ReviewCurrent rheumatology reports2000
Familial autoimmunity and the idiopathic inflammatory myopathies.
Review in Current rheumatology reports, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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
6 citing papers in PubMed, 36 citations in OpenAlex.
- Mitochondrial extracellular vesicles, autoimmunity and myocarditis.Frontiers in immunology · 2024Review
- Familial aggregation and heritability: a nationwide family-based study of idiopathic inflammatory myopathies.Annals of the rheumatic diseases · 2021Article
- Polymyositis and dermatomyositis - challenges in diagnosis and management.Journal of translational autoimmunity · 2019Article
- Evaluation and management of bradycardia in neonates and children.European journal of pediatrics · 2016Review
- Autoimmune joint diseases in Late Medieval skeletal sample from Croatia.Rheumatology international · 2010Article
- Concomitant diseases in a cohort of patients with idiopathic myositis during long-term follow-up.Clinical rheumatology · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many lines of evidence suggest that autoimmune diseases result from chronic immune activation following environmental exposures in genetically susceptible individuals. A genetic basis for autoimmunity is supported by twin and family studies, candidate gene investigations, animal models, and whole genome microsatellite scans. These findings predict, and clinical observations support, familial clustering of a number of individual autoimmune diseases, notably lupus, multiple sclerosis, type-1 diabetes mellitus, rheumatoid arthritis, and recently the idiopathic inflammatory myopathies. Yet, not only is the same autoimmune disease increased in prevalence in pedigrees of persons affected with a given disorder, but other autoimmune diseases are as well. We review these data and propose a hypothesis consistent with these findings. This model posits that a rheumatic disease, as currently classified, is actually composed of a number of elemental disorders. Each of these is defined by the minimal necessary and sufficient environmental exposures and genes that result in a pathology leading to a given sign-symptom complex.
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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.