Rheumatic musculoskeletal disease (RMD) patients when family planning must consider fertility, disease activity and management from pre-conception to lactation. We have developed, in conjunction with the National Maternity Hospital, Holles St., a dedicated Rheumatology Reproductive service for women with RMD. This service includes a comprehensive multidisciplinary team including a rheumatologist and rheumatology nurse specialist, obstetric and midwifery, maternal medicine, anaesthesia and pharmacy. We identify patients’ emotional and healthcare needs, provide expert advice and aim to achieve maintenance of good disease control and positive reproductive outcomes.   To date, ninety-eight women (mean age (range) = 35 years (19-48)) have been managed. The majority of patients (66%) had inflammatory arthritis and a minority connective tissue disease, vasculitis or other diagnosis. Following analysis of these data and literature review we established an evidence-based care pathway for women with RMD. In conclusion, we describe the first evidence-based reproductive care pathway for women with rheumatic musculoskeletal diseases RMDs in a unique rheumatology reproductive health service, RRHS.

The joints of patients with inflammatory arthritis (IA) show a complex microenvironment of neoangiogenesis, immune cell and fibroblast activation leading to inflammation and joint destruction. T cells play a key role in the pathogenesis of both Rheumatoid Arthritis and Psoriatic arthritis, with differential T cell populations associated with both diseases. It has now emerged that T cell subsets can exhibit functional plasticity, particularly, making it difficult to identify discrete T cell subsets on the basis of their cytokine production. Th17 cells appear to be particularly unstable under inflammatory conditions and can become so-called ex-Th17 cells or nonclassical Th1 cells, which start to produce IFN-γ with the eventual loss of IL-17 expression. Interestingly, we have shown enrichment of polyfunctional Th1, Th17 and Ex-Th17 cells in the periphery and synovial fluid of patients with RA and PsA. In addition, the frequency of polyfunctional T cells are associated with disease activity and response to therapy, suggesting they play a key pathogenic role in disease.  Regulatory T cells (Tregs) represent an important peripheral tolerance mechanism that serves to prevent autoimmunity, but fails to constrain inflammation in autoimmune diseases such as RA and PsA. Several studies examining Treg phenotype have reported a decrease in the frequency in peripheral blood of patients with RA/PsA compared with healthy control (HCs), however, studies have also demonstrated enrichment of Tregs at the site of inflammation.  However, they have reduced suppressive function thus allowing pathogenic polyfunctional CD161+ cells to further potentiate inflammation. In this study, we investigated the regulation of effector T cells taken from the RA SF by Tregs. The reduced suppression was in part mediated by the CD161⁺ Th cells, which exhibited enhanced pathogenicity which were resistant to Treg suppression.

In Rheumatology Reproductive Medicine clinic, RA and PsA patients wishing to achieve pregnancy are assessed when they present with active arthritis and intervention is designed to induce remission before conception. Patients are then followed and closely monitored during pregnancy and post-partum to assess disease activity and possible flare. Studies have shown increased frequency and function of Treg cells that are protective in RA patients who are pregnant, however little is known about polyfunctional T cells.

The present study will investigate effector T cells polyfunctionality and Treg cell function in patients with inflammatory arthritis who are pregnant in (i) remission; (ii) during disease flare, if it occurs; and (iii) post-partum.

RA is a complex autoimmune disease resulting from apparently stochastic interactions between genetic and environmental factors. Important environmental factors include smoking, especially heavy smoking, which is the greatest lifestyle risk factor for the development of RA. Environmental factors implicated in addition to smoking include education/social class, breastfeeding, body fat, vitamin D levels, and caffeine and alcohol consumption. According to the WHO, worldwide obesity has nearly tripled since 1975. In parallel with its increase in the general population, obesity has become increasingly common in RA patients.

BMI has been the obesity measure of choice in many previous studies in inflammatory arthritis. However, it has been shown that BMI is not an accurate anthropometric method to diagnose obesity, especially in individuals with altered body compositions (such as inflammatory arthritis patients) due to its inability to discriminate between lean mass and fat mass. Waist circumference has been shown to be superior to BMI in its correlation with visceral fat and has become the preferred measure for abdominal  obesity.Central obesity is defined as having a waist circumference of ≥94 cm in men and ≥80 cm in women The pro-inflammatory nature of fat tissue is now well established. These effects are mediated through the secretion of numerous pro-inflammatory cytokines by adipose tissue, coined adipokines. It is suggested that increased adiposity may have a role in the pathogenesis of inflammatory diseases, however the evidence is conflicting. Numerous studies have demonstrated a positive correlation between BMI and the risk of developing RA. An association between obesity and disease activity in RA has been reported in several previous studies. The Better Anti‐Rheumatic Farmacotherapy observational (BARFOT) study demonstrated that obese patients had higher disease activity and lower rates of remission). Obesity has also been associated with a reduced response to TNF-inhibitors (TNFi).

The aim of this study was to evaluate body composition in seropositive and seronegative rheumatoid arthritis (RA) and psoriatic arthritis (PsA) patients and assess associations with disease characteristics and baseline synovial arthroscopic findings. We will also access the effect of Obesity on immune cell responses.