cholecalciferol and Alopecia

Lipids and lipid metabolism are critical factors in hair follicle (HF) biology, and cholesterol has long been suspected of influencing hair growth. Altered cholesterol homeostasis is involved in the pathogenesis of primary cicatricial alopecia, mutations in a cholesterol transporter are associated with congenital hypertrichosis, and dyslipidaemia has been linked to androgenic alopecia. The underlying molecular mechanisms by which cholesterol influences pathways involved in proliferation and differentiation within HF cell populations remain largely unknown. As such, expanding our knowledge of the role for cholesterol in regulating these processes is likely to provide new leads in the development of treatments for disorders of hair growth and cycling. This review describes the current state of knowledge with respect to cholesterol homeostasis in the HF along with known and putative links to hair pathologies.

Topics: Alopecia; Animals; Cell Differentiation; Cell Proliferation; Cholecalciferol; Cholesterol; Cicatrix; Hair; Hair Diseases; Hair Follicle; Homeostasis; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hypertrichosis; Ichthyosis; Keratinocytes; Lipid Metabolism; Lipids; Mice; Mutation; Peroxisome Proliferator-Activated Receptors; Phenotype; Signal Transduction; Skin Physiological Phenomena; Steroids; Sterols

Our aim is to investigate the protective effect of vitamin D3 especially from radiation-induced hair toxicity. A model of skin radiation injury was developed and a single fraction of 20 Gy Gamma irradiation was applied to the right dorsal skin of fourteen rats. All animals were randomly divided into 2 groups: Group I: irradiation alone (n = 7) and Group II: irradiation and 0.2 microg vitamin D3 given IM (n = 7). Fifty days after post-irradiation rats were sacrificed. The outcomes were evaluated on the basis of histopathological findings and immunohistochemical staining for Vitamin D receptor (VDR) in skin and hair follicles. The number of hair follicles in the radiation field for the group of animals irradiated without pretreatment was significantly lower than outside of the irradiated area (p = 0.016) as it is expected. Contrarily the number of hair follicles did not show significant difference in the pretreated group between the irradiated field and outside of the fields (p = 0,14). Skin of the vitamin D3 pretreated group demonstrated stronger immunoreactivity for VDR compared to irradiation alone group. These results indicate that administration of vitamin D3 may protect hair follicles from radiation toxicity. Further clinical trials should be conducted to prove the preventive effect of vitamin D3 as well as dosing and timing of the agent on radiation-induced alopecia.

Topics: Alopecia; Animals; Cholecalciferol; Female; Gamma Rays; Hair; Hair Follicle; Radiation Injuries, Experimental; Radiation-Protective Agents; Rats; Rats, Wistar; Receptors, Calcitriol; Skin

The active form of vitamin D3 can regulate epidermal keratinization by inducing terminal differentiation; and mice lacking the vitamin D receptor display defects leading to postnatal alopecia. These observations implicate the vitamin D3 pathway in regulation of hair growth. We tested the ability of 1,25 dihydroxyvitamin D3 and its synthetic analogs to stimulate hair growth in biege/nude/xid (BNX) nu/nu (nude) mice exhibiting congenital alopecia. Nude mice were treated with different vitamin D3 analogs at doses that we had previously found to be the highest dose without inducing toxicity (hypercalcemia). The mice were monitored for hair growth and were scored according to a defined scale. Skin samples were taken for histological observation of hair follicles and for extraction of RNA and protein. Vitamin D3 analogs dramatically stimulated the hair growth of nude mice, although parental 1,25 dihydroxyvitamin D3 had no effect. Hair growth occurred in a cyclical pattern, accompanied by formation of normal hair follicles and increased expression of certain keratins (Ha7, Ha8, and Hb3). Vitamin D3 analogs seem to act on keratinocytes to initiate hair follicle cycling and stimulate hair growth in mice that otherwise do not grow hair.

Topics: Alopecia; Animals; Calcitriol; Cholecalciferol; Female; Hair; Hair Follicle; Keratinocytes; Keratins; Male; Mice; Mice, Inbred C57BL; Mice, Nude; Skin

We report about a pair of Turkish siblings suffering from alopecia and severe rickets. In the elder sister we could show the causal role of extreme resistance of target organs to 1.25-(OH)2-cholecalciferol. The birth of a brother who developed the same symptoms together with two other similar cases in siblings recently published by other authors, made it possible to recognize the disorder as a typical syndrome-like entity, based on a hereditary defect. By successful administration of excessive (and so-far not previously published) doses of Vitamin-D3 a way for therapeutic progress in this new type of vitamin-D-dependent rickets is shown.

Topics: Alopecia; Cholecalciferol; Drug Resistance; Female; Humans; Hydroxycholecalciferols; Infant; Male; Rickets

Topics: Alopecia; Cholecalciferol; Cholesterol; Drug Combinations; Hair; Humans; Plant Extracts; Pyridoxine; Thallium; Vitamin A

Topics: Alopecia; Cholecalciferol; Diagnosis, Differential; Female; Humans; Male; Pyridoxine; Thallium; Vitamin A