Difficult to treat psoriatic arthritis - how should we manage?

Psoriatic arthritis (PsA) is a chronic, multi-domain immune-mediated inflammatory arthritis with a high disease burden. PsA patients have significant co-morbidities like obesity, depression, fibromyalgia which can impact disease activity assessment. The management of PsA has undergone a paradigm shift over the last decade due to the availability of multiple biologic and targeted synthetic disease modifying anti-rheumatic drugs. Despite the availability of multiple therapeutic agents, it is not uncommon to find patients not responding adequately and continuing to have active disease and/or high disease burden. In our review, we propose what is "difficult to treat PsA", discuss differential diagnosis, commonly overlooked factors, co-morbidities that affect treatment responses, and suggest a stepwise algorithm to manage these patients.

The arthritis connection to inflammatory bowel disease (IBD): why has it taken so long to understand it?

Inflammatory bowel disease (IBD) associated arthritis is a subgroup of spondyloarthritis (SpA) that has suffered from lack of recognition in rheumatology clinical and research circles for over 100 years. Although clinically distinguishable from rheumatoid arthritis and ankylosing spondylitis, it took advances in detection systems in the middle of the last century (rheumatoid factor, HLA-B27) to convincingly make the final separations. We now know that significant numbers of patients with SpA have associated clinical IBD and almost half of them show subclinical gut inflammation, yet the connection between the gut and the musculoskeletal system has remained a vexing problem. Two publications from Nathan Zvaifler (one in 1960, the other in 1975) presciently described the relationship between the gut and the spine/peripheral joints heralding much of the work present today in laboratories around the world trying to examine basic mechanisms for the connections (there are likely to be many) between the gut, the environment (presumably our intestinal flora) and the downstream effect on the musculoskeletal system. The role of dysregulated microbiome along with microbiome-driven T helper 17 cell expansion and immune cell migration to the joints has been recognised, all of which occur in the appropriate context of genetic background inside and outside of the human leucocyte antigen system. Moreover, different adhesion molecules that mediate immune cells homing to the gut and joints have been noted. In this review, we studied the origins and evolution of IBD-arthritis, proposed pathogenic mechanisms and the current gaps that need to be filled for a complete understanding of IBD-arthritis.

How Point-of-Care Ultrasound Led to a Diagnosis of May-Thurner Syndrome.

A 65-year-old man with a history of a left-sided inguinal hernia presented with three days of left-sided groin pain worsened with exertion and fatigue. The patient was afebrile but tachycardic, and physical examination revealed a tender, erythematous immobile bulge in his left groin. Laboratory studies revealed leukocytosis. Lymphadenopathy secondary to infectious or inflammatory etiology was suspected. However, point-of-care ultrasound (POCUS) identified extensive deep vein thrombosis (DVT) of the lower left limb. Follow-up imaging revealed this to be secondary to May-Thurner syndrome, a mechanical compression of an iliocaval vein against the lumbar vertebrae by a common iliac artery. This report demonstrates how POCUS can be used to identify lower extremity DVT, thereby expediting diagnosis and treatment and potentially preventing complications.

Spondyloarthritis evolution: what is in your history?

PURPOSE OF REVIEW: This review encompasses a detailed history of spondyloarthritis (SpA) evolution as early as the 17th century, continues on to the current concept of SpA, and ends with current gaps in our understandings of SpA. RECENT FINDINGS: Until the early 1960s, ankylosing spondylitis and other SpA family members were considered to be variants of rheumatoid arthritis (RA). The formal medical community separated them from RA at that time, and shortly thereafter they were recognized to be inter-connected based on shared clinical, laboratory, and imaging features. The last two decades have witnessed the formal distinction between axial and peripheral SpA and the connections that exist between nonradiographic and radiographic axial SpA. Recent studies have revealed different microbial compositions among patients with SpA and healthy controls and also between HLA-B27 positive and negative healthy individuals. SUMMARY: Further investigation of the roles of intestinal microbiome and physical force transduction toward SpA pathogenesis, strategies to improve delay in SpA diagnosis, biomarkers to better predict radiographic progression, and modification of current classification criteria to better address the axial and peripheral groups are gaps in our understandings that pose top priorities for SpA research.