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This study found that Kyoh®, a flavonol-rich extract from rocket leaves, may promote hair growth by enhancing the expression of hair growth-related genes in laboratory conditions.

This report describes two sisters with rickets and alopecia unresponsive to high doses of vitamin D2, where oral phosphorus supplements led to significant clinical improvement.

This study observed that children with a genetically transmitted defect in the 1,25-dihydroxyvitamin D3 receptor experienced spontaneous healing of rickets as they aged, despite persistent mineral imbalances during treatment.

In this study, distinct clinical responses and long-term resistances were observed in two pediatric patients with vitamin D-dependency type II, associated with abnormalities in their skin fibroblast interactions with 1,25-(OH)2D3.

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 alopecia in four children was linked to severe calcitriol-resistant rickets, suggesting this condition should be considered among inherited hair growth disorders.

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 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.

In this study, researchers concluded that hereditary 1,25-dihydroxyvitamin D-resistant rickets, characterized by specific mutations in the vitamin D receptor gene, may resolve metabolic abnormalities with age, though associated alopecia remains.

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

This study characterized two siblings with hereditary vitamin D resistant rickets and a mutation in the vitamin D receptor, finding no immune-related disorders despite a defective T cell response to vitamin D.

This study found that calcitriol-resistant rickets is associated with alopecia in children and should be considered in the differential diagnosis of hair loss.

This case report documents a female toddler with novel compound heterozygous mutations in the VDR gene causing hereditary 1,25-dihydroxyvitamin D-resistant rickets, expanding the known mutation spectrum for this disease.

In this study, a Chinese Han family with hereditary vitamin D-resistant rickets was found to have a homozygous missense mutation in the VDR gene, and the affected individual uniquely responded well to treatment with oral calcium and low-dose calcitriol.

This review discusses the link between various skin diseases, such as ichthyosis and psoriasis, and the occurrence of rickets, though no new clinical results were reported.

This case series describes three siblings with hereditary vitamin D-resistant rickets, highlighting variations in their clinical presentations.

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.

Hair loss can happen after a fever caused by Rickettsia conorii infection.

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.

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 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 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 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 highlights the importance of recognizing non-nutritional forms of rickets, which can manifest with subtle symptoms like alopecia and cataracts, and emphasizes that a comprehensive diagnostic approach, including genetic testing, can improve management and treatment outcomes.

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 study describes a case of vitamin D resistant rickets in a young girl due to end organ unresponsiveness, highlighting a possible new subtype of the disorder with distinct clinical features.

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 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 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.

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.