Excess Productivity Costs of Systemic Lupus Erythematosus, Systemic Sclerosis, and Sjögren's Syndrome: A General Population–Based Study

2018 ◽  
Vol 71 (1) ◽  
pp. 142-154
Author(s):  
Natalie McCormick ◽  
Carlo A. Marra ◽  
Mohsen Sadatsafavi ◽  
Jacek A. Kopec ◽  
J. Antonio Aviña‐Zubieta
2017 ◽  
Vol 69 (6) ◽  
pp. 849-856 ◽  
Author(s):  
J. Antonio Aviña-Zubieta ◽  
Fergus To ◽  
Kateryna Vostretsova ◽  
Mary De Vera ◽  
Eric C. Sayre ◽  
...  

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Rossella Talotta ◽  
Fabiola Atzeni ◽  
Maria Chiara Ditto ◽  
Maria Chiara Gerardi ◽  
Piercarlo Sarzi-Puttini

Objective. To provide a narrative review of the most recent data concerning the involvement of the microbiome in the pathogenesis of connective tissue diseases (CTDs) and vasculitides.Methods. The PubMed database was searched for articles using combinations of words or terms that included systemic lupus erythematosus, systemic sclerosis, autoimmune myositis, Sjögren’s syndrome, undifferentiated and mixed CTD, vasculitis, microbiota, microbiome, and dysbiosis. Papers from the reference lists of the articles and book chapters were reviewed, and relevant publications were identified. Abstracts and articles written in languages other than English were excluded.Results.We found some evidence that dysbiosis participates in the pathogenesis of systemic lupus erythematosus, systemic sclerosis, Sjögren’s syndrome, and Behçet’s disease, but there are still few data concerning the role of dysbiosis in other CTDs or vasculitides.Conclusions.Numerous studies suggest that alterations in human microbiota may be involved in the pathogenesis of inflammatory arthritides as a result of the aberrant activation of the innate and adaptive immune responses. Only a few studies have explored the involvement of dysbiosis in other CTDs or vasculitides, and further research is needed.


2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
I. Missala ◽  
U. Kassner ◽  
E. Steinhagen-Thiessen

Objective. To investigate the association of lipoprotein(a) and atherosclerosis-related autoimmune diseases, to provide information on possible pathophysiologic mechanisms, and to give recommendations for Lp(a) determination and therapeutic options.Methods. We performed a systematic review of English language citations referring to the keywords “Lp(a)” AND “autoimmune disease” AND “atherosclerosis,” “Lp(a)” AND “immune system” OR “antiphospholipid (Hughes) syndrome (APS)” OR “rheumatoid arthritis” OR “Sjögren’s syndrome” OR “systemic lupus erythematosus” OR “systemic sclerosis” OR “systemic vasculitis” published between 1991 and 2011 using Medline database.Results. 22 out of 65 found articles were identified as relevant. Lp(a) association was highest in rheumatoid arthritis (RA), followed by systemic lupus erythematosus (SLE), moderate in APS and lowest in systemic sclerosis (SSc). There was no association found between Lp(a) and systemic vasculitis or Sjögren’s syndrome.Conclusion. Immune reactions are highly relevant in the pathophysiology of atherosclerosis, and patients with specific autoimmune diseases are at high risk for CVD. Elevated Lp(a) is an important risk factor for premature atherosclerosis and high Lp(a) levels are also associated with autoimmune diseases. Anti-Lp(a)-antibodies might be a possible explanation. Therapeutic approaches thus far include niacin, Lp(a)-apheresis, farnesoid x-receptor-agonists, and CETP-inhibitors being currently under investigation.


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