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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 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 literature review highlights the effectiveness of topical vitamin D (e.g., calcipotriol, calcitriol) in treating vitiligo, emphasizing its role in melanogenesis and as an immunomodulator, either alone or combined with topical corticosteroids, offering minimal side effects.

Vitamin D is crucial for skin health and managing skin diseases.

This review discusses the regulation and function of vitamin D and its receptor in skin cells, highlighting their roles in processes such as proliferation inhibition, differentiation, and innate immunity, but reports no new results.

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 study observed that the vitamin D receptor is crucial for hair follicle formation and altering tumor development in the Wnt signaling pathway, suggesting therapeutic potential for vitamin D analogues in related tumors.

Adequate vitamin D is crucial for skin health and should be considered in dermatology.

Vitamin D receptor mutations can cause alopecia by affecting hair growth genes.

This abstract reviews hereditary vitamin D-resistant rickets, a rare genetic condition causing severe early childhood rickets, and reports no new results; effective treatment typically requires high doses of calcium to address hypocalcemia and secondary hyperparathyroidism.

This case study describes a child with an unusual form of vitamin D-dependent rickets, characterized by alopecia and a deficient response to active vitamin D.

This study found that measuring 24-OHase induction by 1,25(OH)2D3 in cultured skin fibroblasts is a sensitive test for detecting genetic defects in the 1,25(OH)2D effector pathway.

This study found that the absence of unliganded vitamin D receptor significantly impairs cWnt and hedgehog signaling pathways necessary for hair cycle initiation in VDR-null mice.

This study suggests that vitamin D and its receptor may protect against the development of epidermal tumors following UV radiation by regulating specific cellular signaling pathways.

This study found that while calcium can substitute for the Vitamin D receptor in maintaining epidermal keratinocyte differentiation, it cannot compensate for hair follicle dysfunction caused by the absence of the receptor.

This study identified a novel V26M mutation in the vitamin D receptor as the cause of hereditary vitamin D resistant rickets in a patient, characterized by severe rickets and an unusual pattern of alopecia.

This study found that 1,25-dihydroxyvitamin D3/VDR inhibits β-catenin's role in keratinocyte proliferation but enhances its role in hair follicle differentiation.

This review discusses the various roles of vitamin D in skin disorders, including established use in psoriasis and potential applications for atopic dermatitis and skin cancer prevention, but reports no new clinical results.

In this study, researchers identified a unique Arg30stop mutation in the vitamin D receptor gene that causes hereditary vitamin D-resistant rickets in a young French-Canadian boy by truncating the receptor and causing hormone resistance.

This study found that in a mouse model with hereditary 1,25-dihydroxyvitamin D resistant rickets, a mutant vitamin D receptor lacking hormone-binding ability could restore normal hair cycling and affect parathyroid hormone regulation.

This study reported a case of hereditary vitamin D–resistant rickets caused by a single heterozygous missense mutation in the VDR gene, showing dominant-negative effects and reduced response to 1,25-dihydroxyvitamin D3.

This study identified a novel nonsense mutation in the VDR gene in two patients with hereditary vitamin D resistant rickets and alopecia, leading to resistance to 1,25-dihydroxyvitamin D3.

This study found that vitamin D receptor activation in primary keratinocytes can occur independently of the 1,25-dihydroxyvitamin D₃ ligand, likely through interaction with retinoid X receptors.

This report describes a unique case of hereditary vitamin D-resistant rickets (HVDRR) in a dog, caused by a VDR gene mutation resulting in severe hypocalcemia and bone issues, which presented with symptoms similar to those observed in humans.

This study found that vitamin D deficiency in patients with alopecia areata was associated with greater disease severity and longer duration, but not with disease pattern or vitamin D receptor expression.

In this study, researchers observed that the absence of a functional vitamin D receptor in mice leads to impaired hair follicle regeneration due to defects in keratinocyte stem cells, resulting in alopecia.

This study found that while vitamin D deficiency is not the sole cause of alopecia areata, it may worsen the disease, suggesting supplementation could help in pediatric cases.

This study provides evidence-based recommendations for the off-label use of topical vitamin D in treating certain skin conditions, but highlights the need for higher quality studies for further validation.

This study suggests that while VDR is crucial for maintaining hair follicles in mice, their degeneration may be linked to impaired cell migration during hair growth phases rather than stem cell loss.

This study found no significant association between vitamin D intake or estimated vitamin D status and the risk of developing alopecia areata among women.