ReviewMediators of inflammation2019
Hints for Genetic and Clinical Differentiation of Adult-Onset Monogenic Autoinflammatory Diseases.
Review in Mediators of inflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
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.
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Who cites it
12 citing papers in PubMed, 99 citations in OpenAlex.
- Clinical and laboratory manifestations and treatment of children withWorld journal of clinical pediatrics · 2026Article
- Recurrent aseptic meningitis in adults: a potential indicator of undetermined autoinflammatory disease.Frontiers in immunology · 2026Article
- Real-world therapeutic strategies in active adult-onset Still's disease: clinical insights from the GIRRCS-AOSD study group.Frontiers in immunology · 2026Article
- Knowledge and Current Practices in Monogenic Uveitis: An International Survey by IUSG and AIDA Network.Ophthalmology and therapy · 2024Article
- What General Neurologists Should Know about Autoinflammatory Syndromes?Brain sciences · 2023Review
- Autoinflammatory diseases and the kidney.Immunologic research · 2023Review
- Review
- Rare genetic causes of meningitis and encephalitis.Encephalitis (Seoul, Korea) · 2022Review
- Improving Diagnosis and Clinical Management of Acquired Systemic Autoinflammatory Diseases.Journal of inflammation research · 2022Review
- The everchanging framework of autoinflammation.Internal and emergency medicine · 2021Review
- Children and Adults with PFAPA Syndrome: Similarities and Divergences in a Real-Life Clinical Setting.Advances in therapy · 2021Article
- Computational Modeling of NLRP3 Identifies Enhanced ATP Binding and Multimerization in Cryopyrin-Associated Periodic Syndromes.Frontiers in immunology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Monogenic autoinflammatory diseases (mAIDs) are inherited errors of innate immunity characterized by systemic inflammation recurring with variable frequency and involving the skin, serosal membranes, synovial membranes, joints, the gastrointestinal tube, and/or the central nervous system, with reactive amyloidosis as a potential severe long-term consequence. Although individually uncommon, all mAIDs set up an emerging chapter of internal medicine: recent findings have modified our knowledge regarding mAID pathophysiology and clarified that protean inflammatory symptoms can be variably associated with periodic fevers, depicting multiple specific conditions which usually start in childhood, such as familial Mediterranean fever, tumor necrosis factor receptor-associated periodic syndrome, cryopyrin-associated periodic syndrome, and mevalonate kinase deficiency. There are no evidence-based studies to establish which potential genotype analysis is the most appropriate in adult patients with clinical phenotypes suggestive of mAIDs. This review discusses genetic and clinical hints for an ideal diagnostic approach to mAIDs in adult patients, as their early identification is essential to prompt effective treatment and improve quality of life, and also highlights the most recent developments in the diagnostic work-up for the most frequent hereditary periodic febrile syndromes worldwide.
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Registered trials
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.