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This case report describes a 37-year-old female with non-classical congenital adrenal hyperplasia who presented with severe acne, progressive hair loss, and primary infertility, managed with prednisolone.

In this study, researchers investigated factors predicting resistance to clomiphene citrate in women with anovulatory PCOS, identifying AMH and SHBG levels as significant indicators, but they found no reliable thresholds for predicting resistance to the standard 50 mg/day dose.

This study found that hirsutism patients had a strong correlation with polycystic ovary syndrome and elevated levels of certain hormones, such as 17-OHP and serum testosterone.

This study found that children with classic congenital adrenal hyperplasia had elevated epicardial fat thickness, which was associated with increased carotid intima media thickness, left ventricular mass, and mitral deceleration time.

This article discusses the ongoing care needs for individuals with 21-hydroxylase deficiency due to mutations in the CYP21A2 gene but does not present new clinical findings.

This study found that premenopausal women with female-pattern hair loss had significantly lower serum vitamin D levels compared to healthy controls, suggesting a potential role of vitamin D deficiency in this condition.

This research highlights that engineered mice lacking the vitamin D receptor show multiple health issues similar to human vitamin D deficiency, underscoring the widespread impacts of the vitamin D endocrine system.

This minireview discusses a proposed model of the vitamin D receptor that explains how 1alpha,25(OH)2D3 can mediate both genomic and rapid responses through different ligand shapes and cellular locations, without presenting new research findings.

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 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 review examines the functions of vitamin D and its receptor in skin and explores how these are regulated, reporting no new clinical results.

This study found that mice lacking the vitamin D receptor (VDR) developed skin tumors more rapidly than those with normal VDR activity, regardless of 1,25-dihydroxyvitamin D(3) presence.

This study found that mice lacking the 1αOHase enzyme, which is responsible for producing a key vitamin D metabolite, showed impaired epidermal differentiation and delayed recovery of skin barrier function after disruption.

This study highlights the complex role of the vitamin D receptor in skin processes, where its disruption, along with calcium and co-regulator imbalances, could contribute to skin cancer development by altering skin differentiation and hair follicle cycling.

This study identified a novel I268T mutation in the vitamin D receptor that reduces its function, contributing to hereditary vitamin D-resistant rickets, and found that a potent vitamin D analog could improve receptor function.

This study found that both the natural ligand 1alpha,25(OH)(2)D(3) and the synthetic agonist LG190178 bind similarly to the vitamin D receptor's coregulator motifs, suggesting similar biological functions.

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.

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 article discusses various causes of hyperandrogenism in women and highlights diagnostic considerations for conditions such as PCOS, NCCAH, Cushing's disease, and androgen-secreting tumors, without reporting new clinical results.

This article reviews the multifaceted roles of vitamin D beyond bone health and notes its potential involvement in reducing risks of certain cancers and autoimmune diseases, but it presents no new clinical results.

This chapter discusses the molecular biology of the vitamin D receptor in gene transcription and reports no new results; it highlights recent findings on receptor activity independent of its usual ligand.

This study found that VDR deficiency in mice leads to various skin pathologies but does not affect the phenotype or function of Langerhans cells.

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 review discusses the role of the unliganded vitamin D receptor in hair follicle cycling and tumor formation in mice and reports no new experimental findings.

Vitamin D3 may prevent hair loss from chemotherapy, but side effects and cancer cell protection are concerns.

This study found that a novel R343H mutation in the vitamin D receptor gene impairs its transcription activity, contributing to hereditary vitamin D-resistant rickets and alopecia in the affected family.