Evidence map›Paper›PMID 39039206›Full record

ReviewNature reviews. Endocrinology2024

Graves disease: latest understanding of pathogenesis and treatment options.

Giulia Lanzolla, Michele Marinò, Francesca Menconi

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Endocrinology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 6 pooled it
–field-weighted citation impact
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

64 citing papers in PubMed, 6 syntheses or guidelines pooled it.

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4 more citing papers are in PubMed but not listed here.

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

3 authors.

Giulia LanzollaDepartment of Clinical and Experimental Medicine, Endocrinology Unit II, University of Pisa and University Hospital of Pisa, Pisa, Italy.
Michele MarinòDepartment of Clinical and Experimental Medicine, Endocrinology Unit II, University of Pisa and University Hospital of Pisa, Pisa, Italy.
Francesca MenconiU.O. Endocrinologia II, Azienda Ospedaliero Universitaria Pisana, University Hospital of Pisa, Pisa, Italy. fmenconi.mail@gmail.com.ORCID http://orcid.org/0000-0003-2100-3123

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Graves disease is the most common cause of hyperthyroidism in iodine-sufficient areas. The main responsible mechanism is related to autoantibodies that bind and activate the thyrotropin receptor (TSHR). Although Graves hyperthyroidism is relatively common, no causal treatment options are available. Established treatment modalities are antithyroid drugs, which reduce thyroid hormone synthesis, radioactive iodine and surgery. However, emerging drugs that target the main autoantigen (monoclonal antibodies, small molecules, peptides) or block the immune pathway have been recently tested in clinical trials. Graves disease can involve the thyroid exclusively or it can be associated with extrathyroidal manifestations, among which Graves orbitopathy is the most common. The presence of Graves orbitopathy can change the management of the disease. An established treatment for moderate-to-severe Graves orbitopathy is intravenous glucocorticoids. However, recent advances in understanding the pathogenesis of Graves orbitopathy have allowed the development of new target-based therapies by blocking pro-inflammatory cytokine receptors, lymphocytic infiltration or the insulin-like growth factor 1 receptor (IGF1R), with several clinical trials providing promising results. This article reviews the new discoveries in the pathogenesis of Graves hyperthyroidism and Graves orbitopathy that offer several important tools in disease management.

Indexed as

Antithyroid AgentsGraves DiseaseGraves OphthalmopathyAutoantibodiesGlucocorticoidsHumansReceptor, IGF Type 1Receptors, ThyrotropinAntithyroid AgentsAutoantibodiesGlucocorticoidsReceptor, IGF Type 1Receptors, Thyrotropin

Identifiers

PMID39039206

What OpenQuestion holds

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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.