ArticleCureus2020
Persistent Tenosynovitis, Steroid Dependency and a Hyperpigmented Scaly Macular Rash in a Child With Juvenile Idiopathic Arthritis.
Article in Cureus, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it, 4 citations in OpenAlex.
- Off-label use of canakinumab in pediatric rheumatology and rare diseases.Frontiers in medicine · 2022Pooled it
- Immunological analysis of Blau syndrome, a unique autoinflammatory state.Frontiers in immunology · 2026Review
- Safety and efficacy of canakinumab treatment for undifferentiated autoinflammatory diseases: the data of a retrospective cohort two-centered study.Frontiers in medicine · 2023Article
- Potential Benefits of TNF Targeting Therapy in Blau Syndrome, a NOD2-Associated Systemic Autoinflammatory Granulomatosis.Frontiers in immunology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Blau syndrome is a rare autoinflammatory disease, characterized by granulomatous symmetric arthritis, skin rash and uveitis. It is caused by mutations in the CARD15/NOD2 gene, which is a significant part of innate immunity. We describe the case of a patient with Blau syndrome, initially misdiagnosed as juvenile idiopathic arthritis. Genetic analysis showed R334Q mutation in the NOD2 gene that is known to be linked to Blau syndrome. Our patient was successfully treated with the IL-1β blocking agent canakinumab, with clinical and laboratory remission without any adverse effects. To our knowledge this is one of the rare cases of Blau syndrome successfully treated with canakinumab. After moving abroad, canakinumab was discontinued and she was treated with adalimumab instead. Change in her treatment resulted in a relapse of her disease. Prompt recognition of Blau syndrome and the optimal treatment, are vital for the prevention of severe sequelae such as vision loss and joint deformities. Canakinumab constitutes a promising therapeutic approach for Blau syndrome and requires further investigation.
Indexed as
Identifiers
What OpenQuestion holds
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.