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Hair Loss Regrowth

August 30th, 2010

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Prolactin and Hair loss

August 23rd, 2010

Am J Pathol. 2006 March; 168(3): 748–756.
doi: 10.2353/ajpath.2006.050468. PMCID: PMC1606541

Copyright © American Society for Investigative Pathology

Title: Human Scalp Hair Follicles Are Both a Target and a Source of Prolactin, which Serves as an Autocrine and/or Paracrine Promoter of Apoptosis-Driven Hair Follicle Regression

Kerstin Foitzik et al

From "discussion" section

" Here, we provide the first evidence that human scalp HFs not only express functional PRL-R but also serve as an important extrapituitary site of PRL expression on the gene and protein level (Figure 1, A–D, and Figure 4). Given that human skin has been calculated to display ~5 million HFs, this calls attention to a very substantial, newly identified source of potential PRL synthesis in humans. This deserves further scrutiny and characterization, eg, in healthy versus inflamed human skin, and definition of the quantity of HF-derived PRL that is actually secreted systemically and thus exerts genuine endocrine, rather than autocrine or paracrine activities.Although our finding of intracutaneous transcription of the PRL gene in human skin in situ is well in line with the previous finding of PRL transcription in murine skin in vivo and in human cultured dermal fibroblasts, keratinocytes, and sweat glands in vitro,36,39 it conflicts with the report of Slominski and colleagues40 who could not detect PRL mRNA in human skin by RT-PCR. In our experiments, we detected PRL transcripts of the expected length both in human full-thickness skin and in isolated human HFs, using pituitary gland as positive control, and confirmed our data by sequencing the PRL RT-PCR product. The negative PRL expression data of Slominski and colleagues40 may be related to the fact that these investigators studied sun-exposed truncal skin (containing primarily vellus HFs, approximately half of which are in the telogen stage of the hair cycle), whereas we analyzed scalp skin, which is unusually rich in very large terminal HFs, 80 to 90% of which are in anagen VI HF. In addition, we used different primer sequences and PCR conditions than these investigators, who may well have identified an alternatively spliced PRL mRNA variant that could not be detected because of the exonal location of their primers. The sense primer used by Slominski and colleagues40 was located in exon 3, and the anti-sense primer contained both the end of exon 4 sequences and the initial part of exon 5 sequences. In contrast, our sense primer is in exon 2 and anti-sense primer is in exon 4.PRL mRNA as well as PRL and PRL-R immunoreactivity can be detected within the same epithelial human HF compartments (Figure 1, A–D, and Figure 4), and culture of microdissected, denervated, and avascular HFs in the presence of exogenous PRL exerts significant growth-modulatory effects (Figure 1, E–H, and Figure 2, a and b). This supports the hypothesis that PRL acts in an autocrine and/or paracrine manner on locally expressed high-affinity receptors and functions as a catagen-promoting signal in human HFs just as it does in mouse HFs. The strictly epithelial immunoreactivity pattern of PRL and PRL-R identified here for human scalp HFs corresponds well to the one previously described in mice. However, in ovine HFs, PRL-R expression has also been detected in the dermal papilla. Thus, expression of PRL-R seems to be differentially regulated in seasonally dependent HFs (ovine) compared to seasonally independent HFs (mouse, human).Steroid hormones stimulate cognate receptors in the HF epithelium and mesenchyme and change the secretion of potent hair growth modulators such as TGF-â, which then act back on the epithelium. In contrast, the polypeptide hormone PRL seems capable of signaling more directly within the HF epithelium as an autocrine and/or paracrine promoter of apoptosis-driven HF regression. However, our currently available data do not allow us to exclude that the observed HF effects of PRL were mediated at least in part also indirectly. This could happen via the recognized effects of PRL on peripheral androgen27 and estrogen metabolism, and/or via induction of changes in the intrafollicular expression of PRL-sensitive growth factors, cytokines, and enzymes with recognized hair growth-modulatory functions,21 such as TGF-â1,55 vascular endothelial growth factor,2 IGF-2, interferon-ã, and ornithine decarboxylase.58Treatment of isolated human HFs in culture with PRL results in apoptosis-driven HF regression (catagen), decreased proliferation, and increased apoptosis of follicular keratinocytes (Figure 3). These data correspond well to the rapid, premature induction of apoptosis-driven catagen development in murine anagen skin organ culture22 and to the reported catagen induction by PRL in sheep in vivo. However, PRL has also been shown to exert anti-apoptotic functions, eg, in cultured human breast cancer cell lines in vitro, to act as a larval growth hormone and to be required for limb regeneration in amphibians.61 Therefore, the anti-proliferative and proapoptotic properties of PRL in HF epithelium may not extend to all epithelial-mesenchymal interaction systems and may be developmentally controlled.Although it remains to be clarified how PRL exerts its activities on human HFs, we show that PRL is a potent catagen-promoter of human HFs in vitro, with efficacy comparable to that of TGF-â2, yet is lower than that of interferon-ã. We also show that the catagen-promoting activity of PRL is independent of the hypothalamus-pituitary-adrenal axis and systemic hormone levels. It applies to HFs of a mammalian species with mosaic and seasonally independent HF cycling (=human scalp HF). PRL has long been recognized to play a role in hair growth control in seasonally dependent coat changes, because both rising and falling daily plasma PRL levels can induce moulting. The current human data fit well with the previous reports that PRL induces premature catagen in the, also seasonally independent, murine hair cycle22 and that murine PRL-R-null mutants show longer and coarser hair as well as hair cycle perturbations.23 The present data, therefore, underscore the importance of PRL as a hair growth modulator for both seasonally dependent and independent HF cycling across different mammalian species.PRL has also been implicated in the pathogenesis of androgenetic alopecia25 by modulation of androgens, and hyperprolactemia is associated with an androgenetic alopecia-type hair loss pattern, along with hirsutism (in females). Usually, occipital scalp HFs are insensitive to hormones such as androgens. In our experiments we used mostly occipital scalp HFs and additionally frontal HFs. It is therefore particularly interesting that PRL was able to induce catagen in these hormone-insensitive HFs. It is important to mention that PRL may have distinct functions on distinct areas of scalp and body HFs and that this will be an interesting issue to investigate in the future. Recently, it has been shown that neuroendocrine factors mediate stress-induced acne. HFs and the sebaceous glands express functional receptors for stress-related hormones, which are able to modulate androgen metabolism in the sebaceous gland. These up-regulated androgens in the sebaceous gland could also be involved in stress-induced hair loss. Therefore, it will be interesting to investigate whether PRL is able to modulate androgen receptor expression and/or androgen metabolism in the human pilosebaceous unit. In summary, our study shows that human anagen scalp HFs are very sensitive for inhibitory PRL-R-mediated signals. This is clinically relevant, because it provides a reasonable mechanism to explain the, as yet ill-understood, telogen effluvium associated with hyperprolactinemia.25 It also points to novel therapeutic strategies for the management of stress-related and hormonal hair loss in men and women, by use of recently developed PRL-R antagonists...."

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Keywords: hair loss treatment hair regrowth balding minoxidil nano shampoo Dr Droctor tempol hair loss regrowth propecia proxiphen (tm).

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Prolactin and Hair loss

August 23rd, 2010

Interesting paper on the role of prolactin in the hair cycle. One more thing that seems to drive the hair loss process. Dr Proctor

Am J Pathol. 2006 Mar;168(3):748-56.

Human scalp hair follicles are both a target and a source of prolactin, which serves as an autocrine and/or paracrine promoter of apoptosis-driven hair follicle regression.

Foitzik K, et al

Abstract
The prototypic pituitary hormone prolactin (PRL) exerts a wide variety of bioregulatory effects in mammals and is also found in extrapituitary sites, including murine skin. Here, we show by reverse transcriptase-polymerase chain reaction and immunohistology that, contrary to a previous report, human skin and normal human scalp hair follicles (HFs), in particular, express both PRL and PRL receptors (PRL-R) at the mRNA and protein level. PRL and PRL-R immunoreactivity can be detected in the epithelium of human anagen VI HFs, while the HF mesenchyme is negative. During the HF transformation from growth (anagen) to apoptosis-driven regression (catagen), PRL and PRL-R immunoreactivity appear up-regulated. Treatment of organ-cultured human scalp HFs with high-dose PRL (400 ng/ml) results in a significant inhibition of hair shaft elongation and premature catagen development, along with reduced proliferation and increased apoptosis of hair bulb keratinocytes (Ki-67/terminal dUTP nick-end labeling immunohistomorphometry). This shows that PRL receptors, expressed in HFs, are functional and that human skin and human scalp HFs are both direct targets and sources of PRL. Our data suggest that PRL acts as an autocrine hair regrowth modulator with catagen-promoting functions and that the hair growth-inhibitory effects of PRL demonstrated here may underlie the as yet ill-understood hair loss in patients with hyper-prolactinemia.

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Hair loss Treatment at the Proctor clinic

August 12th, 2010

Hair loss treatment at the Proctor clinic.

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Hair regrowth inducers

August 12th, 2010

FASEB J. 2009 Dec 29

Identification of novel hair-growth inducers by means of connectivity mapping.
Ishimatsu-Tsuji Y, Soma T, Kishimoto J.

The aim of this study was to identify novel inducers of hair regrowth using gene expression profiling at various stages of hair-regrowth induction. First, we analyzed gene expression at the onset of hair growth in mice induced by cyclosporin A (CsA), a well-known hair-growth inducer, using DNA microarray analysis. The results unveiled genes involved in the step-by-step progression of hair growth, including increases in melanin biosynthesis and decreases in immune response at d 2 and the subsequent stimulation of cell proliferation at d 4, followed by the up-regulation of hair specific keratins at d 7 after CsA treatment. With the use of the connectivity map (Cmap), agents that had a similar "gene signature" to that of the profiles of CsA-treated mice were identified. Several agents, including CsA, were identified by the Cmap and were evaluated for hair induction activity in vivo. One of the proposed agents, fluphenazine (from the d 2 signature) actually induced hair growth in vivo (ED50: 2 mM for single application), and the subsequent application of 5 mM iloprost (from the d 4 signature) significantly enhanced the hair-growth effect of fluphenazine. From these results, Cmap analysis was proven to be a useful method that connects gene expression profiles of complicated biological processes, such as hair-growth induction, to effective agents.-Ishimatsu-Tsuji, Y., Soma, T., Kishimoto, J. Identification of novel hair-growth inducers by means of connectivity mapping.

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Hair Loss Treatment with Low Level Light Therapy

August 11th, 2010

South Med J. 2010 Aug 4

Types of Hair Loss and Treatment Options, Including the Novel Low-Level Light Therapy and Its Proposed Mechanism.

Ghanaat M.

From the Department of Dermatology, SUNY Downstate Medical Center, Brooklyn, NY.

Androgenetic alopecia (AGA) is the most common form of hair loss in men, and female pattern hair loss (FPHL) is the most common form of hair loss in women. Traditional methods of treating hair loss have included minoxidil, finasteride, and surgical transplantation. Currently there is a myriad of new and experimental treatments. In addition, low-level light therapy (LLLT) has recently been approved by the United States Food and Drug Administration (FDA) for the treatment of hair loss. There are several theories and minimal clinical evidence of the safety and efficacy of LLLT, although most experts agree that it is safe.

More in vitro studies are necessary to elucidate the mechanism and effectiveness at the cellular level, and more controlled studies are necessary to assess the role of this new treatment in the general population.

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Finasteride treatment for hair loss in women

August 10th, 2010

J Eur Acad Dermatol Venereol. 2010

5 mg/day finasteride treatment for normoandrogenic Asian women with female pattern hair loss.

Yeon JH, et al

Abstract Background Various treatments have been attempted for female pattern hair loss (FPHL), including topical minoxidil, oral antiandrogen and finasteride. But, there is no consensus on the standard hair loss treatment options. Clinical efficacy of finasteride in treating FPHL is still in controversy, but there is a tendency to high dose finasteride, which is more effective than lower dose.

Objectives

The purpose of this study was to evaluate the clinical efficacy of high dose (5 mg/day) oral finasteride in normoandrogenic Asian women with FPHL. Methods Total of 87 normoandrogenic, pre and post-menopausal women with FPHL were enrolled in this study. They were treated with oral finasteride (Proscar((R))), 5 mg daily for 12 months. Efficacy was evaluated with hair density and thickness changes assessed by phototrichogram and global photographs using 7-point scale.

Results

Eighty-six patients completed 12 months of finasteride treatment schedule. One patient withdrew due to headache. At initial visits, mean hair density was 90 +/- 22/cm(2) and mean hair thickness was 64 +/- 11 mum. After 12 months of finasteride treatment, hair density was significantly increased to 107 +/- 23/cm(2), and hair thickness was also significantly increased to 70+/- 9 mum. In global photographs, 70 (81.4%) of the 86 patients were improved (57 were slightly, 10 were moderately and four were greatly improved). Patients without any changes were 13 (15.1%) and 3 (3.5%) patients reported slightly aggravated. Four patients (4.6%) reported adverse events (headache,menstrual irregularity, dizziness and increased body hair growth). However, these adverse events were mild and disappeared soon.

Conclusions Oral finasteride, 5 mg/day, may be an effective and safe treatment for normoandrogenic women with femal pattern hair loss.

hair loss treatment and hair regrowth. Hair loss in women

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Treatment of hair loss

August 10th, 2010

Am Fam Physician. 2009;80:356

Diagnosing and treating hair loss.

Mounsey AL, Reed SW.
edited and modified for hair loss blog

Physicians should be not underestimate the impact of hair loss on some patients. Hair loss may present as focal patches or as more diffuse loss. Ths may include predominant hair thinning or increased hair shedding. Focal hair loss can be further broken down into scarring and nonscarring. Scarring alopecia is best evaluated by a dermatologist. Focal hair loss can be diagnosed by appearance and examination for fungal agents. A biopsy may be necessary if the cause of hair loss is unclear. Alopecia areata presents with smooth rounded hair-less patches....snip.... Male and female pattern hair loss both have recognizable patterns and can be treated with topical minoxidil, and also with finasteride in men. Sudden loss of hair is usually telogen effluvium, but can also be diffuse alopecia areata. In telogen effluvium, once the precipitating cause is removed, hair regrowth will likely occur.

Regrowth of hair loss

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Hair loss in alopecia areata

August 9th, 2010

Calif Med. 1958;89:322.

Noncicatrizing alopecias; with special reference to hair loss due to alopecia areata.
NEW WN, NICKEL WR.

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....there has been general acceptance of the causal relationship of the male sex hormone testosterone, age and inheritance in development of male pattern baldness. snip... Hair loss that accompanies disease states is probably due to generalized toxemia and disturbances in metabolism. Sometimes male pattern baldness occurs in physiologic states, as exemplified by diffuse hair loss occasionally in the postpartum period. snip... The development of alopecia totalis or universalis in 50 per cent of the prepuberal cases of alopecia areata is of real significance, especially since so very few patients regrow normal scalp hair....snip... A few conditions simulate alopecia areata. Probably the ones which are seen most often are trichotillomania and patchy baldness caused by agents used in hair waving and straightening. In 22 cases we found an inflammatory perivascular and perifollicular infiltrate, massive plugging of the ostia, disappearance of robust hair follicles and diminution in total number of hair follicles and sometimes fibrosis are not necessarily diagnostic of alopecia areata but seem to be very definitely characteristic.Treatment for hair regrowth in alopecia areata is of little avail. snip....

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New model of male pattern hair loss

August 9th, 2010

Endocrinology. 2010 Mar 16.

A Mouse Model of Androgenetic Alopecia ( Pattern Hair Loss )
Crabtree JS, et al

Androgenetic alopecia (AGA), commonly known as male pattern baldness, is a form of hair loss that occurs in both males and females. Although the exact cause is unknown, pattern hair loss is associated with genetic predisposition through traits related to androgen synthesis/metabolism and androgen signaling mediated by the androgen receptor (AR). Current therapies for AGA show limited efficacy at hair regrowth and are often associated with undesirable side effects. A major hurdle to developing new therapies for male pattern hairloss is the lack of small animal models to support hair loss drug discovery research. Here, we report the first rodent model of pattern hair loss. Previous work demonstrating that the interaction between androgen-bound AR and beta-catenin can inhibit Wnt signaling led us to test the hypothesis that expression of AR in hair follicle cells could interfere with hair regrowth in an androgen-dependent manner. Transgenic mice overexpressing human AR in the skin under control of the keratin 5 promoter were generated. Keratin 5-human AR transgenic mice exposed to high levels of 5 alpha-dihydrotestosterone (DHT) showed delayed hair regeneration, mimicking the AGA scalp. This effect is AR mediated, because treatment with the androgen receptor antagonist hydroxyflutamide inhibited the effect of dihydrotestosterone on hair regrowth. These results support the hypothesis that androgen-mediated hair loss is androgen receptor dependent and suggest that AR and beta-catenin mediate this effect. These mice can now be used to test new therapeutic agents for hair loss treatment, accelerating the drug discovery process.

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Hair loss and hair loss treatment

August 9th, 2010

Expert Opin Pharmacother. 2010 Apr 29

Male androgenetic alopecia ( Pattern Hair Loss ).
Rathnayake D, Sinclair R.

Abstract
Androgenetic alopecia ( ed: male pattern hair loss ) affects up to 80% of males by the age of 80. The synonym 'male-pattern hair loss' highlights the fact that hair loss occurs in a defined and reproducible pattern. Hair loss results in reduced self esteem, loss of confidence and anxiety in affected men. An effective treatment for hair baldness would be desirable. Areas covered in this review: In androgenetic alopecia, hair follicles undergo progressive miniaturization. Genetic factors and androgens play a major role in the pathogenesis of the disease. Polymorphism of the androgen receptor gene was first identified in association with androgenetic alopecia. Identification of new susceptibility genes on chromosomes 3q26 and 20p11 suggest that non-androgen-dependent pathways also are involved. What the reader will gain: Topical monoxidil and oral finasteride are commonly in use and have FDA approval for the treatment of male androgenetic alopecia; dutasteride, a type I and II 5-alpha-reductase inhibitor, is on hold in Phase III trials. A combination of medical treatment and hair transplant surgery has shown superior efficacy. Androgenetic alopecia is a progressive condition and although the current available treatments are effective in arresting the progression of the disease, they allow only partial hair regrowth. Early treatment achieves the best desirable outcome.

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Another Treatment of Hair Loss in Alopecia Areata

August 9th, 2010

Ann Dermatol. 2009 May;21(2):142-6.

The Therapeutic Effect and the Changed Serum Zinc Level after Zinc Supplementation in Alopecia Areata Patients Who Had a Low Serum Zinc Level Hoon Park, M.D., et al

Some alopecia areata patients may have zinc deficiency. There are also reports concerning oral zinc sulfate treatment in some alopecia areata patients.

Objective
The purpose of this study was to evaluate the therapeutic effects of oral zinc supplementation for twelve weeks in alopecia areata patients who had a low serum zinc level.

Methods
Oral zinc gluconate (50 mg/T/day) supplementation was given to alopecia areata patients without any other treatment for twelve weeks. The serum zinc level was measured before and after zinc supplementation. A four-point scale of hair regrowth was used to evaluate the therapeutic effect of oral zinc supplementation in these patients.Results
Fifteen alopecia areata patients were enrolled in this study. After the therapy, the serum zinc levels increased significantly from 56.9 µg/ to 84.5 µg/dl. Positive therapeutic effects were observed for 9 out of 15 patients (66.7%) although this was not statistically significant. The serum zinc levels of the positive response group increased more than those of the negative response group (p=0.003).

Conclusion

Zinc supplementation needs to be given to the alopecia areata patients who have a low serum zinc level. We suggest that zinc supplementation could become an adjuvant therapy for the alopecia areata patients with a low serum zinc level and for whom the traditional therapeutic methods have been unsuccessful.

Keywords: Alopecia areata, Serum zinc level, Zinc supplementation,hai rloss treatment regrowth.

Oral zinc compounds have been used for decades for treating disorders such as telogen effluvium1,2 and alopecia areata3,4. Reports have also been published on oral zinc sulfate therapy with encouraging results for some cases of alopecia areata. In 1976 Wolowa and Jablonska5 reported that two patients with alopecia areata regrew their hair after treatment with oral zinc sulfate. It has been reported that some alopecia areata patients have zinc deficiency6-8. Zinc is an essential cofactor for multiple enzymes and it is involved with important functional activities in the hair follicle. Further, zinc is a potent inhibitor of hair follicle regression and it accelerates hair follicle recovery6,7. In the present study, we examined the serum levels of zinc in alopecia areata patients. We studied the therapeutic effect of 12 weeks oral zinc supplementation for treating alopecia areata patients who have a low serum zinc level and we checked their serum zinc level after this oral zinc supplementation.

Patients

Forty four alopecia areata patients with hair loss were checked for their serum zinc levels. After the zinc levels were checked, 15 alopecia areata patients who each had a low serum zinc level (Zn≤70 µg/dl) were enrolled in this study. Ten were males and five were females (mean age: 29.1±16.2 years). All of these patients had had alopecia areata for at least 6 months before visiting our clinic for treatment. These patients had reported no effect from other therapeutic methods or they had had no treatment history for more than 6 months before visiting our clinic. The sera obtained from the 15 alopecia areata patients were used as test materials.

Methods

Supplementation with oral zinc gluconate tablet (50 mg/tablet/day, zinc 50, GNC, USA) was used as a therapeutic method for twelve weeks without any other treatment. Each patient's serum zinc level was measured before and after supplementation therapy. We defined a mild type of alopecia areata as hair loss of less than 25% of the total scalp hair, a moderate type of alopecia areata was defined as hair loss between 25% and 50% of the total scalp hair and a severe type of alopecia areata was defined as hair loss of more than 50% of total scalp hair. The therapeutic effects of oral zinc supplementation in alopecia areata patients were evaluated through the extent of vellus hair and terminal hair regrowth on the scalp. We graded the therapeutic effects as follows:(1) Marked recovery: cosmetic satisfaction or terminal hair regrowth of more than 60% on the hair loss patch(2) Partial recovery: terminal hair regrowth less than 60% on the hair loss patch(3) Poor recovery: only vellus hair regrowth on the hair loss patch(4) No recovery: aggravation or an unchanged alopecia areata state as compared to before therapyOf the 4 grades, we defined that the positive therapeutic effects were marked and partial recovery9,10. With maintaining zinc supplementation for at least 6 months, the positive response group was followed up for continuous terminal hair regrowth and recurrence of alopecia areata.

Statistical analysis

The results were expressed as means±standard deviations. The Chi-square test was used for statistical analysis. A p value≤0.05 was considered statistically significant.

RESULTS

All of the 15 subjects completed this study. They were enrolled from September 2006 to August 2007. The patient information is shown in Table 1. After the zinc supplementation the mean serum zinc level changed from 56.9 µg/dl to 84.5 µg/dl. The results of the changed serum zinc levels are shown in Table 2, and the differences of the zinc serum levels were statistically significant before and after supplementation therapy (p=0.002). Positive therapeutic effects were seen in 9 out of 15 patients (66.7%). Out of the 9 patients with positive therapeutic effects, 7 patients showed a marked recovery (Fig. 1) and 2 patients showed a partial recovery. However, the therapeutic effects were not statistically significant (p=0.439, Table 3). After zinc supplementation, there was a difference of the serum zinc level between the positive response group and the negative response group. The serum zinc level of the positive response group increased by 40.9 µg/dl and that of the negative response group increased by 7.7 µg/dl. In the positive response group, the serum zinc levels after therapy were significantly higher than those before therapy (p=0.003). The changed serum zinc levels are shown in Table 4. The patients with mild alopecia areata and who had a single alopecia areata patch displayed more positive results than the patients who had multiple alopecia areata patches (Table 5). Two patients complained of mild nausea as a side effect. The summary of the patients is shown in Table 6. Table 1
Clinical data of the 15 patients with alopecia areata patients.

DISCUSSION

There are several reports stating that the serum zinc level is low in alopecia areata patients7,11-13. However, the pathogenesis of this reduced serum zinc level is unknown. As cofactors of metalloenzymes, zinc has considerable effects on nearly all aspects of the metabolism that takes place in the organs of the body, including the skin. In fact, congenital and acquired zinc deficiencies are usually expressed as a variety of skin manifestations such as acrodermatitis enteropathica, psoriasis-like eruptions, blisters, onychopathy and loss of hair6,14. Several reports have shown that oral administration of zinc compounds improved hair growth5. Yet in 1981, Ead15 reported that oral administration of zinc compounds had no therapeutic effect on hair loss. Ead15 found that after zinc supplementation, the serum zinc level changed from 77.5 µg/dl to 112.2 µg/dl and the serum zinc level increased by 34.7 µg/dl, but the patients did not show a positive therapeutic effect. In this study, 6 out of 15 patients belonged to the negative response group. Among this negative response group, 4 patients' serum zinc levels increased and 2 patients' serum zinc levels decreased. We think that the increased serum zinc levels in the 4 patients are related to another cause. The serum zinc level of three patients except patient No. 12, increased less than those of the positive response group. We thought that the No.12 patient's cause of hair loss was related to stress and fatigue. Two patients with decreased serum zinc levels had an irregular oral zinc tablet intake during this study. Zinc is a metal moiety of many enzymes and it is indispensable for normal cellular function and it has important roles in bone formation, cell-mediated immunity, the general immunological defense of the host and tissue growth. Zinc provides structural integrity to enzymes and/or it participates directly in catalysis. Examples of zinc metalloenzymes include DNA and RNA nucleotidyl transferases, alcohol dehydrogenase, glutamic, lactic and malic dehydrogenase and δ-aminolevulinic acid dehydratase16. The etiology of alopecia areata is still unknown. Several kinds of treatments have been tried with various results, i.e., oral and topical corticosteroids, triamcinolone intralesional injection, photochemotherapy, topical irritants and allergens, immunosuppressants and cryotherapy. Checking the serum zinc level is necessary to evaluate hair loss of an unknown cause, and zinc supplementation may be needed in the alopecia areata patients who have a low serum zinc level. In this study, after adhering to zinc supplementation for twelve weeks, the patients' mean serum zinc level changed from 56.9 µg/dl to 84.5 µg/dl, and the level increased by 27.60 µg/dl. When analyzing the differences between the positive and negative response groups, the positive response group increased their serum zinc level by 40.9 µg/dl, and the negative response group increased their serum zinc level by 7.7 µg/dl. This difference was statistically significant. Those patients with mild alopecia areata and those with a single alopecia areata patch had a greater positive response than the patients with moderate alopecia areata and those with multiple alopecia areata patches. The positive response group maintained zinc supplementation for at least 6 months with no recurrence of their hair loss being seen during their follow-up. The positive response group also showed continuous terminal hair regrowth during follow-up. Although these patients had a mild type of long term alopecia areata, zinc supplementation can become a possible adjuvant therapy when combined with other therapeutic methods, and especially for those alopecia areata patients with a low serum zinc level. Prior to this study, there has only been one report of alopecia areata patients having a low serum zinc level in the Korean medical literature3 and there has been no report about the therapeutic effects of zinc supplementation in Korea. This study was the first in Korea to evaluate the therapeutic effects of twelve weeks of oral zinc supplementation in alopecia areata patients with a low serum zinc level and we reported on the changing serum zinc levels after oral zinc supplementation. Positive therapeutic effects were seen in 9 out of 15 patients, but because of the small numbers of patients, the therapeutic effects were not statistically significant. Subsequent studies with a large number of alopecia areata patients are needed to clarify the therapeutic effects of oral zinc supplementation.

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Hair loss in women of color

August 9th, 2010

Semin Cutan Med Surg.2009;28:109
Hair loss in women of color.

Fu JM, Price VH.

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Hair loss in women of color represents a unique diagnostic challenge that requires a systematic approach. In women of color, clinical examination of the hair and scalp is most helpful when performed first and used to guide subsequent history-taking to arrive at a clinical assessment. The most common hair problems in women of color are hair breakage, traction alopecia, and central centrifugal cicatricial alopecia. A careful detailed clinical examination and history will guide the clinician to appropriate counseling and management. It is important to recognize that a patient may have more than one of these 3 diagnoses and each requires separate attention. Traction alopecia is completely preventable with appropriate education of the public and medical establishment.

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Minoxidil for hair loss treatment

August 6th, 2010

J Dermatol. 2009;36:437

Minoxidil for the treatment of male pattern hair loss

Tsuboi R, et al

Minoxidil induces hair regrowth in pattern hair loss by inducing follicles to transition from the early to the late anagen phase. ..... The objective of this trial was to verify the efficacy of minoxidil in a double-blind controlled study with male, pattern hair loss patients as the subjects. ..... The incidence of adverse events was 8.7% the 5% minoxidil group and 5.3% in the 1% minoxidil group, with no significant difference between the groups. This confirms the superiority of 5% topical minoxidil to 1% topical minoxidil in treatment of androgenetic alopecia.

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Laser treatment for hair regrowth in mice

August 6th, 2010

Skin Pharmacol Physiol.2009;23:79

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Effect of Helium-Neon Laser Irradiation on Hair Follicle Regrowth Cycle of Swiss Albino Mice.
Shukla S, et al .

We report the results of a study carried out to investigate the effect of helium-neon (He-Ne) laser (632.8 nm) irradiation on the hair regrowth cycle of testosterone-treated and untreated mice. Both histology and optical coherence tomography (OCT) were used for the measurement of hair regrowth and the relative percentage of hair follicles in different growth phases. A positive correlation was observed for the lengths of hair follicles measured by both methods. Further, the ratios of the lengths of hair follicles in the anagen and catagen phases obtained by both methods were nearly the same. However, the length of the hair follicles measured by both methods differed by a factor of 1.6, with histology showing smaller lengths. He-Ne laser irradiation (at approximately 1 J/cm(2)) of the skin of both the control and the testosterone-treated mice was observed to lead to a significant increase in % anagen hair, indicating stimulation of hair regrowth. The study also demonstrates that OCT can be used to monitor the hair follicle growth cycle, and thus hair follicle disorders or hair loss treatment.

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