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

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 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 article highlights a lack of published data on vitamin D deficiency prevalence among individuals with central centrifugal cicatricial alopecia, despite its known link to other forms of hair loss.

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 study found that patients with alopecia, particularly alopecia areata and female pattern hair loss, often have vitamin D deficiency, suggesting that screening for vitamin D could benefit these patients.

The authors maintain there is a significant link between vitamin D deficiency and central centrifugal cicatricial alopecia in Black patients, and call for more research on the topic.

This study highlights a rare case of vitamin D-dependent rickets type 2A caused by a heterozygous mutation in the vitamin D receptor gene, emphasizing the complexity of managing this condition with high-dose calcium and vitamin D therapy.

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 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 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.

This report describes siblings with vitamin D-dependent rickets type 2, characterized by growth retardation, alopecia totalis, and low 25(OH)D3 levels, highlighting its autosomal recessive pattern and distinction from other rickets types.

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.

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.

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.

In a case study of vitamin D-dependent rickets type 2A, researchers observed that while active vitamin D treatment failed to improve bone and laboratory abnormalities, oral calcium lactate significantly ameliorated these issues, although skin and hair problems remained unresponsive.

This case study described a girl with vitamin D-dependent rickets type 2A who developed long-standing tertiary hyperparathyroidism, yet this did not hinder the healing of her rickets or normalization of hypophosphatemia; high doses of intravenous calcium were pivotal for recovery.

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 reported that growth hormone therapy dramatically improved rickets symptoms and growth in three children with vitamin-D dependent rickets type 2 who had not responded to standard treatments.

This case study reports on a rare form of vitamin D resistant rickets in a 37-year-old male, highlighting the condition's clinical features and the necessity for a thorough understanding of calcium and vitamin D metabolism in the diagnosis and management of metabolic bone diseases.

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 study observed that knocking out the 1α-hydroxylase gene in mice resulted in rickets and growth retardation, demonstrating the enzyme's crucial role in vitamin D function in animals.

This study found that 89.3% of female college students in Aden, Yemen, had hypovitaminosis D, with sunscreen use and lack of vitamin D supplements significantly associated with this condition.

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.

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.

In this study, eight patients with hereditary vitamin D-resistant rickets who share a specific VDR mutation showed improved clinical symptoms except alopecia after up to 11 years of treatment.