Female Pattern Hair Loss: Epidemiology, Mechanism, Classification, Diagnosis and Treatment Options
Dr Shahram Sadeghi M.D,FRACGP, Ph.D, Registrar Australasian College of Cosmetic Surgery, Dr Russell Knudsen MBBS, FFMACCS
Introduction: Hair loss is a frequent and stressful event for women(1). Despite being prevalent in up to 50% among women as they age, its’ severity is underestimated by women. In addition, due to complexity of treatment, it is undertreated or even ignored by doctors(2, 3).Among many different causes of hair loss in women, female pattern hair loss (FPHL) is the most common cause of hair loss. FPHL is most often described as reduced hair density in crown and frontal scalp while the frontal hairline remains intact(2, 4). Affected women may experience psychological distress and it can deteriorate their quality of life by affecting their appearance.
Hyperandrogenism and the role of these hormones on hair follicles has been well explained and related to MPHL, however its’ role in FPHL is less certain. Probably the best way to describe FPHL is that anagen phase of scalp hair reduces and activation of local androgens in scalp skin accelerates this process (5).Furthermore, unlike male pattern hair loss, family history is not always a easily identified risk factor. Due to this ambiguity in aetiology, there hasn’t been a worldwide accepted algorithm for the treatment of FPHL.
Diagnosis should be made based on history, close clinical examination, biochemical and hormonal tests and scalp biopsy to rule out other causes including acute telogen effluvium and chronic telogen effluvium. Pharmacological interventions, including topical minoxidil, 5α reductase inhibitors (finasteride and dutasteride), anti-androgenic medications (including spironolactone and cyproterone) have all been suggested. Furthermore, low energy laser treatment also has been used successfully in some institutions. In some suitable candidates, surgical interventions, such as hair transplants have also been employed. There hasn’t, however, been a clear comprehensive publication to present these interventions in a practical order.
We used “Embase”, “Medline” and “Cochrane” databases to search for latest publications about FPHL, including all identified studies and systematic reviews with interest in diagnosis, classification and treatment of this condition. They were critically reviewed and their findings were summarised in a practical format. This review aims to provide a sound knowledge about prevalence and incidence and classification of FPHL, its’ patterns, possible causes, diagnosis and treatment options. In this summary we will try to provide a practical algorithm about how to approach and manage FPHL.
Hair is a major factor of the self-esteem and the feeling of attractiveness among women(1). Interestingly, women tend to underestimate the severity of their hair loss more than their treating doctors and therefore there are potentially more patients with hair loss than those already seeking treatment (2). Hair loss can be classified as scarring (rare) and non-scarring hair loss. Discoid lupus erythematosus is an examples for scarring hair loss. The main causes of non-scarring hair loss are alopecia areata or alopecia totalis, telogen effluvium, anagen effluvium and female pattern hair loss (FPHL). Differentiation of these types of hair loss is crucial as each of them needs a different approach. Appropriate history, physical examination, and biochemical and histological investigations are the key to the right diagnosis (6). Alopecia areata represents itself as distinct patches of hair loss on hair bearing areas of the scalp while alopecia totalis involves the whole scalp. In both of these conditions hair loss is complete and is characterised by presence of hair loss and hair breakage (7). Telogen effluvium is categorised as acute or chronic. Acute telogen effluvium can be seen among patients with previous history of severe physical or psychological illness, prolonged surgery or anaesthesia, pregnancy, blood loss, or crash dieting. Chronic telogen effluvium is seen in patients with underactive thyroid, SLE, iron deficiency anaemia or history of taking certain medications (8, 9). Sometimes there seems to be no initiating cause. The history of these medical conditions can go back as much as 6 to 8 months (9). The most commonly reported drugs that can cause hair loss include chemotherapy agents, amphetamines, allopurinol, aspirin, carbamazepine, beta blockers, warfarin, heparin, isotretinoin, levodopa, lithium, propylthiouracil and Vitamine A (10-12). There has also been case reports of hair loss by bromocriptine, an ergot derivate used for the treatment of hyperprolactinemia(13) and Paroxetine a Selective Serotonin Reuptake Inhibitor (SSRI) (14).
Female pattern hair loss (FPHL) is the most common cause of hair loss among women(2). In this type of hair loss, terminal hair follicles transform to small and unpigmented vellus hair follicles and there is also reduction in the number of pilosebaceous units of scalp.Clinically it is generally described as reduced hair density in the crown and frontal scalp while frontal hairline remains intact (4). In severe cases it can extend variably into the lower scalp. Affected women may experience psychological distress and it can deteriorate their quality of life as women pay more attention to their looks than men. Prevalence and the intensity of FPHL increases with age from 12% among women younger than 30 to 25%-32% among women aged 65 to 80 and more than 50% in women 80 years or older(3). Olsen has categorised FPHL occurrence into two peaks: early onset in teen age with more severe hair loss if left untreated, and late onset in the 40s or later in life with less severe presentation of hair loss but with a higher incidence (15). Despite being a common problem, our knowledge about FPHL is limited and there is not a general agreement on how to treat it.
Aetiology of FPHL:
One of the mechanisms of FPHL is considered to be due to androgenic factors.In women testosterone formation occurs mainly in the skin. Dehydroepiandrosterone (DHEA), DHEA sulphate and androstenedione are secreted via the adrenals and ovaries and then peripherally converted to testosterone (16). Testosterone needs to be converted to dihydrotestosterone by 5α reductase (Type 1 and 2) expressed in various tissues such as sex organs and skin in order to be biologically active on the pilosebaceous unit and initiate hair loss. Furthermore recent studies also have found an association between FPHL and lack of p450 α aromatase enzyme, an enzyme that catalyses conversion of testosterone to oestradiol thereby reducing the amount of intrafollicular testosterone available for conversion to dihydrotestosterone (DHT) (17).However these are not the only causes of hair loss and it can even occur in women with normal circulatory androgens. In fact most women with FPHL show no clinical or biochemical evidence of androgen excess (18). This is where the role of genetic and family history becomes important and in fact due to lack of the clear role of androgens, the term FPHL is preferred to androgenetic hair loss (15, 19). Finally sometimes even the history and family history fails to explain the cause of hair loss and that makes FPHL even more confusing (18).
History: As discussed before, a proper history is the key for the right diagnosis. Family history of hair loss (male and female), previous illnesses, surgeries, pregnancy and exposure to medications should be elucidated.
Physical examination of the hair is still an important part of making the right diagnosis, although recently, dermatoscopy, digital hair microscopy and scalp biopsy have extensively replaced physical testing. Some of the useful exams are summarised here(9):
Pull test or traction test or “Sabouraud’s sign”: normally after a gentle pull not more than five hair can be retrieved, while in hair loss this number increases (20, 21).
Tug test: in this test a group of 50 to 70 hairs are pulled using a haemostat and then examined under the microscope. This technique has mainly been replaced with skin biopsy as it is a quite painful examination.
Slide technique: holding hair with two fingers and then rubbing it toward the scalp with other thumb and index finger of other hand. If it resists the movement and loses its’ shape, it is a sign of cuticle damage.
Roll technique: rolling few hair shafts between thumb and index finger can give some idea about the hair shaft diameter and the progression of terminal hair toward vellus hair.
Hair count: the patient is asked to keep the count of their daily hair loss and collect the hair lost in one day and bring to the practice for examination under the microscope. Because of its difficulty, the hair wash method has been suggested instead, where the patient collects their hair after each shower for five days and brings them to their doctor (22).
Density mapping: by scoring the hair density from 0 to 10 in a pictorial manner one can clarify the pattern of hair loss.
All previous examinations can still be very useful but have been mostly replaced by dermatoscopic examination or scalp biopsy. In dermatoscopic examination some of the commonly signs during examination are – seeing hair shafts with different diameters, brown halo spots at the follicular ostium around the hair shaft, empty follicles and finally scalp pigmentation due to sun damage (23).
For performing scalp biopsy it is recommended to take three, 4 mm core biopsies in the direction of the hair follicles from the central scalp to rule out chronic telogen effluvium, diffuse alopecia areata or cicatricial hair loss (mainly in African women) and differentiate it from FPHL. In normal scalp the ratio of terminal to vellus or vellus like hair is usually 7:1 In FPHL it is 2.2-4:1 and it is more than 8:1 in chronic telogen effluvium. 5-6:1 is considered indeterminate. The total number of hairs/cm2 in FPHL is usually significantly less than the normal 240-400 /cm2. It may be as low as 30-50 hairs/cm2(8, 18).
Laboratory tests: Full blood count (FBC), TSH, Iron studies, serum zinc, ANA and Rheumatoid factor are a good start(24, 25). Most women with FPHL don’t have any signs of hyperandrogenism and androgenic tests might not be necessary. Patients who have hirsuitism or are overweight, those with moderate to severe acne, or acne that is resistant to treatment, patients with acanthosis nigricans ,women with irregular periods or presence of galactorrhea are good candidates for androgen studies. For these patients, free testosterone, DHEA sulphate and Sex Hormone Binding Globulin (SHBG), 5α Dihydrotestosterone, FSH, LH, Progesterone and Oestrogen levels (preferably at day 1-14 of cycle) should be tested while patients are off hormonal contraceptives for a month. Prostate specific antigen (PSA) also has been considered as a marker of androgenisation (0.02 ng/ml in premenopausal and 0.04 in postmenopausal women) (26).Testosterone or DHEA sulphate more than twice as the normal range should be referred to an endocrinologist to rule out malignancies. A Prolactin level should be requested if there are suspicions of galactorrhea(18)
Minoxidil is used as 2% or 5% topical lotion. Minoxidil sulphate is the active form of this medication in the body and is a potassium channel opener that relaxes smooth muscles and initiates vasodilatation. In vitro studies however have shown that its’ effect on hair growth is independent from its vasodilatory effect (27, 28). In fact it works by initiating the transition from telogen to anagen and maintaining anagen in the follicular life cycle (29). Minoxidils effect on hair growth can vary from 16% to a 44% increase(30). The main side effect of minoxidil is contact dermatitis due to irritation by its’ carrier vehicle propylene glycol. This problem can be resolved by switching to its foam preparation (Regaine Foam) that doesn’t have propylene glycol but instead uses glycerine as its’ vehicle (31). Finally, a study by Shine et al showed that mixing minoxidil with tretinoin once a day makes it as effective of twice a day minoxidil only (27). It is worth noting that minoxidil is mostly absorbed within 90 minutes but is retained in the stratum corneum for us to 21 hours.
Beside minoxidil, topical combinations of 0.025% progesterone and 0.03% spironolactone have also been tried successfully in premenopausal women. For postmenopausal women, 0.03% of estradiol valerate has been recommended (30).
Fluridil (Eucapil) is a topical anti-androgenic medication that has been used widely in Europe and found to be effective in treatment of FPHL(32).
Systemic and anti-androgenic treatments:
Finasteride is a testosterone conversion inhibitor that inhibits the 5α reductase type 2 isonenzyme and has been examined in different studies with controversial results in women .Overall it seems a 12 months intake of 2.5 mg/day to 5 mg/day finasteride in norm-androgenic women can improve hair density and hair thickness with no difference between pre and post menopausal women (33-35). Similarly, 12 months of 2.5 mg/day finasteride with oral contraceptives has been reported to improve hair loss in norm-androgenic premenopausal women(36). For women with hyper-androgenism a lower dose of finasteride (1.25 mg/day) was also found to be effective (37). One explanation for why finasteride in higher doses has been more successful in norm-androgenic women is that those women might have had higher activity of 5α reductase enzyme in their scalp(38). Finasteride is a well tolerated medication with infrequent side effects including breast tenderness and increased libido(8). Dutasteride is a combined 5α reductase type 1 and 2 inhibitor and has been tested is small studies with results still not that clear(39), however other small studies have shown significant improvement of hair loss even with 0.25 mg/day of dutasteride (40).
Spironolactone works as an androgen inhibitor by suppression of the testosterone production in adrenal it also competitively inhibits binding of the androgens to the hair follicles and suppresses their action (41). Spironolactone has been used successfully for decades in Australia (100 to 200 mg/day) for the treatment of FPHL. It is recommended to start spironolactone with 50 mg a day and increase by 50 mg monthtly to the maximum dose of 200 mg/day (30). The combination of Spironolactone and Finasteride has been shown to be superior to each of them used alone . Common side effects of spironolactone are hyperkalaemia, orthostatic hypotension, fatigue and urticaria as well as reduced libido and irregular vaginal bleeding. Regular blood pressure and potassium control, especially in the first few months after initiating it, as well as prescribing oral contraceptives are crucial(30).
All anti-androgenic medications potentially carry risks of genital abnormalities in a male foetus therefore a reliable contraceptive is recommended in premenopausal women(15). At the same time, the benefit of the combined oral contraceptives have been known for a while on pilosebaceous unit (PSU) disorders including acne vulgaris and hirsutism, and can benefit FPHL, another form of “PSU disorder”. Ethinyloestradiol reduces circulating androgens by inhibiting FSH and LH and increasing sex hormone binding proteins. Progesterone on the other hand, blocks androgen binding receptors in the PSU(42).
Cyproterone acetate is an anti-androgen that inhibits gonadotropin releasing hormone (GnRH) and blocks androgen receptors. It is readily available in Australia in a very low dose (2 mg) combined with estradiol (Diane-35) however higher dosages have been used for the treatment of FPHL, including continuous 50 mg a day with side effects including loss of libido, hypertension, weight gain (30), depression and menstrual disturbance (43). We couldn’t identify any study to find cypreterone superior to other anti-androgenic medications even though its’ side effects seem to be more serious. Finally with recent outcomes of French study on Diane-35 and risk of death from thrombo-embolic events and the alert by the TGA on Diane-35, the risks using the much higher dose of cyproterone acetate should be examined (44).
Flutamide is a potent anti-androgen, acting via androgenreceptor antagonism. As such, it is commonly used to treat advanced prostate cancer and hirsutism. Previous studies showed its superiority over finasteride and cyproterone acetate on a daily dose of 250 mg/day however its adverse effects including dose related hepatotoxicity made it less attractive (20, 45). A new prospective cohort study however showed its efficacy on FPHL treatment with higher tolerability and no hepatotoxicity when prescribed at 62.5 mg/day (46). It is still recommended during the early months of treatment to regularly follow up the liver enzymes and stop the treatment if transaminase levels exceed the twice level of normal range (45).
Low-Level Light Therapy
Low-level light therapy (LLLT) was initially used to create cancer in mice but it grew hair instead (47).Later on it was used by the National Aeronautics and Space Administration (NASA) to improve wound healing in space and in 2007, was approved by the FDA as a treatment for hair loss(48). LLLT, as is clear from its’ name, uses low power light (as small as 5mW) in a wavelength varying from 600 nm to 1400 nm. Some studies at 1500nm using different sources of light including IPL, diode laser, long-pulsed alexandrite lasers as well as erbium-glass laser have been tried (24, 49).This range of wavelength is very close to the absorption spectrum of haemoglobin, water and cytochrome C a respiratory chain component (24, 50). It is hypothesized that the light absorbed by cytochrome C mayultimately result in increased ATP production, which may alter cell metabolism(50). In a study on 28 Korean patients, a 1550 nm fractional erbium–glass laser was used for five months to treat FPHL and showed an increase in mean hair density from 100 to 158 / cm2 and increased mean hair thickness from 58 to 75 µm (24). Overall this method is new and larger studies are needed, however, it seems to be effective in some patients (49).
This is a surgical treatment with more visible outcomes and can be very successful in women with good occipital donor hair. Some clinicians keep this as a last resort though it should be considered as a possible part of the treatment strategy in more severe cases right from the beginning. Even for women who are on topical and systemic medication, hair transplants can be used to improve the outcome while continuing medical treatment can help to keep the transplanted hair in place longer and also slow down the hair loss in other areas.
Cell Therapy/Follicular Cell Implantation is also potentially a novel treatment that uses stem cells in the hair follicle to grow hairs in culture and reimplant them to the scalp. Currently being researched, if successful, this method is going to be the ultimate treatment of hair loss (32).
1. Cash TF. The psychology of hair loss and its implications for patient care. Clinics in dermatology. 2001;19(2):161-6. Epub 2001/06/09.
2. Biondo S, Goble D, Sinclair R. Women who present with female pattern hair loss tend to underestimate the severity of their hair loss. The British journal of dermatology. 2004;150(4):750-2. Epub 2004/04/22.
3. Norwood OT. Incidence of female androgenetic alopecia (female pattern alopecia). Dermatologic surgery : official publication for American Society for Dermatologic Surgery [et al]. 2001;27(1):53-4. Epub 2001/03/07.
4. Ludwig E. Classification of the types of androgenetic alopecia (common baldness) occurring in the female sex. The British journal of dermatology. 1977;97(3):247-54. Epub 1977/09/01.
5. Wiegratz I, Kuhl H. Managing cutaneous manifestations of hyperandrogenic disorders: the role of oral contraceptives. Treatments in endocrinology. 2002;1(6):372-86. Epub 2005/04/19.
6. Mounsey AL, Reed SW. Diagnosing and treating hair loss. American family physician. 2009;80(4):356-62. Epub 2009/08/15.
7. Aldridge RD. Hair loss. British medical journal. 1984;289(6450):985-9. Epub 1984/10/13.
8. Dinh QQ, Sinclair R. Female pattern hair loss: current treatment concepts. Clinical interventions in aging. 2007;2(2):189-99. Epub 2007/11/30.
9. Reid RL, van Vugt DA. Hair loss in the female. Obstetrical & gynecological survey. 1988;43(3):135-41. Epub 1988/03/01.
10. Herten RJ. Nonscarring hair loss disorders: the basis for recognition and treatment. Postgraduate medicine. 1982;72(4):231-6, 43-6. Epub 1982/10/01.
11. Jillson OF. Alopecia. III. Diffuse hair loss (nonscarring). Cutis; cutaneous medicine for the practitioner. 1983;31(5):465, 9, 72 passim. Epub 1983/05/01.
12. Price VH, Roberts JL, Hordinsky M, Olsen EA, Savin R, Bergfeld W, et al. Lack of efficacy of finasteride in postmenopausal women with androgenetic alopecia. Journal of the American Academy of Dermatology. 2000;43(5 Pt 1):768-76. Epub 2000/10/26.
13. Fabre N, Montastruc JL, Rascol O. Alopecia: an adverse effect of bromocriptine. Clinical neuropharmacology. 1993;16(3):266-8. Epub 1993/06/01.
14. Zalsman G, Sever J, Munitz H. Hair loss associated with paroxetine treatment: a case report. Clinical neuropharmacology. 1999;22(4):246-7. Epub 1999/08/12.
15. Olsen EA. Female pattern hair loss. Journal of the American Academy of Dermatology. 2001;45(3 Suppl):S70-80. Epub 2001/08/21.
16. Deplewski D, Rosenfield RL. Role of hormones in pilosebaceous unit development. Endocrine reviews. 2000;21(4):363-92. Epub 2000/08/19.
17. Rathnayake D, Sinclair R. Innovative use of spironolactone as an antiandrogen in the treatment of female pattern hair loss. Dermatologic clinics. 2010;28(3):611-8. Epub 2010/06/01.
18. Olsen EA, Messenger AG, Shapiro J, Bergfeld WF, Hordinsky MK, Roberts JL, et al. Evaluation and treatment of male and female pattern hair loss. Journal of the American Academy of Dermatology. 2005;52(2):301-11. Epub 2005/02/05.
19. Messenger AG, Sinclair R. Follicular miniaturization in female pattern hair loss: clinicopathological correlations. The British journal of dermatology. 2006;155(5):926-30. Epub 2006/10/13.
20. Carmina E, Lobo RA. Treatment of hyperandrogenic alopecia in women. Fertility and sterility. 2003;79(1):91-5. Epub 2003/01/14.
21. Rebora A, Guarrera M, Baldari M, Vecchio F. Distinguishing androgenetic alopecia from chronic telogen effluvium when associated in the same patient: a simple noninvasive method. Archives of dermatology. 2005;141(10):1243-5. Epub 2005/10/19.
22. Trueb RM. Systematic approach to hair loss in women. Journal der Deutschen Dermatologischen Gesellschaft = Journal of the German Society of Dermatology : JDDG. 2010;8(4):284-97, -98. Epub 2010/01/29.
23. Tosti A, Gray J. Assessment of hair and scalp disorders. The journal of investigative dermatology Symposium proceedings / the Society for Investigative Dermatology, Inc [and] European Society for Dermatological Research. 2007;12(2):23-7. Epub 2007/11/16.
24. Lee GY, Lee SJ, Kim WS. The effect of a 1550 nm fractional erbium-glass laser in female pattern hair loss. Journal of the European Academy of Dermatology and Venereology : JEADV. 2011;25(12):1450-4. Epub 2011/08/05.
25. Ross EK, Shapiro J. Management of hair loss. Dermatologic clinics. 2005;23(2):227-43. Epub 2005/04/20.
26. Camacho FM, Lopez-Elorza F, Rodriguez-Rey EM, Coronel-Perez IM. Prostate-specific antigen levels as hyperandrogenism marker in women. Journal of the European Academy of Dermatology and Venereology : JEADV. 2009;23(2):221-3. Epub 2008/06/11.
27. Shin HS, Won CH, Lee SH, Kwon OS, Kim KH, Eun HC. Efficacy of 5% minoxidil versus combined 5% minoxidil and 0.01% tretinoin for male pattern hair loss: a randomized, double-blind, comparative clinical trial. American journal of clinical dermatology. 2007;8(5):285-90. Epub 2007/10/02.
28. Haber RS. Pharmacologic management of pattern hair loss. Facial plastic surgery clinics of North America. 2004;12(2):181-9. Epub 2004/05/12.
29. Messenger AG, Rundegren J. Minoxidil: mechanisms of action on hair growth. The British journal of dermatology. 2004;150(2):186-94. Epub 2004/03/05.
30. Camacho-Martinez FM. Hair loss in women. Seminars in cutaneous medicine and surgery. 2009;28(1):19-32. Epub 2009/04/04.
31. Otberg N, Finner AM, Shapiro J. Androgenetic alopecia. Endocrinology and metabolism clinics of North America. 2007;36(2):379-98. Epub 2007/06/05.
32. Banka N, Bunagan MJ, Shapiro J. Pattern hair loss in men: diagnosis and medical treatment. Dermatologic clinics. 2013;31(1):129-40. Epub 2012/11/20.
33. Yeon JH, Jung JY, Choi JW, Kim BJ, Youn SW, Park KC, et al. 5 mg/day finasteride treatment for normoandrogenic Asian women with female pattern hair loss. Journal of the European Academy of Dermatology and Venereology : JEADV. 2011;25(2):211-4. Epub 2010/06/24.
34. Trueb RM, Swiss Trichology Study G. Finasteride treatment of patterned hair loss in normoandrogenic postmenopausal women. Dermatology. 2004;209(3):202-7. Epub 2004/10/02.
35. Scheinfeld N. A review of hormonal therapy for female pattern (androgenic) alopecia. Dermatology online journal. 2008;14(3):1. Epub 2008/07/17.
36. Iorizzo M, Vincenzi C, Voudouris S, Piraccini BM, Tosti A. Finasteride treatment of female pattern hair loss. Archives of dermatology. 2006;142(3):298-302. Epub 2006/03/22.
37. Shum KW, Cullen DR, Messenger AG. Hair loss in women with hyperandrogenism: four cases responding to finasteride. Journal of the American Academy of Dermatology. 2002;47(5):733-9. Epub 2002/10/26.
38. Rogers NE, Avram MR. Medical treatments for male and female pattern hair loss. Journal of the American Academy of Dermatology. 2008;59(4):547-66; quiz 67-8. Epub 2008/09/17.
39. Olszewska M, Rudnicka L. Effective treatment of female androgenic alopecia with dutasteride. Journal of drugs in dermatology : JDD. 2005;4(5):637-40. Epub 2005/09/20.
40. Olsen EA, Hordinsky M, Whiting D, Stough D, Hobbs S, Ellis ML, et al. The importance of dual 5alpha-reductase inhibition in the treatment of male pattern hair loss: results of a randomized placebo-controlled study of dutasteride versus finasteride. Journal of the American Academy of Dermatology. 2006;55(6):1014-23. Epub 2006/11/18.
41. Shaw JC. Antiandrogen therapy in dermatology. International journal of dermatology. 1996;35(11):770-8. Epub 1996/11/01.
42. Guerra-Tapia A, Sancho Perez B. Ethinylestradiol/Chlormadinone acetate: dermatological benefits. American journal of clinical dermatology. 2011;12 Suppl 1:3-11. Epub 2011/09/16.
43. Ghanaat M. Types of hair loss and treatment options, including the novel low-level light therapy and its proposed mechanism. Southern medical journal. 2010;103(9):917-21. Epub 2010/08/07.
44. TGA. Diane-35. 2013; Available from: http://www.tga.gov.au/safety/alerts-medicine-diane-35-130205.htm.
45. Sinclair R, Wewerinke M, Jolley D. Treatment of female pattern hair loss with oral antiandrogens. The British journal of dermatology. 2005;152(3):466-73. Epub 2005/03/25.
46. Paradisi R, Porcu E, Fabbri R, Seracchioli R, Battaglia C, Venturoli S. Prospective cohort study on the effects and tolerability of flutamide in patients with female pattern hair loss. The Annals of pharmacotherapy. 2011;45(4):469-75. Epub 2011/04/14.
47. Mester E, Szende B, Gartner P. [The effect of laser beams on the growth of hair in mice]. Radiobiologia, radiotherapia. 1968;9(5):621-6. Epub 1968/01/01. Die Wirkung der Lasstrahlen auf den Haarwuchs der Maus.
48. Sobanko JF, Alster TS. Efficacy of low-level laser therapy for chronic cutaneous ulceration in humans: a review and discussion. Dermatologic surgery : official publication for American Society for Dermatologic Surgery [et al]. 2008;34(8):991-1000. Epub 2008/04/24.
49. Avram MR, Rogers NE. The use of low-level light for hair growth: part I. Journal of cosmetic and laser therapy : official publication of the European Society for Laser Dermatology. 2009;11(2):110-7. Epub 2009/05/26.
50. Hamblin MR, TN D. Mechanisms of low level light therapy. Proc SPIE. 2006;6140:1-12.