Harv Mens Health Watch. 2002 Jun;6(11):8

"I am a 64-year-old man, and I've always been proud of my perfect health record. I've also been proud of my full head of hair, even after the gray started creeping in. Four months ago I caught pneumonia and spent eight days in the hospital (three in intensive care). It took a while, but I'm finally back to normal - except that my hair is falling out. It comes out in clumps when I shampoo or even comb it, and it's gotten noticeably thin all over. I remember reading about Propecia in your newsletter but I don't have the old issue. Should I try the medication?"
Simon HB.

Harv Mens Health Watch. 2002 Jun;6(11):8

"I am a 64-year-old man, and I've always been proud of my perfect health record. I've also been proud of my full head of hair, even after the gray started creeping in. Four months ago I caught pneumonia and spent eight days in the hospital (three in intensive care). It took a while, but I'm finally back to normal - except that my hair is falling out. It comes out in clumps when I shampoo or even comb it, and it's gotten noticeably thin all over. I remember reading about Propecia in your newsletter but I don't have the old issue. Should I try the medication?"
Simon HB.

Int J Dermatol. 1999 Dec;38(12):928-30.

Improvement in androgenetic alopecia (male pattern hair loss) in 53-76-year-old men using oral finasteride.
Brenner S, Matz H.

Twenty-eight men with AGA, aged 53-76 years (mean, 65 years), were selected to participate in this trial from a double blind, placebo controlled, multicenter study of subjects with moderate symptoms of BPH. Patients received either finasteride 5 mg or placebo daily for 24 months. Hair counts were performed at entry to the study and at 6, 12, 18, and 24 months. Hair counts were made directly on the scalp in a circular target area 1 in in diameter, located in the center of a template. The template was applied in such a way that its counting window fell on the most balding scalp area, which remained the same for each patient.11 At each hair counting session, patients were asked about side-effects and questioned about their sex life. Time trend and differences between groups were examined using a one-way (treatment) MANOVA with repeated measures (baseline, 6, 12, 18, and 24 months). Additional two-tailed t-tests were performed to compare the two groups at each point of time was considered to be significant.

Journal of Clinical Endocrinology & Metabolism, Vol 79, 703-706, Copyright © 1994 by Endocrine Society

The effect of finasteride, a 5 alpha-reductase inhibitor, on scalp skin testosterone and dihydrotestosterone concentrations in patients with male pattern baldness

AL Dallob, NS Sadick, W Unger, S Lipert, LA Geissler, SL Gregoire, HH Nguyen, EC Moore and WK Tanaka
Merck Research Laboratories, Rahway, New Jersey 07065.

The effects of the 5 alpha-reductase inhibitor, finasteride, on scalp skin testosterone (T) and dihydrotestosterone (DHT) levels were studied in patients with male pattern baldness ande hair loss. In a double blind study, male patients undergoing hair transplantation were treated with oral finasteride (5 mg/day) or placebo for 28 days. Scalp skin biopsies were obtained before and after treatment for measurement of T and DHT by high pressure liquid chromatography-RIA. In 10 male subjects studied at baseline, mean (+/- SEM) DHT levels were significantly higher in bald (7.37 +/- 1.24 pmol/g) compared to hair-containing (4.20 +/- 0.65 pmol/g) scalp, whereas there was no difference in mean T levels at baseline. In bald scalp from 8 patients treated with finasteride, the mean DHT concentration decreased from 6.40 +/- 1.07 pmol/g at baseline to 3.62 +/- 0.38 pmol/g on day 28. Scalp T levels increased in 6 of 8 subjects treated with finasteride. Finasteride decreased the mean serum DHT concentration from 1.36 +/- 0.18 nmol/L (n = 8) at baseline to 0.46 +/- 0.10 nmol/L on day 28 and had no effect on serum T. There were no significant changes in scalp or serum T or DHT in placebo-treated patients. In this study, male subjects treated with 5 mg/day finasteride for 4 weeks had significantly decreased concentrations of DHT in bald scalp, resulting in a mean level similar to the baseline levels found in hair-containing scalp.

Arch Dermatol Res. 1989;281(4):247-53.

Animal models of androgen-dependent disorders of the pilosebaceous apparatus. 1. The androchronogenetic alopecia (AGA) mouse as a model for male-pattern baldness.

Matias JR, Malloy V, Orentreich N.

Orentreich Foundation for the Advancement of Science, Inc., Biomedical Research Station, Cold Spring-on-Hudson, NY 10516.

The androchronogenetic alopecia (AGA) mouse if a mutant strain which expresses androgen-dependent baldness. Daily s.c. injection of testosterone (T) induced thinning of the hair coat along the upper dorsum after 4 weeks of treatment. After 12 to 14 weeks this diffuse alopecia eventually eveloped into a bald area which extended to the middorsum. Dihydrotestosterone was more effective than T in stimulating the onset of AGA. In this model, T produced the alopecia by decreasing the rate of hair growth, decreasing the duration of anagen, and markedly prolonging the duration of telogen. When applied topically at a concentration of 5%, cyproterone acetate delayed the progression of the T-mediated hair loss. However, this inhibitory effect occurred through systemic means as evidenced by decrease in the size of the submaxillary gland. Chronic feeding of androgen-treated female AGA mice with a diet containing 0.01% minoxidil also inhibited the development of alopecia. Skin and core temperatures were found to be higher in minoxidil-treated animals than in the placebo-treated controls. Minoxidil at a topical dose of 1% did not produce any effect. Increasing the dose to 2% caused a slight retardation of the development of alopecia. However, a 60% inhibition was observed at a topical dose of 5% minoxidil after 12 weeks of treatmen. The data demonstrate that hair loss in the AGA mouse is androgen dependent and that this mutant strain can serve as a suitable model for the screening of compounds, such as antiandrogens and vasodilators, which may influence the balding process.

Hair Loss blog

Ther Umsch. 2002 May;59(5):217-22.

Diffuse hair loss in women

Hair Loss Blog

Trüeb RM.

The complaint "Doctor, I am losing my hair" represents a particular challenge to the physician, and involves making a specific diagnosis, selecting an appropriate therapy, and expressing empathy for the patient's anxiety. Diffuse hair loss in women was formerly classified as an entity of its own. Since the identification of female pattern hair loss, most cases have been recognized to be due to androgenetic alopecia, often during phases of life characterized by fluctuations of sexual hormone levels or in connection with intake or cessation of hormonal therapy. The most difficult differential diagnosis includes androgenetic alopecia, chronic telogen effluvium, and psychogenic pseudo efflvuium. Androgenetic alopecia is due to androgen-induced, non-synchronized, progressive shortening of the hair growth cycle and gradually leads to thinning of the central scalp area. Idiopathic chronic telogen effluvium typically occurs in women, starting abruptly without a recognizable initiating factor, and involves the entire scalp area with increased shedding of telogen hair. It is believed to be due to synchronization phenomena of the cyclic hair growth. Psychogenic pseudo effluvium affects fashion-oriented, self-conscious women suffering of a discrepancy between the actual state of their hair and idealized expectations. Later the problem of age-related hair thinning oft becomes a surrogate for the more generalized problem of senescence. Rational therapy of androgenetic alopecia aims at blocking the androgen effect on hair follicles with estrogens and antiandrogens or at pharmacologically reversing vellus hair transformation with topical minoxidil. In contrast, women with idiopathic chronic telogen effluvium should be reassured that their problem is rather a state of exaggerated "hair shedding" than of actual "hair loss".

Hair loss treatment regrowth alopecia antiandrogens minoxidil nano drproctor proxiphen

Alopecia in Women, Am Fam Physician. 2003 Mar 1;67(5):1007-14.

C. CAROLYN THIEDKE, M.D., Copyright © 2003 by the American Academy of Family Physicians.

Androgenetic Alopecia

Brief exerpt:

".....Androgenetic alopecia, or hair loss mediated by the presence of the androgen dihydrotestosterone, is the most common form of alopecia in men and women. Almost all persons have some degree of androgenetic alopecia.7 The hair loss usually begins between the ages of 12 and 40 years and is frequently insufficient to be noticed. However, visible hair loss occurs in approximately one half of all persons by the age of 50 years8 (Figure 2). In women, hairstyling may mask early hair loss.

Hair follicles contain androgen receptors. In the presence of androgens, genes that shorten the anagen phase are activated, and hair follicles shrink or become miniaturized. With successive anagen cycles, the follicles become smaller (leading to shorter, finer hair), and nonpigmented vellus hairs replace pigmented terminal hairs. In women, the thinning is diffuse, but more marked in the frontal and parietal regions. Even persons with severe androgenetic alopecia almost always have a thin fringe of hair frontally. The remaining hair configuration may resemble a monk's haircut.

An extensive hormonal work-up is not needed in women with androgenetic alopecia who have normal menses, fertility, and endocrine function.

Women with androgenetic alopecia do not have higher levels of circulating androgens. However, they have been found to have higher levels of 5a-reductase (which converts testosterone to dihydrotestosterone), more androgen receptors, and lower levels of cytochrome P450 (which converts testosterone to estrogen).6

Most women with androgenetic alopecia have normal menses, normal fertility, and normal endocrine function, including gender-appropriate levels of circulating androgens. Therefore, an extensive hormonal work-up is unnecessary. If a woman has irregular menses, abrupt hair loss, hirsutism, or acne recurrence, an endocrine evaluation is appropriate. In this situation, total testosterone, free testosterone, dehydroepiandrosterone sulfate, and prolactin levels should be obtained.6

Because the hair loss in androgenetic alopecia is an aberration of the normal hair cycle, it is theoretically reversible. Advanced androgenetic alopecia, however, may not respond to treatment, because the inflammation that surrounds the bulge area of the follicle may irreparably damage the follicular stem cell...."

J Eur Acad Dermatol Venereol. 2003 May;17(3):271-5.

Hypertrichosis in females applying minoxidil topical solution and in normal controls.
Dawber RP, Rundegren J.

BACKGROUND: Hypertrichosis has been reported more frequently in females than in males who use minoxidil topical solution (MTS) for the treatment of androgenetic alopecia (AGA) or pattern hair loss. This article examines the occurrence of MTS-induced hypertrichosis in females. METHODS: Data from placebo-controlled clinical trials in females (up to 5% MTS) were analysed based on spontaneous reports of hypertrichosis/facial hair and investigators' inquiries (solicited) about the presence of any new hair regrowth on body parts other than the scalp. A postmarketing drug surveillance database for MTS was also examined for reports of hypertrichosis/facial hair. RESULTS: In the clinical trials involving a total of 1333 females, spontaneous reports of hypertrichosis/facial hair were noted for 50 (4%) females in a dose-related pattern of response. Nine females (seven and two in the 5% MTS and 2% MTS groups, respectively) discontinued treatment because of hypertrichosis/facial hair. Solicited reports of excessive hair growth (primarily facial) also showed a dose-related pattern of response. Post-marketing data showed a lower occurrence (0.5%) of hypertrichosis/facial hair than in the clinical trials. Of interest, in one clinical trial, 27% of the females enrolled (MTS and placebo treated) had facial hair growth reported at baseline. CONCLUSIONS: Females with some hirsutism are particularly prone to seek treatment for AGA, and this may explain the high occurrence of hypertrichosis/facial hair found in the MTS clinical trials. Furthermore, some demographic groups of females are prone to develop facial hair and the problem of unwanted facial hair growth seems to be underestimated. Some females may have hair follicles that are very sensitive to MTS and should use the lowest strength of MTS (2%) to help avoid unwanted hair growth. The hypertrichotic effect of MTS on other sites than the scalp, including the face, is reversible and does not always require discontinuation of therapy.

Am J Clin Dermatol. 2000 Mar-Apr;1(2):101-5

Alopecia areata. Pathogenesis, diagnosis, and therapy.

Papadopoulos AJ, et al

Alopecia areata is a common form of non-scarring alopecia that appears equally in males and females of any age, although children and adolescents are more commonly affected. The disorder is usually characterized by limited alopecic patches on the scalp, but more severe forms may affect the entire scalp (alopecia totalis) or body (alopecia universalis). Characteristic nail changes may also accompany hair loss. Alopecia areata has been linked with certain human leukocyte antigen (HLA) class II alleles, indicating a probable autoimmune etiology. Current research implicates T lymphocytes in the pathogenetic mechanism of disease. Other autoimmune diseases are also linked with alopecia areata. The diagnosis of alopecia areata is usually made clinically, although a biopsy is diagnostic for this condition. Treatment is challenging and aims at the regrowth of hair in affected individuals. Intralesional corticosteroid injections are widely used in mild disease. Topical anthralin and minoxidil may also be clinically efficacious. Topical sensitizers, such as squaric acid dibutlyester and diphenyl-cyclopropenone, are sometimes employed. Various therapies for the disease may have efficacy in different patients, making a universal treatment algorithm difficult to implement. Patients should be handled on an individual basis, with the final outcome based on the cosmetic regrowth of hair. Maintenance therapy is also important in patients that do achieve acceptable regrowth, necessitating a highly motivated patient and good rapport with the treating physician.

Arch Dermatol. 1984 Apr;120(4):457-63.

Alopecia areata treated with topical minoxidil.

Hair Loss Blog

Weiss VC, West DP, Fu TS, Robinson LA, Cook B, Cohen RL, Chambers DA.

A 1% minoxidil topical solution was used to treat 48 patients with alopecia areata, ie, 24 patients with patchy disease and 24 patients with alopecia totalis or alopecia universalis ( complete hair loss ). Twenty-five patients had terminal hair regrowth; in 11 of the 25 patients, it was cosmetically acceptable. No clinical features of the disease seemed to indicate the likelihood of hair regrowth. Hair regrowth began approximately two months after the initiation of treatment and was not uniformly well maintained after the treatment was terminated. One patient had an allergic contact dermatitis reaction to the minoxidil solution; no systemic side effects were seen. No notable systemic absorption was found in 18 adult patients. Effects on cutaneous blood flow or the immune system or some direct effect on hair follicles are possible mechanisms by which minoxidil therapy might stimulate hair growth.

Hair loss and hair loss treatment