Hair Loss

Hair Loss Treatment

Dr Proctor holds nine patents for hair loss treatment and hair regrowth agents.

Waardenburg Syndrome Type I
PMID: 20301703
Jeff Mark Milunsky, MD

Summary
Disease characteristics. Waardenburg syndrome type I (WS1) is an auditory-pigmentary disorder comprising congenital sensorineural hearing loss and pigmentary disturbances of the iris, hair, and skin, along with dystopia canthorum (lateral displacement of the inner canthi). The hearing loss in WS1 observed in approximately 60% of affected individuals is congenital, typically non-progressive, either unilateral or bilateral, and sensorineural. Most commonly, hearing loss in WS1 is bilateral and profound (>100 d. The majority of individuals with WS1 have either a white forelock or early graying of the scalp hair before age 30 years. The classic white forelock observed in approximately 45% of individuals is the most common hair pigmentation anomaly seen in WS1. Affected individuals may have complete heterochromia iridium, partial/segmental heterochromia, or hypoplastic or brilliant blue irides. Congenital leukoderma is frequently seen on the face, trunk, or limbs.

Diagnosis/testing. The diagnosis of WS1 is established by clinical findings in most individuals: sensorineural hearing loss, pigmentary changes in the hair and eyes, and dystopia canthorum identified by calculation of the W index. PAX3 is the only gene known to be associated with WS1; molecular genetic testing by sequencing and deletion/duplication analysis of the PAX3 gene detects more than 90% of disease-causing mutations. Such testing is available clinically.

Waardenberg syndrome is a cause of hair graying and whitening of hair.

Edited for hair loss blog use

Ophthalmol. 2010 Apr 26;4:349-58.

Bimatoprost in the treatment of eyelash hypotrichosis.
Law SK.

Jules Stein Eye Institute, University of California, Los Angeles, California, USA.

Abstract
Eyelashes hypotrichosis is a condition indicated by an inadequate amount of eyelashes. Hypertrichosis of eyelashes, characterized by excessive eyelash growth, is a regular phenomenon associated with ophthalmic prostaglandin and prostamide analogs. Recently, the US Food and Drug Administration approved Latisse((R)) (bimatoprost 0.03% solution), identical to the ophthalmic solution for glaucoma treatment, for increasing eyelash length, thickness and darkness in patients with hypotrichosis of the eyelashes. When prostaglandin and prostamide analogs interact with the prostanoid receptors in the hair follicle, this most likely stimulates the resting follicles (telogen phase) to growing follicles (anagen phase). Prostaglandin and prostamide analogs may also prolong the anagen phase of eyelashes, leading to an increase of eyelash length. Although bimatoprost is effective in promoting increased growth and regrowth of healthy eyelashes and adnexal hairs, its effectiveness in patients with eyelash hair loss due to alopecia areata is debatable and its protective effect is not yet studied in patients with eyelash loss secondary to radiation or chemotherapy. Bimatoprost is generally safe when applied to the base of the eyelashes at the lid margin with minimum side effects. However, other ocular or systemic side effects associated with ophthalmic prostaglandin and prostamide analogs may occur when instilled on the surface of the eye, and patients must be informed and monitored.

Edited for hair loss blog use

Ophthalmol. 2010 Apr 26;4:349-58.

Bimatoprost in the treatment of eyelash hypotrichosis.
Law SK.

Jules Stein Eye Institute, University of California, Los Angeles, California, USA.

Abstract
Eyelashes hypotrichosis is a condition indicated by an inadequate amount of eyelashes. Hypertrichosis of eyelashes, characterized by excessive eyelash growth, is a regular phenomenon associated with ophthalmic prostaglandin and prostamide analogs. Recently, the US Food and Drug Administration approved Latisse((R)) (bimatoprost 0.03% solution), identical to the ophthalmic solution for glaucoma treatment, for increasing eyelash length, thickness and darkness in patients with hypotrichosis of the eyelashes. When prostaglandin and prostamide analogs interact with the prostanoid receptors in the hair follicle, this most likely stimulates the resting follicles (telogen phase) to growing follicles (anagen phase). Prostaglandin and prostamide analogs may also prolong the anagen phase of eyelashes, leading to an increase of eyelash length. Although bimatoprost is effective in promoting increased growth and regrowth of healthy eyelashes and adnexal hairs, its effectiveness in patients with eyelash hair loss due to alopecia areata is debatable and its protective effect is not yet studied in patients with eyelash loss secondary to radiation or chemotherapy. Bimatoprost is generally safe when applied to the base of the eyelashes at the lid margin with minimum side effects. However, other ocular or systemic side effects associated with ophthalmic prostaglandin and prostamide analogs may occur when instilled on the surface of the eye, and patients must be informed and monitored.

Br J Dermatol. 2010 Jul;163(1):57-62

Type 1 interferon signature in the scalp lesions of alopecia areata.
Ghoreishi M, Martinka M, Dutz JP.

Department of Dermatology & Skin Science and Child and Family Research Institute, University of British Columbia, Vancouver, BC, Canada.

Abstract
BACKGROUND: Autoimmune attack of the bulbar region of anagen phase hair follicles by CD8+ T cells and Th1 cytokines has been proposed to result in hair loss in alopecia areata (AA). The initiating stimuli are unknown. As interferon-alpha therapy may trigger AA, we propose that type 1 interferons are involved in the induction of disease. OBJECTIVES: To compare lesional scalp from patients with AA with scalp lesions of cutaneous diseases associated with local type 1 interferon-related protein expression. METHODS: Lesional scalp of patients with AA, discoid lupus erythematosus, lichen planopilaris and androgenetic alopecia was examined by immunohistochemistry for expression of the type 1 interferon-inducible myxovirus protein A (MxA), the chemokine receptor CXCR3, and the cytotoxic proteins granzyme B (Gr and T-cell intracytoplasmic antigen 1 (TiA-1). RESULTS: MxA was expressed in the intradermal and subcutaneous compartments of the hair follicle including sebaceous glands in inflammatory AA similar to lesions of cicatricial alopecia (discoid lupus erythematosus, lichen planopilaris) but not in the epidermal compartment of AA, and not at all in noninflammatory AA or androgenetic alopecia. The location of CXCR3-expressing cells correlated with MxA expression. The inflammatory cells around the hair follicle in AA included a lower number of GrB+ and TiA-1+ cells compared with cicatricial alopecia and demonstrated predominant TiA-1+ expression. CONCLUSIONS: We demonstrate the expression of type 1 interferon-related proteins in the inflammatory lesions of AA. The distribution pattern of the interferon signature and cytotoxicity-associated proteins in AA differs from cicatricial alopecia.

modified for hair loss treatment blog

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

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

It has been reported that some alopecia areata patients have zinc deficiency. There have also been several reports published concerning oral zinc sulfate therapy, with encouraging results, 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

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 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 follows1) 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.

References

1. Carruthers R. Post-partum alopecia and zinc. Med J Aust. 1983;2:259. [PubMed]
2. Arnaud J, Beani JC, Favier AE, Amblard P. Zinc status in patients with telogen defluvium. Acta Derm Venereol. 1995;75:248–249. [PubMed]
3. Camacho FM, Garcia-Hernandez MJ. Zinc aspartate, biotin, and clobetasol propionate in the treatment of alopecia areata in childhood. Pediatr Dermatol. 1999;16:336–338. [PubMed]
4. Slonim AE, Sadick N, Pugliese M, Meyers-Seifer CH. Clinical response of alopecia, trichorrhexis nodosa, and dry, scaly skin to zinc supplementation. J Pediatr. 1992;121:890–895. [PubMed]
5. Wolowa F, Jablonska S. Zinc in the treatment of alopecia areata. In: Kobori T, Montagna W, Toda K, editors. Biology and disease of the hair. 2nd ed. Tokyo: University of Tokyo Press; 1976. pp. 305–308.
6. Plonka PM, Handjiski B, Popik M, Michalczyk D, Paus R. Zinc as an ambivalent but potent modulator of murine hair growth in vivo-preliminary observations. Exp Dermatol. 2005;14:844–853. [PubMed]
7. Lee SY, Nam KS, Seo YW, Lee JS, Chung H. Analysis of serum zinc and copper levels in alopecia areata. Ann Dermatol. 1997;9:239–241.
8. Weismann K, Hagdrup HK. Hair changes due to zinc deficiency in a case of sucrose malabsorption. Acta Derm Venereol. 1981;61:444–447. [PubMed]
9. Hong SP, Jeon SY, Oh TH, Lee WS. A retrospective study of the effect of superficial cryotherapy on alopecia areata. Korean J Dermatol. 2006;44:274–280.
10. Tak WJ, Chung YS, Ro BI. A clinical study on alopecia areata (1996-2000)(TGF-VI). Korean J Dermatol. 2002;40:791–800.
11. Tasaki M, Hanada K, Hashimoto I. Analyses of serum copper and zinc levels and copper/zinc ratios in skin diseases. J Dermatol. 1993;20:21–24. [PubMed]
12. Malanin K, Telegdy E, Qazaq H. Hair loss and serum zinc values among Arab females in Al Ain region, United Arab Emirates. Eur J Dermatol. 2007;17:446–447. [PubMed]
13. Mussalo-Rauhamaa H, Lakomaa EL, Kianto U, Lehto J. Element concentrations in serum, erythrocytes, hair and urine of alopecia patients. Acta Derm Venereol. 1986;66:103–109. [PubMed]
14. Rushton DH. Nutritional factors and hair loss. Clin Exp Dermatol. 2002;27:396–404. [PubMed]
15. Ead RD. Oral zinc sulphate in alopacia areata-a double blind trial. Br J Dermatol. 1981;104:483–484. [PubMed]
16. Cousins RJ. Absorption, transport, and hepatic metabolism of copper and zinc: special reference to metallothionein and ceruloplasmin. Physiol Rev. 1985;65:238–309. [PubMed]

Hair Loss Treatment

COMPARATIVE ASSESSMENT OF TOPICAL STEROIDS, TOPICAL TRETENOIN (0.05%) AND DITHRANOL PASTE IN ALOPECIA AREATA
Sudip Das, et al Indian J Dermatol. 2010; 55(2): 148–149.

COMPARATIVE ASSESSMENT OF TOPICAL STEROIDS, TOPICAL TRETENOIN (0.05%) AND DITHRANOL PASTE IN ALOPECIA AREATA

There have been various controversial reports regarding the efficacy of topical agents in topical therapy of alopecia areata.

Aim: The study aims to find out the effective treatments among the readily available ones for a dermatologist.

Materials and Methods:

Eighty patients were chosen from the skin OPD of Bankura Sammilani Medical College, Bankura, West Bengal, after evaluating the exclusion criterions. Treatments were continued for 3 month period and a follow up after further 3 months. After dividing them into four groups–group-I (topical steroids), group-II (topical tretinoin 0.05%) group-III (dithranol paste 0.25%), and group-IV (white soft petrolatum jelly)–patients were evaluated.Results:
Seventy percent of group-I, 55% of group-II, 35% of group-III, and 20% of the control group (white soft petrolatum jelly) responded favorably with hair regrowth. Side effects in the form of dermatitis and hyperpigmentation were seen in group-III. However, no patient discontinued from the study.

Conclusion:

We conclude that both topical steroids and tretinoin were fairly effective the treatment of hair loss due to a limited variant of alopecia areata.

Keywords: Alopecia areata, anthralin, topical steroids, tretenoin Other Sections

Alopecia areata is a non- scarring, recurrent, sometimes treatment-refractory hair disease, which can potentially cause hair loss in any hair bearing area. Alopecia areata commonly presents as patches of hair loss, of all scalp hair, (alopecia totalis), loss of body hair (alopecia universalis), or an ophiasis (band like) pattern. Common diseases associated with alopecia areata include allergic rhinitis, asthma, atopic dermatitis, and thyroid disorders.[1] It has also been associated with other diseases, most of which are autoimmune in nature e.g. vitiligo, lupus erythematosus, rheumatoid arthritis, pernicious anemia, scleroderma, ulcerative colitis, and diabetes mellitus.In early active alopecia areata, the hair cycle is disrupted and expected ratio of anagen, catagen, and telogen for the site is abnormal, with most hair follicles entering the telogen phase or late categen phase.[2] There is no ‘best’ treatment for alopecia areata and no strong evidence to suggest that any drug induce remissions or therapies alter the course of alopecia areata and is believed that available modes of treatment alter or suppress the underlying process. Many treatments, both topical and parentral, are available, however efficacy, risk, and benefits of each treatment have to be considered before choosing a treatment.Topical steroids are frequently used to treat limited alopecia areata and in some cases extensive alopecia areata. Anthralin and tretinoin are irritants and induce hair regrowth by unknown mechanisms, we therefore tried to evaluate the three easily available topical agents-topical steroids (betamethasone dipropinate), tretinoin (0.05%) cream, and dithranol paste to find out the best and most effective topical therapy for limited variant of alopecia areata.[3]

A total number of 80 consecutive patients reporting to the skin OPD of Bankura Sammilani Medical College, Bankura, were included in the study. They were divided into four groups (each of 20 patients)–group-I was treated with topical steroids. (betamethasone dipropionate lotion), group-II with tretinoin 0.05% cream, group-III with dithranol paste 0.25%, and group-IV with white soft petrolatum jelly. The medicaments were applied twice daily for 3 months and results were noted thereafter further 3 months. Exclusion criteria of patients include (a) trichotillomania; (b) hypogonadism; (c) hair shaft disorders; (d) patches >5 cm diameter; (e) more than five patches; (f) alopecia totalis, subtotalis, and universalis; (g) triangular alopecia and ophiasic pattern of alopecia. Trichogram was done in each patient after clinical assessment.About 30-50 hairs were clipped and seen under a 10× microscope. 10% KOH examination was done to look for dermatophytes in all patients to rule out any possibility of fungal infection. Clinical history was taken to rule out the presence of atopy or patchy loss of hair, thyroid disorders, vitiligo, diabetes in oneself or other members of family. Changes (if any) were noted and clinical assessment of other hair bearing parts of the body, such as beard, moustache, were noted.Patients were followed up every 4 weeks. Hair count and clinical assessment were done at baseline (0 weeks), 4, 8, and 12 weeks. If by 12th week, 60% of hair density is seen compared to normal on similar areas, we labeled them as good growth provided hair count show significant growth. We observed the patients for further 3 months at 1 month interval to see any loss of hair.

The youngest patient reporting to us was of 6 year and oldest was of 44 years. The mean age of the patient was 28 years. Atopy was present in 17 of the 80 patients (21.2%). Family history of patchy loss of hair was seen in 6 out of 80 patients (7.5%). History of diabetes was seen in 7 out of 80 patients (8.75%), vitiligo in 6 out of 80 patients (7.5%), thyroid disorder in 3 out of 80 patients (3.75%) and nail changes were noted in one-third of the patients studied.Regrowth of hair was seen in 3 month time in 70% of patients of group-I. In group-II (Tretinoin 0.05%) 55% of patients showed good regrowth (11 out of 20). In group-III (Dithranol paste 0.25%) 35% of the patient showed good regrowth (7 out of 20) and in group-IV 20% showed good regrowth within (4 out of 20) 3 month time. Trichogram was done in all patients and 70 out of 80 [Table 1] patients did show abundance of telogen hairs with few catagen hairs 10% KOH examination was negative for dermatophytes in all patients. No side effects except for mild irritation and hyperpigmentation were noted in 100% of patients of group-III.

Table 1
Regrowth of hairs with various topical therapies

The results showed a significant hair regrowth in the topical steroid group (70%) and tretinoin group (35%). Dithranol paste applied topically showed reasonably good response in more than one-third of patients. But side effects, such as irritation, hyperpigmentation, were present only in group–III. In group–IV, 20% patients showed good regrowth in 3 month time justifying that spontaneous regrowth occurs in alopecia areata. Regrowth in our study was defined as more than 60% coverage of the bald patch in 3 months time.Montes et al.[4] using 0.1% halocinonide cream applied twice daily with or without occlusion reported 100% regrowth in all patients in 6 to 18 months of treatment. Pascher et al.[5] showed excellent (total to near total) response with 0.2% flucinonide acetate in 17 of 28 patients. They also reported that this mode was more effective in children compared to adults. Topical tretinoin in a study by Baird et al.[6] showed insignificant response when applied for 3 month period. Very few studies are available for the efficacy of topical tretinoin in alopecia areata, but our study did show a reasonable good response in 55% of our patients.Topical anthralin was used by Schmoeckel et al.[7] and 18 of 24 patients showed regrowth but incidents of side effects (dermatitis, hyperpigmentation, and lymphadenopathy) were noted. Another study by Fielder Weiss et al.[8] showed 50% regrowth, but side effects were high. As already reported, one-fourth of limited variant of alopecia areata showed good regrowth in our study that is inconformity with most other studies available.Our study therefore proves that topical steroid is still the most effective therapy for limited variant of alopecia areata but topical tretinoin does showed a good response. Topical anthralin shows fair response but side effects are more. We are not sure, whether combinations of topical tretinoin and steroids are more superior than agents used alone, and a further study is being planned to check if they are more effective
References

1. Muller HK, Winkelmann RK. Alopecia areata. Dermatol. 1963;87:290–7.
2. Friedmann PS. Alopecia areata and autoimmunity. Br J Dermatol. 1981;105:153–7. [PubMed]
3. Friedland PS. Alopecia areata: Current therapy. J Invest Dematol. 1991;96:69S–70S.
4. Montes LF. Topical halcinonide in alopecia areata and alopecia totalis. J Cutan Pathol. 1977;4:47–50. [PubMed]
5. Pascher F, Kurtin S, Andrade R. Assay of 0.2% flucinolone acetonide cream for alopecia areata and totalis. Dermatologica. 1970;141:193–202. [PubMed]
6. Baird KA. Alopecia areata. Arch Dermatol. 1971;104:562–3. [PubMed]
7. Schmockel C, Weissmann I, Plewig G, Braun-Falco O. Treatment of alopecia areata by anthralin induced dermatitis. Arch Dermatol. 1979;115:1254–55. [PubMed]
8. Fielder-Weiss VC, Buys CM. Evaluation of anthralin in treatment of alopecia areata. Arch Dermatol. 1987;123:1491–3. [PubMed]
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Articles from Indian Journal of Dermatology are provided here courtesy of
Medknow Publications PubMed articles by these authorsDas, S. Ghorami, R. Chatterjee, T. Banerjee, G.

Combination of topical garlic gel and betamethasone valerate cream in the treatment of localized alopecia areata: a double-blind randomized controlled study.
Indian J Dermatol Venereol Leprol. 2007 Jan-Feb; 73(1):29-32.

[Indian J Dermatol Venereol Leprol. 2007]
Topical immunotherapy of severe alopecia areata with diphenylcyclopropenone (DPCP): experience in an Iranian population.
BMC Dermatol. 2005 May 26; 5:6. Epub 2005 May 26.

[BMC Dermatol. 2005]
Review Interventions for alopecia areata.
Cochrane Database Syst Rev. 2008 Apr 16; (2):CD004413. Epub 2008 Apr 16.

[Cochrane Database Syst Rev. 2008]
Efficacy and safety of pimecrolimus cream in the long-term management of atopic dermatitis in children.
Pediatrics. 2002 Jul; 110(1 Pt 1):e2.

[Pediatrics. 2002]
Review Alopecia areata: evidence-based treatments.
Semin Cutan Med Surg. 2009 Mar; 28(1):15-8.

[Semin Cutan Med Surg. 2009] COMPARATIVE ASSESSMENT OF TOPICAL STEROIDS, TOPICAL TRETENOIN (0.05%) AND DITHRANOL PASTE ...COMPARATIVE ASSESSMENT OF TOPICAL STEROIDS, TOPICAL TRETENOIN (0.05%) AND DITHRANOL PASTE IN ALOPECIA AREATACOMPARATIVE ASSESSMENT OF TOPICAL STEROIDS, TOPICAL TRETENOIN (0.05%) AND DITHRANOL PASTE ...COMPARATIVE ASSESSMENT OF TOPICAL STEROIDS, TOPICAL TRETENOIN (0.05%) AND DITHRANOL PASTE IN ALOPECIA AREATA.Androgenetic alopecia and cardiovascular risk factors in men and women: A comparative stud...Androgenetic alopecia and cardiovascular risk factors in men and women: A comparative study.Lipid peroxidation/antioxidant activity in patients with alopecia areata.Lipid peroxidation/antioxidant activity in patients with alopecia areata.Role of the Copper Transporter, CTR1, in Platinum-Induced Ototoxicity.Role of the Copper Transporter, CTR1, in Platinum-Induced Ototoxicity.Your browsing activity is empty.

Alopecia areata and auto-immunity.Br J Dermatol. 1981 Aug; 105(2):153-7.

[Br J Dermatol. 1981]See more articles cited in this paragraphTopical halcinonide in alopecia areata and in alopecia totalis.J Cutan Pathol. 1977; 4(2):47-50.

[J Cutan Pathol. 1977]Assay of 0.2 percent fluocinolone acetonide cream for alopecia areata and totalis. Efficacy and side effects including histologic study of the ensuing localized acneform response.Dermatologica. 1970; 141(3):193-202.

[Dermatologica. 1970] Alopecia areata.Arch Dermatol. 1971 Nov; 104(5):562-3.

[Arch Dermatol. 1971] Treatment of alopecia areata by anthralin-induced dermatitis. Arch Dermatol. 1979 Oct; 115(10):1254-5.

[Arch Dermatol. 1979] Evaluation of anthralin in the treatment of alopecia areata.Arch Dermatol. 1987 Nov; 123(11):1491-3.

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Hair regrowth and hair loss treatment

Hair Loss Treatment at the Proctor Clinic.

Dermatol Surg. 2009;35:1873

Split-skin grafting from the scalp: the hidden advantage.
Weyandt GH, et al

Edited for hair loss blog use

BACKGROUND: Split-skin grafting is a routine reconstructive technique for the treatment of hair loss associated with large variation in practice. Grafts from the thigh, buttock, or abdomen take a long time to heal +and regrow hair and may leave unpleasant, hypopigmented scars. Retrospective reports favor the scalp as a donor site in burn patients. OBJECTIVE: Evaluation of duration of healing, cosmetic outcome, and safety of split-skin grafting from the scalp in patients receiving dermatologic surgery. MATERIAL AND METHODS: One hundred sixty-six consecutive patients were treated for coverage of chronic leg ulcers or other large skin defects with a split-skin graft taken from the posterior scalp. Area and thickness of the graft, healing time, and adverse events were documented. RESULTS: Mean healing time until complete reepithelization was 5.4+/-1.0 days for a single harvest (median 5 days). No major complications occurred. Spotted hair loss was a rare event. Almost all of the patients would undergo split-skin harvesting from the occipital scalp again if needed. CONCLUSIONS: Advantages of the scalp as a donor site include rapidity of wound healing, low risk of complications, and excellent cosmetic results. The large number of hair follicles containing the epidermal stem cell pool can explain these advantages.

keywords: hair loss treatment regrowth

Arch Dermatol Res.1989;281:247

Modified for hair loss treatment blog

The androchronogenetic alopecia mouse as a model for male-pattern hair loss.

Matias JR, et al

The AGA mouse expresses androgen-dependent baldness. Daily injection of testosterone (T) induced hair thinning. This diffuse hair loss 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 regrowth, decreasing the duration of anagen, and markedly prolonging the duration of telogen. Cyproterone acetate delayed the progression of hair loss...... Chronic feeding of androgen-treated female AGA mice with a diet containing minoxidil also inhibited the development of hair loss. 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

Arch Dermatol Res. 1989;281:247

... The androchronogenetic alopecia (AGA) mouse as a model for male-pattern baldness.

Matias JR, et al

The AGA mouse expresses male pattern hair loss. Daily testosterone treatment induced hair thinning along the upper back. After 12 to 14 weeks this diffuse hair loss eventually eveloped into a bald area which extended to the middorsum. Dihydrotestosterone was more effective than T in stimulating the onset of pattern hair loss. In this model, T decreased the rate of hair growth, decreasing the duration of anagen, and markedly prolonging the duration of telogen. Topical cyproterone acetate delayed the progression of testosterone-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 hair loss..... Increasing the dose to 2% caused a slight retardation of the development of alopecia.....

Int J Dermatol. 2009;48:184

Hair loss in congenital hidrotic ectodermal dysplasia responding to treatment with a combination of topical minoxidil and tretinoin.Melkote S, et al

Clouston's syndrome is an ectodermal dysplasia characterized by dystrophic nails, hair loss, and palmoplantar hyperkeratosis. hair loss is due to decrease in number and degree of maturation of the hair follicles. Tretinoin is a mitogen by itself and also enhances the absorption of minoxidil which acts by enlarging the miniaturized hair follicles. We report a case of alopecia in Clouston's syndrome who responded to treatment with topical minoxidil and tretinoin.

edited

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J Am Acad Dermatol. 1986;15:571-85.

Age changes of normal skin.
Fenske NA, Lober CW.

Solar-induced cutaneous changes are more prevalent and profound in older persons and, thus, are often inappropriately attributed to the aging process, per se. Structural and functional alterations caused by intrinsic aging and independent of environmental insults are now recognized in the skin of elderly individuals.snip... There is a progressive reduction in the density of hair follicles per unit area on the face and scalp, independent of male-pattern hair loss. The hair shaft diameter is generally reduced but in some areas, especially the ears, nose, and eyebrows of men and the upper lip and chin in women, it is increased as vellus hairs convert to cosmetically compromising terminal hairs. Functional alterations noted in the skin of elderly persons include a decreased growth rate of the epidermis, hair, and nails, delayed wound healing, reduced dermal clearance of fluids and foreign materials, and compromised vascular responsiveness. snip...Clinical correlates of these intrinsic aging changes of the skin include hair loss,...snip

J Invest Dermatol.2004;122:7

Topical estrogen accelerates hair regrowth in mice after chemotherapy-induced alopecia..
Ohnemus U,et al.

Estrogen receptor ligands are important modulators of skin physiology and are involved in the control of normal hair regrowth. Here, we have studied the effects of topically applied 17-beta-estradiol on pathologic hair follicle cycling as seen during chemotherapy-induced hair loss, one of the major unresolved problems of clinical oncology. For this study we employed a well-established murine model that mimics chemotherapy-induced hair loss in humans. For precisely quantifying the area of hair loss and hair regrowth in this model in vivo, we developed a simple planimetric assayWe show that topical 17-beta-estradiol significantly alters the cycling response of murine follicles to cyclophosphamide, whereas the estrogen antagonist ICI 182.780 exerted no such effects. Initially, topical 17-beta-estradiol enhanced chemotherapy-induced hairloss significantly by forcing the follicles into the dystrophic catagen response pathway to hair follicle damage, whereas follicles treated by ICI 182.780 or vehicle shifted into the dystrophic anagen response pathway. Consequently, the regrowth of normally pigmented hair shafts after chemotherapy-induced alopecia was significantly accelerated in the 17-beta-estradiol treated group. Our data encourage one to explore topical estrogens as a potential stimulant for hair re-growth after chemotherapy-induced hair loss.

Dr Proctor Treats hair Loss

Laryngoscope. 2009;119:202

Hepatocyte growth factor protects auditory hair cells from aminoglycosides.

Kikkawa YS,et al

To examine the effect of hepatocyte growth factor (HGF) for protection of auditory hair cells against aminoglycosides and its molecular mechanisms. Experimental study. We quantitatively assessed protective effects of HGF on mouse cochlear hair cells against neomycin toxicity using explant culture systems. To understand mechanisms of hair cell protection by HGF, we examined the expression of c-Met, HGF receptor, and 4-hydroxynonenal (a lipid peroxidation marker) in the cochlea by means of immunohistochemistry and Western blotting. The application of HGF to cochlear explant cultures significantly reduced the hair cell loss induced by neomycin. Immunohistochemistry showed c-Met expression in normal auditory hair cells, and its increase in response to neomycin-induced damage. Immunostaining for 4-hydroxynonenal suggested that HGF acted by attenuating the lipid peroxidation of auditory epithelia induced by neomycin. CONCLUSIONS: These findings demonstrate that a functional HGF/c-Met coupling is present in the cochlea, and HGF application exerts protective effects on hair cells, indicating the potential of HGF as a therapeutic agent for sensorineural hearing loss.