Data Entry: Please note that the research database will be replaced by UNIverse by the end of October 2023. Please enter your data into the system https://universe-intern.unibas.ch. Thanks

Login for users with Unibas email account...

Login for registered users without Unibas email account...

 
Secondary Antibody Deficiency Due to Endogenous Hypercortisolism
JournalArticle (Originalarbeit in einer wissenschaftlichen Zeitschrift)
 
ID 4600257
Author(s) Sarcevic, Jelena; Cavelti-Weder, Claudia; Berger, T. Christoph; Trendelenburg, Marten
Author(s) at UniBasel Sarcevic, Jelena
Cavelti-Weder, Claudia
Berger, Christoph
Trendelenburg, Marten
Year 2020
Title Secondary Antibody Deficiency Due to Endogenous Hypercortisolism
Journal Frontiers in Immunology
Volume 11
Pages / Article-Number 1435
Keywords hypogammaglobulinemia, immune deficiency, secondary antibody deficiency, endogenous hypercortisolism
Abstract Therapeutic corticosteroids have an immunosuppressive function involving several pathways, including lymphocytopenia and hypogammaglobulinemia. While these effects have been well-described in patients that received corticosteroids for therapeutic reasons, the effects of endogenous corticosteroids on the immune system are less well-understood. Here, we describe a 21-year old patient with hypercortisolism due to an ACTH producing thymic tumor. In this patient, we observed a decrease in some of the immunoglobulin classes, and in specific B and T cell populations that resembled effects caused by corticosteroid treatment. IgG levels were restored following treatment and normalization of the hypercortisolism.
Publisher Frontiers Media
ISSN/ISBN 1664-3224
URL https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7358340/
edoc-URL https://edoc.unibas.ch/77772/
Full Text on edoc No
Digital Object Identifier DOI 10.3389/fimmu.2020.01435
PubMed ID http://www.ncbi.nlm.nih.gov/pubmed/32733476
ISI-Number WOS:000553406200001
Document type (ISI) Article
 
   

MCSS v5.8 PRO. 0.373 sec, queries - 0.000 sec ©Universität Basel  |  Impressum   |    
30/04/2024