Results 181 to 190 of about 32,701 (297)
Success of transition to adult care in patients with pediatric‐onset chronic liver disease
Abstract Objectives Previous studies on chronic pediatric‐onset conditions have highlighted the risks of loss to follow‐up, disease progression, or therapeutic nonadherence during transition. However, very few studies have focused on liver diseases.
Sarah Mongbo +8 more
wiley +1 more source
Case Report: A case of focal segmental glomerulosclerosis in Wilson's disease induced by penicillamine. [PDF]
Li Q, Yang L, Zheng X, Zhang Y.
europepmc +1 more source
Current status of liver transplantation (Editorial) [PDF]
Koep, LJ, Putnam, CW, Starzl, TE
core
Abstract Metabolic dysfunction‐associated steatotic liver disease (MASLD) affects 30%–40% of youth with obesity and lacks approved pharmacologic therapies. In this single‐center retrospective case series at a tertiary care safety‐net children's hospital, we evaluated five adolescents (mean age: 17.0 years; 100% Hispanic; 60% male; mean body mass index:
Rachel Schenker +3 more
wiley +1 more source
Postoperative Outcomes Following Liver Transplantation for Wilson's Disease: A Systematic Review and Meta-Analysis. [PDF]
Wang A +8 more
europepmc +1 more source
Abstract Wilson disease (WD) is an autosomal recessive disorder of hepatic copper metabolism with varied clinical presentations. We describe a 15‐year‐old male referred for elevated aminotransferases, burning facial pruritis, scalp dysesthesias, and chronic bilateral lower extremity edema.
Tierra L. R. Mosher +2 more
wiley +1 more source
Sixty years of the first studies by Horácio Martins Canelas on Wilson's disease. [PDF]
Barbosa ER +5 more
europepmc +1 more source
A cross-sectional assessment of the diagnostic value of serum ceruloplasmin for Wilson's disease in children. [PDF]
Yaldany M +6 more
europepmc +1 more source
The utility of whole exome sequencing in diagnosing Wilson disease: A case report
Abstract Wilson disease (WD) is an autosomal recessive disorder of copper metabolism caused by mutations in the ATP7B gene, resulting in toxic copper accumulation in the body. Diagnosis is typically based on biochemistries, including low serum ceruloplasmin and elevated 24‐h urine copper excretion, with Kayser–Fleischer (KF) rings being a supportive ...
Mihir J. Palan +4 more
wiley +1 more source

