The Role of Propionibacterium acnes in the Pathogenesis of Sarcoidosis and Ulcerative Colitis: How This Connection May Inspire Novel Management of These Conditions.

A lesser-acknowledged role of Propionibacterium acnes is its effect on the development of sarcoidosis. This literature review not only further explores this association but also that of Propionibacterium acnes and other inflammatory conditions, such as ulcerative colitis and pyoderma gangrenosum, acne, ulcerative colitis syndrome (PAC syndrome). This article reviews the effect that isotretinoin, a commonly used treatment of acne, has on the pathogenesis of ulcerative colitis, and the immune dysregulation and genetic susceptibility of individuals prone to developing acne, sarcoidosis, and ulcerative colitis. Literature for this article review was obtained from PubMed by utilizing both regular keywords and medical subject heading (MeSH) subheadings for data gathering. Regular keywords were: Propionibacterium acnes, sarcoidosis, ulcerative colitis, and isotretinoin. MeSH subheadings used were: Propionibacterium acnes/immunology, Propionibacterium acnes/pathogenicity, Propionibacterium acnes/genetics, sarcoidosis/immunology, and sarcoidosis/genetics. Following the application of inclusion and exclusion criteria, a total of 5172 publications were obtained. A total of 5086 publications were removed due to a lack of relevancy to outcomes of interest. The remaining 86 publications from all the regular and MeSH keywords were selected due to relevancy to outcomes of interest. Following this, a refined manual search was done, with the removal of duplicates, and 33 publications from PubMed were selected for review. Following a review of these records, Propionibacterium acnes was repeatedly concluded to be a causative agent of sarcoidosis. Variable results for the association between Propionibacterium acnes and ulcerative colitis were found. Most studies showed no significant association between the use of isotretinoin and the development of ulcerative colitis. A strong overlapping role of genetic susceptibility and immune dysregulation in the pathogeneses of sarcoidosis, ulcerative colitis, and Propionibacterium acnes was found.

Restless Leg Syndrome in the Setting of Patients With End-Stage Renal Disease on Hemodialysis: A Literature Review.

Restless Leg Syndrome (RLS), or Willis-Ekbom disease (WED), is an irresistible urge to move the legs, predominantly while resting, sitting, or sleeping, which disrupts sleep and impairs quality of life. RLS can occur secondary to uremia in chronic kidney disease (CKD) patients due to inadequate hemodialysis. Early diagnosis is essential to prevent muscular atrophy and to improve the quality of life of RLS patients, especially those with end-stage renal disease (ESRD). Cardiac mortality high in uremic RLS patients due to associated discomfort and lowering the duration of hemodialysis treatment. This review focuses on and discusses the diagnosis, treatment, and associated comorbid conditions of uremic RLS. Though the exact pathophysiology is unknown, altered transferrin expression in the choroid plexus, increased glutamate levels in the thalamus, decreased opioid receptors, dopamine system dysfunction, calcium/phosphate imbalance, and single nucleotide polymorphisms in the BTBD9 and MEIS1 genes are a few nonconfirmatory pathophysiological concepts for uremic RLS. Nonpharmacological options include lowering the temperature of dialysate by 1 degree C and home-based therapies like massages, warm/cold baths, and aerobic exercises. Pharmacological therapy like dopamine agonists ropinirole and pramipexole reduces the symptoms effectively. However, surgical options like parathyroidectomy and renal transplantation are stated as the best treatment options in patients suffering from uremic RLS.

Mechanisms of Beta-Blocker Induced Psoriasis, and Psoriasis De Novo at the Cellular Level.

Beta-blockers are a commonly prescribed medication, but the increase in use goes hand in hand with increasing side effects; one of particular interest lately has been its dermatological reactions. Although rare, beta-blockers can exacerbate pre-existing psoriasis and also cause de novo psoriasis in patients naïve to the disease. The mechanism by which this occurs is still unclear, although numerous articles have been published throughout the years as to how this unusual effect takes place. The most common mechanism suggests that beta-blockers cause intracellular changes in calcium, affecting both keratinocyte proliferation and granulocyte function via decreased cyclic adenosine monophosphate (cAMP) levels. Several inflammatory mediators are known to play a role, as well as reduced expression and desensitization of the beta-adrenergic receptor itself. We discuss these posed pathways in-depth and how each contributes to the worsening or formation of new psoriasis. With this knowledge, future physicians may be more mindful of this side effect should it occur, and why they occur, to better manage our patients on this widely used medication.