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Hyperhidrosis and human leucocyte antigens in the Danish Blood Donor Study

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Familial clustering of the skin disease primary hyperhidrosis suggests a genetic component to the disease. The human leucocyte antigen (HLA) is implicated in a range of diseases, including many comorbidities to hyperhidrosis. No study has investigated whether the HLA genes are involved in the pathogenesis of hyperhidrosis. We, therefore, compared HLA alleles in individuals with and without hyperhidrosis in this study of 65 000 blood donors. In this retrospective cohort study, we retrieved information on individuals with and without hyperhidrosis using self-reported questionnaires, the Danish National Patient Registry and the Danish National Prescription Registry on participants recruited to the Danish Blood Donor Study between 2010 and 2019. Association tests using logistic regression were conducted for each HLA allele corrected for sex, age, body mass index, smoking and principal components. Overall, 145 of 65 795 (0.2%) participants had hospital diagnosed hyperhidrosis. Similarly, 1379 of 15 530 (8.9%) participants had moderate-severe self-reported hyperhidrosis, of whom 447 (2.9%) had severe self-reported hyperhidrosis. Altogether, 28 participants had both hospital diagnosed and moderate-severe self-reported hyperhidrosis. Severe self-reported hyperhidrosis was associated with HLA-A*80:01 (adjusted odds ratio 26.97; 95% confidence interval 5.32-136.70; n = 7; P <.001). Moderate-severe self-reported hyperhidrosis and hospital diagnosed hyperhidrosis were not associated with any HLA. The association between hyperhidrosis and HLA-A*80:01 was based on a very small number of cases and not replicated in other patient subsets, and therefore likely a chance finding. Thus, this study suggests that genes other than the HLA are involved in the pathogenesis of hyperhidrosis.

OriginalsprogEngelsk
Artikelnummere13150
TidsskriftScandinavian Journal of Immunology
Vol/bind95
Udgave nummer5
Sider (fra-til)e13150
ISSN0300-9475
DOI
StatusUdgivet - maj 2022

Bibliografisk note

Funding Information:
Mattias AS Henning was provided a grant for research from the Leo Foundation, Denmark (grant number LF 18002). The generous support of the Leo Foundation, Denmark (grant number LF 18002), is gratefully acknowledged. Karina Banasik acknowledges the Novo Nordisk Foundation (grant NNF14CC0001 and NNF17OC0027594).

Funding Information:
Mattias AS Henning reports grants from Leo Foundation (Grant number LF‐18002), during the conduct of the study. Gregor BE Jemec reports grants and personal fees from Abbvie, personal fees from Coloplast, personal fees from Chemocentryx, personal fees from LEO pharma, grants from LEO Foundation, grants from Afyx, personal fees from Incyte, grants and personal fees from InflaRx, grants from Janssen‐Cilag, grants and personal fees from Novartis, grants and personal fees from UCB, grants from CSL Behring, grants from Regeneron, grants from Sanofi, personal fees from Kymera and personal fees from VielaBio, outside the submitted work. Christoffer Hother received support for the present manuscript from the Department of clinical immunology, University hospital of Copenhagen. Kristina Ibler, Christian Erikstrup, Kathrine Agergård Kaspersen, Henrik Hjalgrim, Henrik Ullum, Betina Sørensen, Karina Banasik, Kaspar Nielsen, Thomas Folkmann Hansen, Susanne Gjørup Sækmose, Ole Pedersen and Sisse R Ostrowski declare that they have no conflicts of interests. No study sponsor had any role in the study design; collection; analysis or interpretation of data; writing of the report or in the decision to submit the report for publication.

Funding Information:
Mattias AS Henning was provided a grant for research from the Leo Foundation, Denmark (grant number LF 18002). Karina Banasik acknowledges the Novo Nordisk Foundation (grant NNF14CC0001 and NNF17OC0027594)

Publisher Copyright:
© 2022 The Scandinavian Foundation for Immunology.

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