Praxis (Bern 1994). 1997 Jun 4;86(23):979-81
Cycle of hair growth and evaluation of alopecia
Piérard-Franchimont C, Piérard GE.
Hair follows a cycle of growth and involution which is asynchronous among follicles. Three phases are distinguished, namely the anagen growth phase and the catagen and telogen phases of regression. Any kind of alopecia results from perturbations of the hair cycle. Among triggering factors, various hormones, cytokines and apoptosis-inducing agents are currently recognized. Some microorganisms inducing inflammation could modulate the severity of selected hair loss disorders.
Skin Pharmacol. 1993;6(3):170-8.
Potassium channel openers stimulate DNA synthesis in mouse epidermal keratinocyte and whole hair follicle cultures.
Harmon CS, et al
We have conducted studies using primary mouse epidermal keratinocyte and whole hair follicle cultures to investigate the mechanism of the hypertrichotic ( hair regrowth-inducing ) activity of potassium channel openers. In a time course study, the extent of stimulation of epidermal keratinocyte DNA synthesis by minoxidil increased as the rate of DNA synthesis in control cultures declined. Minoxidil stimulation of DNA synthesis in 7-day cultures required prolonged exposure to the agent. Pinacidil and diazoxide also stimulated DNA synthesis in mouse epidermal keratinocyte cultures. In addition, minoxidil, pinacidil, diazoxide, and cromakalim stimulated DNA synthesis in whole-organ cultures of mouse hair follicles. These results suggest that potassium channel openers retard the loss of proliferative activity of differentiating keratinocytes and support the hypothesis that these agents stimulate hair regrowth through a direct effect on hair follicles.
Gynecol Obstet Invest. 1991;31(4):235-9.
Hormone studies in females with androgenic hairloss.
Schmidt JB, et al
Reports on hormone analysis in androgenic hair loss in the female show partly contradicting results. Elevated as well as normal-range androgen levels have been found. The present study aimed at the investigation of a possibly more differentiated hormonal constellation by hormone analysis and additional determination of the hypophyseal level by the thyrotropin-releasing hormone (TRH) test. In 46 female patients with androgenic hairloss blood sampling for hormone analysis was performed. Determination of the androgens testosterone (T), androstenedione (A), dehydroepiandrosterone sulfate (DHEAS), 17-hydroxy-progesterone acetate (17-OHP) and free testosterone (FT), of sex-hormone-binding globulin (SHBG), estradiol (E2), cortisol (F) and the hypophyseal luteinizing hormone (LH) and follicle-stimulating hormone (FSH) was performed by standard radioimmunoassay methods. The TRH-test is based on feedback mechanisms between the hypothalamic TRH which stimulates hypophyseal TSH and PRL release. Thus, even mild forms of hypothyroidism or hyperprolactinaemia can be detected. The control group for the TRH test consisted of 45 volunteer females without hairloss or any other hormonal or menstrual disturbances. Statistical analysis was performed according to the Wilcoxon two-sample test. The results of the study show no significant elevation of androgens in females with androgenic hairloss, but a more complex condition with involvement of the glandula suprarenalis and the hypophyseal level. Significantly elevated TSH levels prior to and after TRH stimulation in the hairloss group indicate that hypothyroidism may be an important hormonal disturbance in androgenic hairloss. Interactions between hypothyroidism and androgen metabolism are possible at various links.
J Cell Physiol. 2003 Nov;197(2):272-83.
Decapeptide with fibroblast growth factor (FGF)-5 partial sequence inhibits hair growth suppressing activity of FGF-5.
Ito C, Saitoh Y, Fujita Y, Yamazaki Y, Imamura T, Oka S, Suzuki S.
Earlier studies demonstrated that knock-out of fibroblast growth factor-5 gene (Fgf-5) prolonged anagen VI phase of hair cycle, resulting long hairs in the mice. We showed the activities on hair growth of the two Fgf-5 gene products, one of which, FGF-5 suppressed hair growth by inhibiting anagen proceeding and inducing the transition from anagen to catagen, and FGF-5S, a shorter polypeptide with FGF-5-antagonizing activity translated from alternatively spliced mRNA, suppressed this activity of FGF-5. As the results suggested that FGF-5 antagonist would increase hair regrowth, we synthesized various peptides having partial sequences of human FGF-5 and FGF-5S and determined their FGF-5 antagonist activity. Among them, a decapeptide designated P3 that aligns with receptor binding sites of FGF-1 and FGF-2 suppressed FGF-5-induced proliferation of BALB/3T3 A31 and NIH/3T3 murine fibroblasts, and FGF receptor-1c (FGFR-1c)-transfected Ba/F3 cell line (FR-Ba/F3 cells). IC50s of this peptide on these cell proliferations were 64, 28, 146 microM, respectively. On the other hand, IC50 of this peptide on binding of FGF-5 to the FGFR-1(IIIc)/Fc chimera was 483 microM. Examination in dorsal depilated mice revealed that the P3 peptide reduced the activity of FGF-5 to recover hair pigmentation and hair follicle lengths. The classification of histologically observed skin sections showed FGF-5-induced delations of anagen procedure had reduced by the P3 peptide. The anti-Ki67 antibody staining of hair follicles was inhibited by administration of FGF-5, and this inhibition by FGF-5 was recovered by administration of the P3 peptide. The P3 peptide alone did not affect hair follicle length and hair cell proliferation. These results indicate that the decapeptide antagonized FGF-5 activity in vivo, and reduced the inhibition of FGF-5 in hair growth, confirming that FGF-5 inhibitors are promising substances against hair loss and/or for promoting hair growth. Copyright 2003 Wiley-Liss, Inc.
Arch Dermatol. 1992 May;128(5):653-6. LinksComment in:
Arch Dermatol. 1992. 128(5):678
Proper vehicle selection in the detection of minoxidil sensitivity.
Whitmore SE.
BACKGROUND--The correct selection of vehicles for patch testing specific substances is essential in the evaluation of suspected allergic contact dermatitis. A reaction to a chemical may be dependent not only on the concentration tested but also on the vehicle in which it is tested. In cases of suspected allergic contact dermatitis to minoxidil, propylene glycol, and alcohol formulations used ofr the treatment of pattern hair loss, patch testing is usually done with the formulation of minoxidil in alcohol and/or minoxidil in petrolatum. OBSERVATIONS--An acute contact dermatitis of the scalp developed in a 34-year-old white man while he was using minoxidil solution. Patch testing with 2% minoxidil in alcohol and 2% minoxidil in petrolatum showed no reaction, while both Rogaine solution and 2% minoxidil in propylene glycol produced papulovesicular plaques. CONCLUSIONS--Patch testing in cases of suspected minoxidil allergic contact dermatitis should include testing with minoxidil in propylene glycol. Omitting this testing may cause diagnoses and therapeutic formulation alternatives to go unrecognized.
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Dermatologica. 1980;161(2):124-32.
Local therapy of (pattern hair loss) with 17 alpha-estradiol. A controlled, randomized double-blind study
Orfanos CE, Vogels L.
In a controlled, randomized double-blind study, 51 patients with male pattern hair loss and increased hair loss (telogen rate greater than 20%) were treated by local application of hair loss treatment lotions with and without 17 alpha-estradiol (0.025%).. Before and after therapy trichograms were taken and evaluated under standardized conditions. In 63% of the treated patients a reduction of the amount of telogen hairs appeared, whereas in the control group the same reduction was found in only 37% of the cases. Similarly, in the treated group only 11% of the patients worsened, in contrast to 50% of the control group who showed an increased telogen rate (greater than 10%). The amount of growing anagen hairs and of seborrhea did not change significantly in both groups. Side effects were not seen. These findings indicate that hair lotions containing 17 alpha-estradiol may have a therapeutic value in reducing androgenetic hair loss, if applied topically for a long period of time, similar to 17 beta-estradiol. However, no new hair regrowth occurred.
Acta Derm Venereol. 1983;63(6):546-9.
PUVA treatment of alopecia totalis.
Larkö O, Swanbeck G.
40 patients with hair loss secondary to alopecia totalis have been treated with PUVA. 26 did not respond, 6 experienced a partial hair regrowth, while 8 got a complete regrowth. However, relapses were frequent, occurring at an early stage.
Neurosci Lett. 1987;74(2):139
Classification of aberrant primary afferents in the substantia gelatinosa of the rat following neonatal capsaicin treatment.
Beal JA, Knight DS.
Administration of capsaicin to newborn rats results in a loss of a large percentage of primary afferent C fibers many of which terminate in the substantia gelatinosa (SG). Using the Golgi silver impregnation technique, the present study shows that the loss of C fibers results in an invasion of aberrant myelinated primary afferents in the SG by 10 days after birth. The aberrant afferents, identified on the basis of their distinctive collateral arborizations, are derived from hair follicles and slowly adapting type I mechanoreceptors.
J Invest Dermatol. 1985 Dec;85(6):569-72.Links
Expression of HLA-DR by anagen hair follicles in hair loss due to alopecia areata.
Messenger AG, Bleehen SS.
The expression of HLA-DR within hair follicles in hair loss secondary to alopecia areata was studied using an immunoperoxidase method. Scalp biopsies were taken from 12 patients with hair loss due to alopecia areata and from 6 normal control subjects. Frozen sections were stained with a panel of 4 anti-HLA-DR monoclonal antibodies, Leu 2, Leu 3, Leu 4, and T6 antibodies. The expression of DR in normal hair follicles and in most anagen follicles from nonlesional alopecia skin was confined to dendritic cells which were sparse below the level of the arrector pilorum insertion. ..snip... The aberrant expression of DR antigens by hair follicle epithelium provides direct evidence that immune mechanisms are operating in the pathogenesis of alopecia areata- induced hair loss. In a previous study of alopecia areata we found evidence of cell injury confined to the precortical matrix and presumptive cortex in lesional anagen follicles. The relative restriction of epithelial DR expression to the same site suggests that this region of the follicle is of fundamental importance in the disease process.
Hair Loss Treatment Blog
Int J Dermatol. 1992;31(12):858
Hormonal status in postmenopausal androgenetic alopecia.
Georgala S, et al
edited for blog
Androgenetic alopecia or pattern hair loss is thought to be caused by increased androgen action on hair follicles with menopause. Testosterone, estradiol and sex hormone binding globulin (SHBG) serum levels were determined in ten postmenopausal women with pattern hair loss and in ten sex and age matched healthy controls. No statistically significant differences were found in the hormone levels between the patients and the controls. These findings suggest that a genetically determined functional alteration of androgen receptors and/or a metabolic disturbance may exist in the hair follicle keratinocytes in pattern hair loss.