Overview of infections as an etiologic factor and complication in patients with vasculitides

Abstract

Vasculitides, a form of inflammatory autoimmune disease targeting the vessels, constitute an entity with significant morbidity and mortality. Infections have long been associated with vasculitides as a result of the incident immunosuppression following treatment induction and maintenance. Several microbial pathogens have been described as etiologic factors of infections in this patient population according to the type of vessels affected. Intense research has also been recently conducted in the interplay between vasculitides and certain viral infections, namely human immunodeficiency virus and severe acute respiratory syndrome coronavirus 2. Of note, a plethora of scientific evidence is available regarding the role of infections as triggering factors for vasculitides. Among the main mechanisms implicated in this direction are the activation of B and T cells, the direct endothelial insult, the immune complex-mediated vascular injury, and the cell-mediated, type IV hypersensitivity vessel damage. Therefore, this review aims to summarize all the available evidence concerning this bidirectional interplay between infections and vasculitides.

A clustering approach to improve our understanding of the genetic and phenotypic complexity of chronic kidney disease

“…For the clusters of 'Increased urate' and 'Increased inflammation,' the top traits were confirmed by the PheWAS. CKD is also associated with dyslipidemia comprising high levels of triglycerides and LDL-cholesterol, and low levels of HDL-cholesterol and apolipoprotein A1 [29] . We could observe similar associations in clusters 'Increased inflammation,' 'Reduced lipids,' and 'Reduced inflammation.'…”

High incidence of immune‐mediated inflammatory diseases in sepsis survivors: A nationwide exposed‐nonexposed epidemiological study

“…The strength and temporal pattern of the association between sepsis and increased risk of IMIDs suggest a causal relationship. Some IMIDs have been associated with specific pathogens, such as SLE and MS with Epstein-Barr virus, or polyarteritis nodosa with hepatitis B [16,[45][46][47]. The association between sepsis and IMIDs onset appeared well balanced across pathogen categories and viruses, bacteria, and parasites all induce multiple inflammatory cascades leading to the activation of innate and adaptive immune cells [48].…”

“…Incidences are presented per 100,000 patient-years. IMID incidences in general population, as reported in literature is presented as references[36][37][38][39][40][41][42][43][44][45][46][47][48]. AIHA, autoimmune hemolytic anemia; AAV, ANCAassociated vasculitis; ANCA, anti-neutrophil cytoplasmic antibody; BD, Behçet's disease; GCA, giant cell arteritis; IBD, inflammatory bowel disease; IMIDs, immune-mediated inflammatory diseases; ITP, immune thrombocytopenia; MS, multiple sclerosis; PMR, polymyalgia rheumatic; RA, rheumatoid arthritis; SLE, systemic lupus erythematosus; SS, Sjögren's syndrome; SSs, systemic sclerosis.…”

Hemophagocytic Lymphohistiocytosis and Anti-neutrophil Cytoplasmic Antibody-associated Vasculitis Possibly Caused by <i>Enterococcus faecalis</i> Infective Endocarditis

“…Infection can also trigger vasculitis through a variety of mechanisms, including the activation of autoreactive B and T cells, direct invasion of endothelial cells, cell-mediated type IV hypersensitivity, and immune complex-mediated vascular damage, including formation of ANCA ( 4 ). Recent studies have revealed various pathogenic mechanisms for ANCA formation during infection ( 5 ).…”

“…A study from Taiwan reported that infection-associated HLH is mostly caused by viruses (41%) but occasionally by mycobacteria (23%), bacteria (23%), and fungi (13%), with a high mortality rate without appropriate pathogen-specific therapy ( 2 ). In contrast, the association between infections and the formation of anti-neutrophil cytoplasmic antibodies (ANCAs) has been known for decades ( 3 , 4 ). A fraction of patients with infection-triggered ANCAs develop ANCA-associated vasculitis (AAV) ( 5 ).…”