Observational studyMedicine2018
Familial screening of children with Wilson disease: Necessity of screening in previous generation and screening methods.
Observational study in Medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 9 citations in OpenAlex.
- Spectrum and classification ofSaudi medical journal · 2025Article
- Therapeutic strategies in Wilson disease: pathophysiology and mode of action.Annals of translational medicine · 2021Review
- Population screening and diagnostic strategies in screening family members of Wilson's disease patients.Annals of translational medicine · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Wilson disease (WD) is an autosomal recessive genetic disorder associated with copper metabolism. Early diagnosis and therapy can result in good prognosis of WD. Thus, it is highly recommended to perform familial screening. In this study, we aimed to investigate the range of familial screening of children with WD and determine the appropriate screening methods.We enrolled 20 children with WD and 50 family members of each of these patients (40 parents and 10 siblings). All the subjects underwent a physical examination, Kayser-Fleischer (K-F) rings in the cornea, abdominal ultrasonography (Abdl Ur), cranial magnetic resonance imaging (MRI), serum ceruloplasmin, serum copper, 24-hour urine copper, blood alanine transaminase (ALT) and aspartate transaminase (AST), and ATP7B gene.Two new patients with presymptomatic WD (1 mother and 1 brother) in 2 families were found by screening. They had no clinical symptoms and K-F rings in corneal. Biochemical examination indicated decreased serum ceruloplasmin and serum copper in the mother and decreased serum ceruloplasmin in the brother. Gene sequencing revealed compound heterozygous mutations in them. In addition, 48 heterozygous carriers of Wilson disease (WHDzc) were found in this study. The levels of ceruloplasmin and serum copper in patients of WD were significantly less than WHDzc and 24-hour urinary copper were significantly higher than WHDzc (P = .000). The biochemical profiles of WD and WDHzc overlapped in range of 0.8 to 1.5 g/L in ceruloplasmin, above 9 μmol/L in serum copper and below 100 μg/24 h in urinary copper. Gene sequencing showed 2 pathological mutations in all patients with WD and 1 pathological mutation in all WDHzc.Not only siblings but also the previous generation of children probands with WD should be screened. Genetic testing should be conducted for the diagnosis of presymptomatic patients with WD.
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.