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Other Reactions from Gloves
Published in Robert N. Phalen, Howard I. Maibach, Protective Gloves for Occupational Use, 2023
T. Bullock, A. Sood, J.S. Taylor
In 1984, Anderson and Maibach89 described multiple-application, delayed-onset CU to formalin as possibly related to certain textile reactions. The reaction appeared on normal skin after repeated open applications but only after a single application on diseased skin. Although they described this reaction as possibly a non-clinically relevant epiphenomenon, it could be relevant to unexplained glove reactions.
A Mycobacterial 65 kD Heat-Shock Protein and T Cells in Experimental Arthritis
Published in Thomas F. Kresina, Monoclonal Antibodies, Cytokines, and Arthritis, 2020
Willem van Eden, Claire J. P. Boog, Els J. M. Hogervorst, Marca H. M. Wauben, Ruurd van der Zee, Jan D. A. van Embden
From a number of bacterial and parasitic infections it has become apparent that members of the heat-shock protein (HSP) families are frequent and efficient inducers of immune reactivity (17). This may be related to their enhanced expression during the stress that bacteria undergo being within the hostile environment of the host. Be that as it may, the T cells of the AA model now have also shown that when part of a dead complex antigen, T cells may select the 65 kD protein to respond to, resulting in a pernicious form of autoimmune arthritis. It is tempting to speculate that this responsiveness to these conserved molecules may be similarly responsible for other forms of bacteria-induced autoimmune arthritides. Moreover, it seems attractive to assume that, in such cases, there is an additional role for the homologous endogenous counterpart expressed by the host tissues themselves in the disease. Such a role could be in serving as a target structure for the autoimmune reactivity triggered by the bacterial counterpart. Alternatively, responses directed at such endogenous HSPs could theoretically have an influence on their functioning as chaperone molecules, which could indirectly change processing or presentation, for instance in antigen presenting cells. This could, of course, indirectly contribute to inflammatory responses or cause additional immunologic epiphenomena in the disease process.
The Interaction Between Genetic Factors and Microorganisms in Ankylosing Spondylitis
Published in Irun R. Cohen, Perspectives on Autoimmunity, 2020
L. E. McGuigan, A. F. Geczy, J. K. Prendergast, L. I. Upfold
Even if our data were to gain universal acceptance, a great deal more has to be learned before any real progress can be made to unravel the mechanisms involved in the pathogenesis of AS. Although we have postulated that the cross-reactive bacteria may trigger AS in HLA-B27-positive individuals it may be worth introducing a word of caution. Indeed, the phenomenon we have observed in vitro may simply be an intriguing epiphenomenon of AS, entirely unrelated to the pathogenesis of the disease. A large cohort study of HLA-B27-positive normal individuals (i.e., HLA-B27-positive children of AS probands) examining the association between the acquisition of cross-reactive bacteria in the bowel flora and the subsequent development of AS needs to be performed before a cause-and-effect relationship between cross-reactive bacteria and AS can be established. Furthermore, the reasons for the unusual distribution of the lesions in AS and their propensity to form bone would still require explanation.
Aortic valve stenosis: drivers of disease progression and drug targets for therapeutic opportunities
Published in Expert Opinion on Therapeutic Targets, 2022
Giuseppe Pinto, Gabriele Fragasso
At last, to elucidate pathogenetic mechanisms of initiation and propagation of AS, several studies have tried to investigate potential genes implicated in genetic risk of aortic valve calcification. The familial aggregation of the disease has been established by a nationwide Swedish registry, highlighting a 3.5-fold increase in AS risk for having a sibling with the disease [36]. On the other hand, specific genetic variants have been shown to be associated with an increased risk of developing AS. In vitro studies have suggested a causative role for specific mutations [37], while many single nucleotide polymorphisms (SNPs) mainly involved in lipid and calcium metabolism have been identified [38,39]. Whether these mutations represent a key role in pathogenesis or an epiphenomenon remains to be established.
Pharmacological strategies for sexual recovery in men undergoing antipsychotic treatment
Published in Expert Opinion on Pharmacotherapy, 2022
Tommaso B. Jannini, Andrea Sansone, Rodolfo Rossi, Giorgio Di Lorenzo, Massimiliano Toscano, Alberto Siracusano, Emmanuele A. Jannini
All these risk factors for SD are commonly shared by people with psychiatric disorders. However, other than being simply isolated epiphenomena and independent from one another, they sometimes are both the cause and the expression of a worse clinical picture, that is a non-communicable chronic disease (NCD). World Health Organization defines NCDs as medical conditions that cannot be transmitted, featuring at least 3 months of chronicity and a progressive nature [119]. NCDs include the ‘Big Four’: cardiovascular diseases, type 2 diabetes mellitus, cancer, and chronic respiratory diseases. Evidence strongly suggests how NCDs have a high prevalence among mentally ill patients and how NCD-induced SD may be a significant marker of such conditions, with most of the time even facilitating their prevention, diagnosis, and treatment [21,119].
Management of open‐angle glaucoma by primary eye‐care practitioners: toward a personalised medicine approach
Published in Clinical and Experimental Optometry, 2021
Jack Phu, Ashish Agar, Henrietta Wang, Katherine Masselos, Michael Kalloniatis
An important clinical question is to ask whether the patient is likely to become visually impaired or blind within their lifetime. As expected from clinical trials in glaucoma, higher baseline intraocular pressure has been shown to be a risk factor for eventual progression to blindness. Age was more equivocal, with some studies82,83 reporting it to be a significant risk factor while others84,85 not finding an effect. The severity of disease at the point of diagnosis has been shown to be the most conclusive risk factor for eventual blindness, and it is possible that prevalence of blindness is largely driven by a cohort of fast‐progressing patients.82–86 Other factors, such as the presence of exfoliation, socio‐economic status, treatment compliance and efficacy, follow‐up and other demographic factors may simply be epiphenomena of a more severe disease presentation.