People with osteoarthritis have a higher component of neuropathic pain as compared to those with rheumatoid arthritis: A cross-sectional study.

Neuropathic pain may be present in a proportion of patients with osteoarthritis (OA) and rheumatoid arthritis (RA). Its presence may lead to the requirement of altered management approaches in these conditions. This study investigated the prevalence of neuropathic pain in OA as compared to that in RA. Patients with OA and RA were included cross-sectionally if they had no other known neuropathic disorder. The PainDETECT questionnaire was used to assess neuropathic pain. WOMAC and CDAI scores were used to assess disease severity in OA and RA respectively. 69 patients with OA with a mean WOMAC score of 53.30 ± 16.39 and 98 patients with RA with a mean CDAI of 25.48 ± 16.99 were compared. The median PainDETECT score for OA was 13 (0-30) and RA was 5 (0-37) [p<0.001]. 15 patients with OA and six patients with RA were highly likely to have neuropathic pain, while 15 patients with OA and 30 patients with RA were classified as possibly having neuropathic pain. Thus, the proportion of patients free from neuropathic pain was higher in the RA group (63.3%) than in the OA group (39.1%) [p = 0.003]. Both the prevalence and the severity of neuropathic pain were significantly higher in OA than in RA. These findings suggest that neuropathic pain is an important factor in OA, as in RA, and must be considered in management as well as in future research in both these conditions.

Diagnostic delays in systemic vasculitides.

Systemic vasculitides are among the less common disorders encountered in routine rheumatology practice. The low incidence and heterogeneous presentation at onset can potentially lead to delayed diagnosis. Not recognizing these in the early phase may prove detrimental, as some vasculitis may progress to a catastrophic course with major morbidity or mortality. The causes of diagnostic delay may vary among different types of vasculitis and may also be disease-, patient-, or physician-related. Disease-related factors include the myriad presentations with diverse and non-specific symptoms, mimicking other conditions like infections. In addition, some forms have prolonged prodromal phases before evident organ damage. Limited awareness among healthcare professionals, particularly outside rheumatology, and a lack of readily available diagnostic tools contribute to missed diagnoses. Delays in seeking care due to non-specific symptoms or lack of access to specialist care can worsen outcomes. The economic burden also increases with delayed diagnosis and damage accrual when the disease remains unrecognized or untreated for prolonged periods. Although the causes of vasculitis are numerous, including secondary causes, in this review, we focus on diagnostic delays in primary vasculitides and suggest potential steps to identify and treat these diseases early. These include educating both healthcare professionals and the public about the signs and symptoms of vasculitis; expanding the rheumatology workforce and facilitating timely referrals; implementing readily available and reliable tests for early detection; and streamlining care and diagnostic pathways. Such measures have the potential to improve the overall outcomes of the disease, with prolonged remission, minimal damage accrual, and improved quality of life.

RNAseq-based transcriptomics of treatment-naïve multi-inflammatory syndrome in children (MIS-C) demonstrates predominant activation of matrisome, innate and humoral immune pathways.

MIS-C is a rare, highly inflammatory state resembling incomplete Kawasaki disease, temporarily associated with COVID-19. The pathogenesis is not completely known. RNAseq was carried out on whole blood of six treatment-naïve MIS-C patients. This was compared against RNAseq transcriptomics data of five healthy controls (HC), four Kawasaki Disease (KD) and seven systemic Juvenile Idiopathic Arthritis (sJIA). Using PCA, MIS-C clustered separately from HC, KD and sJIA. Amongst the top 50 significant genes in the three comparisons with HC, KD, and sJIA, common genes were: TMCC2, ITGA2B, DMTN, GFI1B, PF4, QSER1, GRAP2, TUBB1. DSEA revealed that maximum number of hits for overexpressed pathways was for NABA matrisome activation when MIS-C was compared against HC. Cytokine stimulated cellular activation pathways, specifically IL-10 were downregulated. MIS-C had more activated pathways of neutrophil degranulation and acquired immune activation but less of coagulation system or heat-shock system involvement as compared to KD. As compared to sJIA, humoral immune response and complements were activated. Matrisome activation was higher, with increased cell-cell interaction and ECM signalling. This analysis revealed novel insights into the pathogenesis of MIS-C, including the potential role of matrisomes, humoral immune system and down-regulated interleukin-10 pathways.