Evidence map›Paper›PMID 30746508›Full record

ArticleJournal of the Endocrine Society2019

Immune Checkpoint Blockade Anti-PD-L1 as a Trigger for Autoimmune Polyendocrine Syndrome.

Giulia Lanzolla, Alberto Coppelli, Mirco Cosottini, Stefano Del Prato, Claudio Marcocci, Isabella Lupi

Open access · goldAbstract readCase Reports
In one paragraph

Article in Journal of the Endocrine Society, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 3 pooled it
6.5field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 3 syntheses or guidelines pooled it, 62 citations in OpenAlex.

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  10. Blockade of trans PD-L1 interaction with CD80 augments antitumor immunity.Proceedings of the National Academy of Sciences of the United States of America · 2023
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Giulia LanzollaEndocrinology Unit, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
Alberto CoppelliDiabetes Unit, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
Mirco CosottiniNeuroradiology, Department of Translational Research and New Technologies in Medicine and Surgery, University Hospital Pisa, Pisa, Italy.
Stefano Del PratoDiabetes Unit, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
Claudio MarcocciEndocrinology Unit, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
Isabella LupiEndocrinology Unit, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.ORCID 0000-0003-1010-3110
University of Pisa · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

contextThe programmed cell death protein 1 (PD-1)/programmed cell death protein ligand 1 (PD-L1) pathway is a key regulator in T-cell activation and tolerance, limiting effector T-cell function in peripheral tissues. Atezolizumab, an anti-PD-L1 monoclonal antibody, is approved for treatment of some types of advanced cancer. Its main treatment-related adverse events are immune related, such as thyroid dysfunction and hypophysitis. Autoimmune endocrinopathy can occur as isolated manifestations; only a few cases of autoimmune polyendocrine syndromes have been reported thus far. CASE: We report a case of polyendocrine syndrome type 2, characterized by Addison disease (AD), type 1 diabetes mellitus (T1DM), accompanied by hypophysitis, in a patient treated with atezolizumab. Testing was positive for 21-hydroxylase and pituitary antibodies and negative for islet cells antibodies. HLA typing revealed DRB1*04 and DQB1*03 haplotypes, which are associated with increased susceptibility to T1DM and AD.

conclusionThe type and severity of immune-related adverse events in polyendocrine syndrome type 2 are different and depend on the monoclonal antibody used. Although the numerous molecular mechanisms inducing autoimmune endocrine diseases are still unclear, a link exists between HLA haplotypes, gene variants involved in immune checkpoint molecule expression, and increased susceptibility to autoimmune endocrinopathies. Additional studies are needed to identify susceptible patients and adapt therapy to each patient.

Indexed as

Addison diseasediabetes mellitushypophysitisimmune checkpoint inhibitors

Identifiers

PMID30746508
PMCPMC6364624
OpenAlexW2910529725

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.