Chiefs’ Inquiry Corner – 12/31/2021

   Psoriatic arthritis (PsA) is increasingly found to cause progressive joint damage and disability. Management requires coordination between a primary care physician, dermatologist, and rheumatologist. The first line therapy for PsA is NSAIDs, while PsAs unresponsive to NSAIDs is typically managed with non-biologic DMARDs (ie Methotrexate or Leflunomide). However, persistent disease or flares that occurs beyond DMARD or NSAID therapy has typically not been treated with a steroid burst (unlike other inflammatory arthritides) due to concern for erythroderma and exacerbating pustular psoriasis skin lesions on steroid withdrawal after the burst course is completed. The American College of Rheumatology guidelines do not address or recommend steroids. However, several case reports show the use of corticosteroids in low doses (ie prednisone 5 mg, prednisolone 10 mg) with prolonged slow tapers in conjunction with a DMARD has been shown to prevent worsening joint disease. In summary: don’t start burst dose steroids in a psoriatic flare but there may be a role for considering prolonged courses of low dose steroids in controlling symptoms long term/

References: 2018 American College of Rheumatology/National Psoriasis Foundation Guideline for the Treatment of Psoriatic Arthritis

  Historically, there has been a well-established relationship between low density lipoprotein cholesterol (LDL-C) levels and cardiovascular risk. Lipid modifying therapy focuses on reducing LDL-C via several mechanisms. Recently attention has turned toward apolipoprotein B(apoB), as apoB-containing lipoproteins have a causal role in atherogenesis. One large prospective cohort analysis examined two patient populations – those without any baseline coronary artery disease or prior cardiovascular event and those who had established atherosclerosis. All patients had lipids collected (including apoB) and the endpoint was fatal or nonfatal myocardial infarction. On follow-up (11 years in primary prevention and 2.5 in secondary), only apoB remained associated with risk for MI after adjusting for other measures. Oher recent research this year has also suggested that in patients treated with statins already, apoB levels predicted residual risk for CV events. Our current guidelines do not take these levels into account in terms of guiding management, but the European guidelines do comment on apoB as the best marker of atherogenic lipoproteins – whether we see our guidelines change remains to be seen.

References: Association of Apolipoprotein B–Containing Lipoproteins and Risk of Myocardial Infarction in Individuals With and Without Atherosclerosis

 It has been previously shown in large epidemiologic studies that greater amounts of alcohol consumption over time are associated with incident development of atrial fibrillation (AF). The question of whether there is a temporal relationship between acute consumption of alcohol and subsequent episodes of AF has only been more recently examined. One recent study followed patients with continuous ambulatory cardiac monitoring and a transdermal ethanol sensor over 4 weeks. They showed a higher OR (2.02) of subsequent AF in patients who reported even 1 drink in the last 4 hours; the episodes also correlated to a higher blood alcohol concentration. Another recent study (I-STOP-Afib) examined self-selected individual triggers (such as alcohol, caffeine, decreased sleep) and followed patients after they participated in 1 week of exposure versus 1 week of avoidance. Alcohol was the only trigger associated with fewer episodes of AF during the avoidance phase, as measured by a smartphone based ECG. These studies suggest that in certain patients, avoidance of alcohol may be helpful in avoiding episodes of AF in the acute setting.

References: Individualized Studies of Triggers of Paroxysmal Atrial Fibrillation