Hot topic: menopause and inflammatory arthritis outcomes in RA and PsA Save

Across EULAR 2026 abstracts this year and presented in a session called “this is a woman’s world”, strong signals are emerging that the menopausal transition is associated with changes in disease phenotype, disease activity, and treatment response in both RA and PsA. 

In abstract OP0243, Perniola and colleagues use the large multicentre BIOPURE registry to examine how menopausal status influences disease severity and biologic treatment response in women with RA initiating bioDMARDs. Across 2,645 patients, postmenopausal women presented with a more severe immuno-radiographic phenotype compared to women of childbearing age, including higher RF/ACPA positivity (83.2% vs 76.8%), more erosive disease (47.1% vs 37.3%), and higher CRP levels, despite similar baseline DAS28-CRP and CDAI. Importantly, remission rates on bioDMARD therapy were significantly lower in postmenopausal women (53.6% vs 64.9%). However, stratified analyses suggest that this is not a treatment-refractory state per se: early remission remained achievable, particularly in bioDMARD-naïve patients and those without fibromyalgia. This suggests that menopause is associated with a distinct disease phenotype with reduced chances of remission and a potentially narrower therapeutic window. Longitudinal studies through the walk of life would be extremely helpful to understand if this is a dynamic hormonal driven change or part of a distinct phenotype present at diagnosis.

In abstract OP0246, Eder and colleagues extend this concept into PsA focusing specifically on the perimenopausal transition. Using a long-term prospective cohort spanning over 8,000 visits, they demonstrate a clear temporal association between perimenopause and worsening disease activity. DAPSA scores increased significantly during perimenopause compared with both pre- and post-menopausal phases (β ~1.9 vs pre-menopause), with consistent increases in tender and swollen joint counts, as well as PASI scores. Fatigue partially mediated the effect (explaining ~12–18% of the DAPSA increase), while BMI did not appear to play a significant role. Notably, disease activity appeared to improve again after menopause, suggesting a time-limited biological window rather than a sustained shift.

Taken together, these two studies describe complementary aspects of the same signal across RA and PsA. OP0243 suggests that postmenopausal status is associated with a more severe RA phenotype at the point of biologic initiation and lower probability of remission, while OP0246 demonstrates a dynamic increase in PsA disease activity specifically during the perimenopausal transition, with partial reversibility thereafter. 

This raises an important translational gap: while observational data now consistently show an effect of menopausal status on disease expression, interventional evidence remains extremely limited. Hormone replacement therapy is mentioned only indirectly, and there are currently no robust randomized trials testing whether hormonal modulation alters disease activity trajectories or treatment response in RA or PsA.