ArticleHealth science reports2025
Vitamin D Deficiency as a Debatable Modulator of Outcomes in Transfusion-Dependent Thalassemia; An Overview of the Latest Findings: A Narrative Review.
Article in Health science reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Use of romosozumab for osteoporosis in β-thalassemia major.JBMR plus · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background and Aims: Vitamin D deficiency (VDD) is highly prevalent in transfusion-dependent thalassemia (TDT), yet its clinical implications beyond bone health remain controversial. This review explores the risk factors and clinical outcomes of VDD in TDT, with particular focus on its potential roles in cardiac iron deposition, osteoporosis, and musculoskeletal growth disturbances. Methods: We conducted a comprehensive narrative review of 72 eligible studies published between 2003 and 2024, including observational, interventional, and genetic association studies. Databases searched were PubMed, Google Scholar (top 100 records), ScienceDirect, Cochrane Library, Springer, Web of Science, and Wiley Online Library, using keywords such as "thalassemia," "vitamin D," "siderosis," "osteoporosis," and "cardiac dysfunction." Results: VDD in TDT is multifactorial, with key drivers including aging, hepatic iron overload (ferritin > 1000 ng/mL; OR 2.31-2.62), endocrine dysfunction, and VDR polymorphisms (e.g., FokI/ff). More than 60% of TDT patients remain vitamin D deficient despite supplementation. VDD is associated with reduced bone mineral density, impaired growth and development, rickets, osteomalacia, and musculoskeletal weakness. Cardiovascularly, VDD independently correlates with cardiac iron deposition (via l-type calcium channels), elevated PTH, and NT-proBNP, contributing to left ventricular dysfunction (ejection fraction Conclusion: VDD is a critical and underappreciated modulator of cardiac and skeletal complications in TDT. While vitamin D supplementation improves calcium metabolism and reduces secondary hyperparathyroidism, its ability to reverse osteoporosis and cardiac changes is limited unless combined with targeted treatments addressing other contributors, such as hypogonadism and iron overload. Further research is needed to clarify persistent VDD mechanisms in TDT.
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.