Relationship Between <i>LTA4H</i> Promotor Polymorphism and Tuberculosis-Associated Immune Reconstitution Inflammatory Syndrome and Its Prevention With Prednisone-Reference-Cited by-同舟云学术

Relationship Between LTA4H Promotor Polymorphism and Tuberculosis-Associated Immune Reconstitution Inflammatory Syndrome and Its Prevention With Prednisone

Published:2023-07-01 Issue:7 Volume:10 Page:
ISSN:2328-8957
Container-title:Open Forum Infectious Diseases
language:en
Short-container-title:

Author:

Stek Cari¹²³^ORCID,Shey Muki¹³,Mnika Khuthala⁴,Schutz Charlotte¹³,Thienemann Friedrich¹³^ORCID,Wilkinson Robert J¹³⁵⁶,Lynen Lutgarde²,Meintjes Graeme¹³

Affiliation:

1. Wellcome Center for Infectious Diseases Research in Africa, Institute of Infectious Disease and Molecular Medicine, University of Cape Town , Cape Town , South Africa

2. Department of Clinical Sciences, Institute of Tropical Medicine , Antwerp , Belgium

3. Department of Medicine, University of Cape Town , Cape Town , South Africa

4. Division of Human Genetics, Department of Pathology, University of Cape Town , Cape Town , South Africa

5. Francis Crick Institute , London , United Kingdom

6. Department of Infectious Diseases, Imperial College London , London , United Kingdom

Abstract

Abstract The development of paradoxical tuberculosis-associated immune reconstitution inflammatory syndrome (TB-IRIS) and its prevention using prednisone may potentially be mediated by the LTA4H genotype. We assessed this hypothesis in a clinical trial evaluating prednisone to prevent TB-IRIS. We did not find an association between LTA4H genotype and TB-IRIS incidence or prednisone efficacy.

Funder

European and Developing Countries Clinical Trials Partnership

South African Government Department of Science and Technology

Wellcome Trust

Institute for Tropical Medicine

Francis Crick Institute

Publisher

Oxford University Press (OUP)

Subject

Infectious Diseases,Oncology

Link

https://academic.oup.com/ofid/advance-article-pdf/doi/10.1093/ofid/ofad379/50893932/ofad379.pdf

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