BALTIMORE—These timeless words from Sir William Osler, one of the preeminent physicians of the 19th and early 20th centuries, are often worth reflecting on as we consider how best to stay up to date in the field of rheumatology. At the 17th Annual Advances in the Diagnosis and Treatment of the Rheumatic Diseases meeting at Johns Hopkins University School of Medicine, Baltimore, Ana-Maria Orbai, MD, MHS, assistant professor of medicine and director of the Psoriatic Arthritis Program at Johns Hopkins University School of Medicine, followed Osler’s advice and provided outstanding clinical pearls by telling several patient stories.
Infection as a Trigger
Dr. Orbai began her lecture describing a 29-year-old grocery store clerk with a history of severe psoriatic arthritis (PsA) that included erosive arthritis, dactylitis, enthesitis, nail involvement and erythrodermic psoriasis as manifestations of his disease. Over the past year, he had experienced several complications related to both his worsening disease and sequelae of being on immunosuppressive medications.
When reflecting on his case, Dr. Orbai made the point that infection is a known trigger for flares in psoriatic disease. For example, strong evidence exists that a preceding tonsillar Streptococcus pyogenes infection can induce the onset of guttate psoriasis, and the exacerbation of psoriasis has been associated with skin and/or gut colonization by Staphylococcus aureus, Malassezia and Candida albicans.2
Acute infection should also be a consideration when evaluating for worsening arthritis or before committing to escalation of therapy. In this patient’s case, aspiration of a knee effusion revealed a white blood cell count of 135,000 cells/μL (normal range = 4,000–11,000 cells/μL), with 92% of these cells being polymorphonuclear lymphocytes. Although cultures from the synovial fluid did not yield bacteria growth, the clinical context and lab parameters were concerning for septic arthritis, and his condition was treated as such.
A review article from Siegel and Winthrop in 2019 noted that ustekinumab and biologics inhibiting interleukin (IL) 17 or IL-23 appear to have reduced infectious risk estimates compared with anti-tumor necrosis factor (TNF) therapies. The authors note that although infectious risks vary across biologics and small-molecule therapies for psoriasis and psoriatic arthritis, we still have limited real-world data to evaluate these risks.3
In a second patient story, Dr. Orbai described a 34-year-old office worker with PsA who had experienced recurrent dactylitis despite treatment with IL-12/23 inhibition, IL-17 inhibition and multiple anti-TNF therapies.
In discussing this patient, Dr. Orbai shared several important lessons, including: Dactylitis can occur in both the hands and the feet (and is, in fact, more common in the feet). Active disease can re-emerge even while a patient is on biologic treatment. Dactylitis is associated with radiographic progression. And flexor tenosynovitis is a common finding in patients with PsA.