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Rhinology and Facial Plastics
Published in Adnan Darr, Karan Jolly, Jameel Muzaffar, ENT Vivas, 2023
Adnan Darr, Karan Jolly, Shahzada Ahmed, Claire Hopkins
Background: Common site: Fossa of RosenmullerRisk factors: South-Asian origin (Nitrosamines), EBV, geneticHLA-B17 associated with short-term survivalEBV: Early: Intra-cellular antigen (IgA EA)Later: Viral capsule antigen (IgA VCA) – later and most specific finding in NPCEschelon nodes: Retropharyngeal
Psoriatic Arthritis
Published in Jason Liebowitz, Philip Seo, David Hellmann, Michael Zeide, Clinical Innovation in Rheumatology, 2023
Elena Ciofoaia, Ana-Maria Orbai, Jason Liebowitz
HLA-B27 is positive in 25% of patients with PsA. The psoriasis phenotype results from two patterns of MHC effect. One phenotype is mediated by HLA-B alleles, particularly by B27, and it correlates more with musculoskeletal involvement rather than with skin disease. The second phenotype is the classic psoriasis susceptibility of gene C*06, which confers more penetrant skin disease with less prevalent and more time-dependent musculoskeletal symptom development (Winchester, 2012). Studies comparing HLA antigens between patients with psoriasis and PsA have shown that HLA-B13, HLA-B16, HLA-B17, and HLA-Cw6 are associated with psoriasis with or without arthritis, while HLA-B27 and HLA-B7 are specifically associated with PsA (Gladman et al., 1986, 1999). Researchers have also shown an association of HLA-B13, B17, B19, B37, B39, and Cw6 with synovitis and an association of HLA-B27 with axial disease, especially bilateral sacroiliitis (McGonagle, 2001). In PsA there is a stronger association with HLA-B than with HLA-C alleles. There is an association of HLA-C*06 with the form of PsA that demonstrates early onset of skin psoriasis. HLA-C*12/B*38, HLA-B*27 and HLA-C*06/B*57 are haplotypes (alleles) strongly associated with PsA; however, since patients with PsA also have psoriasis, it is difficult to determine whether the primary association is with arthritis or psoriasis (Chandran, 2013).
Psoriasis and lichen planus
Published in Ronald Marks, Richard Motley, Common Skin Diseases, 2019
Psoriasis is associated with human leucocyte antigen (HLA) groups HLA-B13, HLA-B17 and HLA-B37 as well as with the class II antigen DR7. It is even more strongly associated with CW6 – increasing the risk of the disease some 13 times in Caucasians.
Pathogenesis of adult onset still’s disease: current understanding and new insights
Published in Expert Review of Clinical Immunology, 2018
Piero Ruscitti, Roberto Giacomelli
Concerning pathogenesis, AOSD is categorized as a multigenic autoinflammatory disease [18]. It is defined a disorder at the ‘crossroads’ of autoinflammatory and autoimmune diseases, because of the involvement of both arms of immune system, innate and adaptive ones [18]. In this context, unknown factor(s) could act as second hit in genetic susceptible patients; thus, triggering the pathogenic immune response associated with the disease [18,19]. Regarding the genetic background, despite a familial trend has not been described so far, an association of the disease with different susceptibility genes has been proposed [19]. AOSD could be associated with some HLA antigens, such as HLA-B17, -B18, -B35, -DR2 and -DR4 [20]. Polymorphisms in both interleukin (IL)-18 gene and in macrophage migration inhibitory factor (MIF) gene are suggested to be involved [21,22]. Finally, rare variants in MEFV and TNFRSF1, genes implicated in genetic periodic fevers, have been identified in AOSD [23]. Concerning the triggers, due to the abrupt onset and the seasonality, an infectious trigger could be suggested [1,4]. Both viruses and bacteria have been implicated [18,19], but a unique and defined trigger has been not fully identified yet.
Interleukin-6 inhibition: a therapeutic strategy for the management of adult-onset Still’s disease
Published in Expert Opinion on Biological Therapy, 2022
Although familial aggregation has not been reported in adult-onset Still’s disease, some genetic studies have shown associations of the disease with HLA antigens, including HLA-B17, -B18, -B35, and -DR2 [15]. Recently, several polymorphisms associated with genes relevant to the pathogenic mechanism of adult-onset Still’s disease have been reported. For example, a diplotype configuration covering two distinct promoter regions of the IL-18 gene was found to occur significantly more frequently in affected patients and was associated with higher serum IL-18 levels [16]. Additionally, functional promoter polymorphisms in the macrophage migration inhibitory factor (MIF) and IL-6 genes were shown to affect plasma MIF and IL-6 levels, respectively [17,18]