Immune checkpoint inhibitor use and tuberculosis: a systematic review of the literature.

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Citation: European Journal of Cancer. 132:168-175, 2020 06.PMID: 32375103Department: MedStar Georgetown University Hospital ResidentsForm of publication: Journal ArticleMedline article type(s): Journal ArticleSubject headings: *Antineoplastic Agents, Immunological/ae [Adverse Effects] | *Neoplasms/dt [Drug Therapy] | *Tuberculosis/ci [Chemically Induced] | Aged | Aged, 80 and over | Female | Humans | Male | Middle Aged | Neoplasms/pa [Pathology] | Prognosis | Survival Rate | Tuberculosis/pa [Pathology]Year: 2020ISSN:
  • 0959-8049
Name of journal: European journal of cancer (Oxford, England : 1990)Abstract: BACKGROUND: An amassing body of evidence exists to support an association between the use of immune checkpoint inhibitors (ICIs) and the development of tuberculosis (TB).CONCLUSION: Findings from our systematic review indicate that PD-(L)1 inhibitors are linked to TB reactivation. TB activation can occur in various organs and TB-related fatalities have been reported. TB screening before starting immunotherapy should be considered in high-risk patient populations. Further research, including prospective studies with patients whose baseline TB status is known, is necessary to better understand the incidence of TB reactivation during ICI therapy and how best to manage TB that develops during immunotherapy. Copyright (c) 2020 Elsevier Ltd. All rights reserved.METHODS: We performed a systematic review of the literature to assess the nature of this relationship using PubMed, EMBASE and meeting proceedings.RESULTS: We have identified 16 patients who developed active TB during immunotherapy. Median age was 61 (range: 49-87). Twelve (75%) were male and 4 (25%) were female. Lung cancer was the most common type of cancer (n = 8), followed by melanoma (n = 3) and head and neck cancer (n = 3). Median time to TB reactivation after initiation of ICI therapy was 6.3 months (range: 1-24 months). Two (13%) patients died of complications of TB (spinal cord compression, GI perforation). TB reactivation in organs (pericardium, bone, liver, and GI track; one each) other than the lungs has been documented. We did not find any cases of TB reactivation that occurred during anti-CTLA-4 therapy.All authors: Kim C, Zaemes JOriginally published: European Journal of Cancer. 132:168-175, 2020 Jun.Fiscal year: FY2020Digital Object Identifier: Date added to catalog: 2020-07-09
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Journal Article MedStar Authors Catalog Article 32375103 Available 32375103

BACKGROUND: An amassing body of evidence exists to support an association between the use of immune checkpoint inhibitors (ICIs) and the development of tuberculosis (TB).

CONCLUSION: Findings from our systematic review indicate that PD-(L)1 inhibitors are linked to TB reactivation. TB activation can occur in various organs and TB-related fatalities have been reported. TB screening before starting immunotherapy should be considered in high-risk patient populations. Further research, including prospective studies with patients whose baseline TB status is known, is necessary to better understand the incidence of TB reactivation during ICI therapy and how best to manage TB that develops during immunotherapy. Copyright (c) 2020 Elsevier Ltd. All rights reserved.

METHODS: We performed a systematic review of the literature to assess the nature of this relationship using PubMed, EMBASE and meeting proceedings.

RESULTS: We have identified 16 patients who developed active TB during immunotherapy. Median age was 61 (range: 49-87). Twelve (75%) were male and 4 (25%) were female. Lung cancer was the most common type of cancer (n = 8), followed by melanoma (n = 3) and head and neck cancer (n = 3). Median time to TB reactivation after initiation of ICI therapy was 6.3 months (range: 1-24 months). Two (13%) patients died of complications of TB (spinal cord compression, GI perforation). TB reactivation in organs (pericardium, bone, liver, and GI track; one each) other than the lungs has been documented. We did not find any cases of TB reactivation that occurred during anti-CTLA-4 therapy.

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