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This study found that intravenous high dose calcium infusions followed by high dose oral calcium effectively treated vitamin D dependent rickets type II, leading to complete biochemical and radiological healing and improved growth in two patients.

This case study reported that absence of alopecia does not reliably predict responsiveness to vitamin D treatment in Vitamin D-dependent rickets type II, as demonstrated by a patient with normal hair growth who showed extreme resistance.

This case report observed that while a 4-year-old boy with vitamin D-dependent rickets type II showed biochemical and bone improvement after vitamin D and calcium treatment, his alopecia did not improve.

This case study reported on a 3-year-old child with vitamin D-dependent rickets type II treated in the Gaza Strip, whose condition deteriorated despite vitamin D and calcium treatments, leading to recurrent chest infections, respiratory failure, and eventual death.

This case study describes a child with rickets and alopecia who responded to a small dose of 1-a-hydroxyvitamin D3, but her alopecia remained unchanged despite treatment.

This study observed wide clinical diversity among five patients with the same VDR gene mutation causing vitamin D-dependent rickets type II, suggesting involvement of a nuclear accessory factor and a nongenomic action of the vitamin.

This abstract discusses two types of hereditary vitamin D metabolism defects, VDDR I and VDDR II, and reports on their distinct characteristics and treatment responses, without presenting new clinical data.

In this case report, researchers described a two-year-old girl with Vitamin D dependent rickets Type II, noting elevated 1,25-dihydroxyvitamin D3 and alopecia, and observed limited treatment response likely due to poor compliance.

This case report presents the dental challenges faced by a child with vitamin D-dependent rickets type II, including early onset rickets, alopecia, and specific dental abnormalities, emphasizing the need for comprehensive, multidisciplinary management.

This review discusses inherited forms of vitamin D-dependent rickets and explains their genetic and metabolic causes but reports no new clinical findings.

In this study, gene therapy using a VDR-expressing adenoviral vector promoted hair growth in Vdr-KO rats, suggesting its potential for treating alopecia associated with type II rickets.

This case study reports that a 3 ½ year-old male with vitamin D-dependent type II rickets showed partial improvement in alopecia and rickets when treated with high doses of 1,25(OH)2 vitamin D3.

This article reviews Vitamin D-dependent rickets Type II with a focus on alopecia as a potential diagnostic clue for this rare disorder, reporting no new clinical findings.

This case report discusses a 27-month-old girl with vitamin D-dependent rickets type II, who showed minor improvement in skeletal features and alopecia after high-dose oral calcium and vitamin D3 treatment.

A genetic mutation caused severe rickets and alopecia in an Indian patient, but high-dose calcium and phosphate treatment improved their condition.

This article compares two rare genetic diseases, vitamin D-dependent rickets type 1 and type 2, focusing on their similar presentations of hypocalcemia and rickets in infancy, but reports no new clinical results.

This case study describes a 5-year-old boy with vitamin D dependent rickets type 2, motor delays, and alopecia totalis who showed improved biochemical parameters with calcium and calcitriol treatment.

In this case report, a four-year-old girl was diagnosed with vitamin D-dependent rickets type II, manifesting as diffuse alopecia, frontal bossing, hypoplastic teeth, and skin-colored papules, due to a genetic mutation causing resistance to 1.25-dihydroxy vitamin D.

This study found that the vitamin D-VDR system is crucial for mineral and bone metabolism post-weaning and identified missense mutations in 1alpha-hydroxylase causing type I rickets.

This article discusses various causes of rickets in children and describes VDDR-2A as a type of refractory rickets often linked to alopecia totalis in infancy, but reports no new clinical findings.

This study suggests that the vitamin D receptor and hairless gene may directly regulate each other via a transcriptional mechanism, potentially explaining phenotypic similarities between atrichia and VDRRIIa rickets.

This study identified two distinct VDR gene mutations among Lebanese families with hereditary vitamin D-resistant rickets, noting varied treatment responses and promising outcomes despite severe phenotypes.

This report discusses the various causes and clinical assessment of madarosis, emphasizing the importance of recognizing and diagnosing associated vision or life-threatening conditions, without presenting new findings.

This study observed that 25-hydroxyvitamin D3 restored rickets symptoms in genetically modified rats, suggesting its direct action through vitamin D receptor pathways.

The testes significantly contribute to vitamin D metabolism and may affect male reproductive health and conditions like hair loss.

This review suggests that decreased serum 25-hydroxyvitamin D levels may play a role in different types of non-scarring alopecia, but further studies are needed to explore vitamin D supplementation as a therapeutic option.

This study observed that Cyp27b1−/− mice exhibited growth and skeletal abnormalities similar to those of Vdr−/− mice, despite differences like the development of alopecia in Vdr−/− mice, suggesting that 1α,25D3 may directly influence chondrocyte proliferation and differentiation.

This study found that iron deficiency anemia is a key factor in the development of telogen effluvium, and higher 25-hydroxyvitamin D3 levels in TE patients may be linked to increased UV exposure.

The baby’s hair loss was due to a rare genetic condition, not treatable by usual methods.

This study found that vitamin D deficiency was significantly more prevalent among men with androgenetic alopecia in eastern Uttar Pradesh, India, than in age-matched controls, suggesting a potential link between vitamin D levels and the condition's pathogenesis.