HIV infection is unclear , but an increase in prevalence of PsA has been observed in sub Saharan Africa since the HIV epidemic. Both the skin and joint disease is more severe and persistent in these patients, and is often refractory to traditional therapies. Traditional disease modifying antirheumatic drugs (DMARDs) as well as biologic DMARDs have been used with a good safety profile. The advent of antiretroviral therapy has changed the spectrum of rheumatological disease encountered with the immune reconstitution inflammatory syndrome (IRIS) emerging as an important syndrome. Further epidemiological data on the prevalence of psoriatic arthritis in HIV positive patients is required. This review will focus on the epidemiology, clinical presentation and management of PsA in HIV positive patients

Travel- and immigration-related problems in rheumatology.

Health problems are self-reported by up to 64% of travellers to the developing world. Traditionally, rheumatic symptoms are accorded little significance, but many travellers do return home with musculoskeletal complaints. The assessment of these patients is often hindered by the Western clinician's lack of familiarity with the types of infections that the patient may have encountered while travelling. Standard serological tests for autoimmune diseases can be unreliable in the setting of concomitant tropical infection, and these infections themselves can have musculoskeletal manifestations. Even in the absence of tropical infection, laboratory investigation of musculoskeletal symptoms in individuals of different ethnicities is challenging due to genetic and physiological variation. This review focusses on addressing the impact global migration has had on rheumatological clinical practice