Bacterias son gatillos para autoinmunidad en Lupus eritematoso sistemico.
Commensal Bacteria May Be Involved In Triggering SLE In Genetically Predisposed Individuals, Research Suggests.
Medwire News (3/29, Barnard) reports, "Commensal bacteria may be involved in triggering systemic lupus erythematosus (SLE) in genetically predisposed individuals," researchers concluded after examining "bacteria taken from skin, mouth, and stool samples of 13 patients with SLE and seven healthy controls." The findings of the "proof-of-concept" study were published in Science Translational Medicine. Rheumatology News (3/29, Collins) also covers the study.
Dermatology
Chronic pruritus poses a significant burden on society in terms of healthcare cost and treatment challenges.
Additionally, many systemic diseases are also known to be associated with pruritus. Currently, the pathophysiology of pruritus is unclear, but we do know that the substance P/neurokinin 1 receptor (NK1R) pathway is critical in chronic pruritus.
In this original article, the authors evaluated the safety and efficacy of novel agent serlopitant, an NK1R antagonist, for treatment of chronic pruritus in patients with disparate dermatologic diseases and idiopathic pruritus.
In this study, serlopitant treatment resulted in a dose-dependent decrease in pruritus in all groups as well as improvement in the DLQI (quality-of-life assay). Nearly 45% of patients had a primary dermatologic disease. However, it should be noted that improvement in pruritus occurred in the treatment group regardless of the underlying dermatologic disease. This is particularly exciting as treatments for chronic pruritus are not particularly helpful. This was a small patient population, and the high placebo rates should not detract from the potential significance of this study.
This study also demonstrates that more research is needed in evaluating the basic pathophysiology of pruritus. If we are able to discover the key players and pathways in pruritus, we will be able to construct drugs that can target these pathways to block its effects.