ReviewJournal of clinical research in pediatric endocrinology2017
Genetic Causes of Rickets.
Review in Journal of clinical research in pediatric endocrinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 2 of them syntheses 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
44 citing papers in PubMed, 2 syntheses or guidelines pooled it, 88 citations in OpenAlex.
- X-linked hypophosphatemia and spinal cord compression: a systematic review and illustrative case.Acta neurochirurgica · 2026Pooled it
- Evaluating whole genome sequencing for rare diseases in newborn screening: evidence synthesis from a series of systematic reviews.Health technology assessment (Winchester, England) · 2025Pooled it
- SGK3 promoter deletion in late-onset hypophosphatemic rickets, a possible genetic cause of the disease.Orphanet journal of rare diseases · 2026Article
- A new metabolic path in type 3 rickets.The FEBS journal · 2026Review
- Biologics for bone regeneration: advances in cell, protein, gene, and mRNA therapies.Bone research · 2026Review
- Long-term epidemiological insights into rickets: a nationwide population-based retrospective study.Clinical and experimental pediatrics · 2025Article
- Clinical and Laboratory Characteristics of Patients with Genetic Rickets: A Single-Center Experience with Long-Term Outcomes.Turkish archives of pediatrics · 2025Article
- Phenotypes and Genotypes of Children with Vitamin D-Dependent Rickets Type 1A: A Single Tertiary Pediatric Center in Vietnam.Diagnostics (Basel, Switzerland) · 2025Article
- Genetic Polymorphisms in Cytochrome P450 Enzymes Involved in Vitamin D Metabolism and the Vitamin D Receptor: Their Clinical Relevance.Journal of personalized medicine · 2025Review
- HeterozygousFrontiers in physiology · 2025Article
- Rickets Types and Treatment with Vitamin D and Analogues.Nutrients · 2024Review
- Article
- Alopecia with Vitamin D-Dependent Rickets Type 2 A: A Case Report.Clinical, cosmetic and investigational dermatology · 2024Article
- Rickets is Not Always Nutritional!Indian journal of pediatrics · 2023Article
- Exome Sequencing in Monogenic Forms of Rickets.Indian journal of pediatrics · 2023Article
- De Novo Large Deletions in theDiagnostics (Basel, Switzerland) · 2023Article
- An overview of CYP27B1 enzyme mutation and management: A case report and review of the literature.Clinical case reports · 2023Article
- Genetic Forms of Calciopenic Rickets.The Eurasian journal of medicine · 2022Article
- Identification of six novel variants from nine Chinese families with hypophosphatemic rickets.BMC medical genomics · 2022Article
- Vitamin D and Its Receptor from a Structural Perspective.Nutrients · 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
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rickets is a metabolic bone disease that develops as a result of inadequate mineralization of growing bone due to disruption of calcium, phosphorus and/or vitamin D metabolism. Nutritional rickets remains a significant child health problem in developing countries. In addition, several rare genetic causes of rickets have also been described, which can be divided into two groups. The first group consists of genetic disorders of vitamin D biosynthesis and action, such as vitamin D-dependent rickets type 1A (VDDR1A), vitamin D-dependent rickets type 1B (VDDR1B), vitamin D-dependent rickets type 2A (VDDR2A), and vitamin D-dependent rickets type 2B (VDDR2B). The second group involves genetic disorders of excessive renal phosphate loss (hereditary hypophosphatemic rickets) due to impairment in renal tubular phosphate reabsorption as a result of FGF23-related or FGF23-independent causes. In this review, we focus on clinical, laboratory and genetic characteristics of various types of hereditary rickets as well as differential diagnosis and treatment approaches.
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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.