HAIR Disorders.pptx

Trichotillomania (trik-o-til-o-MAY-nee-uh), also called hair-pulling disorder, is a mental disorder that involves recurrent, irresistible urges to pull out hair from your scalp, eyebrows or other areas of your body, despite trying to stop.

Hair pulling from the scalp often leaves patchy bald spots, which causes significant distress and can interfere with social or work functioning. People with trichotillomania may go to great lengths to disguise the loss of hair.

For some people, trichotillomania may be mild and generally manageable. For others, the compulsive urge to pull hair is overwhelming. Some treatment options have helped many people reduce their hair pulling or stop entirely.Symptoms
Signs and symptoms of trichotillomania often include:

Repeatedly pulling your hair out, typically from your scalp, eyebrows or eyelashes, but sometimes from other body areas, and sites may vary over time
An increasing sense of tension before pulling, or when you try to resist pulling
A sense of pleasure or relief after the hair is pulled
Noticeable hair loss, such as shortened hair or thinned or bald areas on the scalp or other areas of your body, including sparse or missing eyelashes or eyebrows
Preference for specific types of hair, rituals that accompany hair pulling or patterns of hair pulling
Biting, chewing or eating pulled-out hair
Playing with pulled-out hair or rubbing it across your lips or face
Repeatedly trying to stop pulling out your hair or trying to do it less often without success
Significant distress or problems at work, school or in social situations related to pulling out your hair
Many people who have trichotillomania also pick their skin, bite their nails or chew their lips. Sometimes pulling hairs from pets or dolls or from materials, such as clothes or blankets, may be a sign. Most people with trichotillomania pull hair in private and generally try to hide the disorder from others.

For people with trichotillomania, hair pulling can be:

Focused. Some people pull their hair intentionally to relieve tension or distress — for example, pulling hair out to get relief from the overwhelming urge to pull hair. Some people may develop elaborate rituals for pulling hair, such as finding just the right hair or biting pulled hairs.
Automatic. Some people pull their hair without even realizing they're doing it, such as when they're bored, reading or watching TV.
The same person may do both focused and automatic hair pulling, depending on the situation and mood. Certain positions or rituals may trigger hair pulling, such as resting your head on your hand or brushing your hair.

Trichotillomania can be related to emotions:

Negative emotions. For many people with trichotillomania, hair pulling is a way of dealing with negative or uncomfortable feelings, such as stress, anxiety, tension, boredom, loneliness, fatigue or frustration.
Positive feelings.

1. HAIR Disorders Presented by :Jagruti Marathe

2. Hair is a unique character found on all mammals but not on other animals In humans it is a special and cherished feature, especially in females. Its main functions are in protection of the skin from possible dameges. Eyebrows and eyelashes, for example, stop things entering the eyes, while scalp hair prevents sunlight, cold, and physical damage to the head and neck. Mammalian skin produces hair almost all over the body surface except for a few areas of the body, i.e., sole of the foot, palm of the hand, buccal surface of the lip, and portions of external genitalia . Human hair is usually classified according to three conventional ethnic human subgroups, i.e., African, Asian, and European .

3. Hair is only found in mammals. Hair is made of epidermal cells that grow out of follicles. In the follicle , hair is nourished by blood vessels. Keratin is a protein (also found in fingernails) that gives hair its hard durable structure. Hair grows about ½ inch per month and 6 inches per month. M e lanocy te s : ce l ls t h at m ake pigment called melanin . Dark hair has more melanin. Gray hair has lost its melanin

4. Hair Shaft Composed of: Cuticle —outside covering, made of overlapping scales, cuticle covers the hair from the root to the tip of the epidermis and is formed by flat overlapping cells. Each cuticle cell is generally 0.3– 0.5lm thick, and its visible length is about 50lm. Cortex —inner layer made of keratin and embedded with pigment; also contains air sacs called cortical fusi cortex , which represents the majority of the hair fiber composition and plays an important role in the physical and mechanical properties of hair, is the peripheral part and is made up of approximately 50–60% of macrofibrils embeded in matrix . Medulla —inside layer running down the center of the cortex

5. The Cuticle The cuticle is the outermost layer of hair which is covered with scales. The scales point toward the tip of the hair. Scales differ among species of animals and are named based on their appearance. The three basic patterns are: Coronal Spinous I m bri c at e

6. The Cortex The cortex gives the hair its shape. It has two major characteristics: Melanin —pigment granules that give hair its color Cortical fusi —air spaces, usually found near the root but may be found throughout the hair shaft

7. The Medulla The medulla is the hair core that is not always visible. The medulla comes in different types and patterns. Types: Intermittent or interrupted Fragmented Continuous Stacked Absent—not present

8. Human medulla may be continuous, fragmented, or absent. Animal hair medullas:

9. Physiology of the hair: hair growth cycle

10. The development of hair is a dynamic, cyclic process in which the duration of growth cycles is coordinated by many hormones and cytokines. Hair growth depends not only on where the hair is growing but also on some other factors, such as the individual’s age and stage of development, nutritional habits, or environmental alterations like day-length. Important players of this cycle are mainly cytokines (hormones), which are able to instruct the follicle to undergo appropriate changes, so that each hair can be in a different stage of growth cycle compared to the adjacent hairs

11. Hair follicles grow in repeated cycles, in which stages of rapid growth and hair shaft formation alternate with stages of apoptosis-driven hair follicle. In particular, the hair growth cycle can be divided into three distinct phases: Anagen or growth phase; Catagen or transitional phase; Telogen or resting phase

12. Anagen: The anagen phase is an active growth phase, during which the hair follicle enlarges reaching its characteristic onion shape and a hair fiber is produced. It can be divided into six stages (I–VI). During anagen I–V (proanagen), hair progenitor cells proliferate, envelope the growing dermal papilla, grow downwards into the skin, and begin to differentiate into the hair shaft and Inner Root Sheath (IRS); then, the newly formed hair shaft begins to develop and the melanocytes located in the hair matrix pigment producing activity In anagen VI (metanagen), full restoration of the hair fiber-producing unit is realized, which is characterized by formation of the epithelial hair bulb surrounding the dermal papilla, located deep in the subcutaneous tissue, and the new hair shaft appears from the skin surface. This phase can last for several years in hair follicles

13. Catagen: The catagen phase starts when the anagen growth phase comes to the end. At the beginning of the catagen phase, differentiation and proliferation of hair matrix keratinocytes decreases significantly, the pigment-producing activity of melanocytes stops, and hair shaft production is completed. The hair follicle undergoes apoptosis-driven regression resulting in a reduction of about one-sixth of the normal diameter. During catagen, a specialized structure, the club hair, is formed. The keratinized brush-like structure at the base of the club hair is surrounded by epithelial cells of the ORS and anchors the hair in the telogen follicle. This phase lasts for a few weeks

14. Telogen : The telogen phase begins after the catagen phase; the hair goes into a resting phase, and this period can last few weeks (eyelashes) to eight months (scalp hair). Although the hair does not grow during this stage, the dermal papilla stays in the resting phase. Telogen hair follicles are characterized by a lack of pigment- producing melanocytes and the IRS. Their dermal papilla is closely attached to a small cap of secondary hair germ keratinocytes containing hair follicle stem cells. Approximately 10–15% of all hairs are in resting phase at any given moment. At the end of this stage, the hair falls (exogen phase); a few weeks later, the hair follicle re-enters the growth phase by stimulating stem cells from the bulge area.

15. Morphologically, there are three types of hair: Vellus : are short, fine, soft, usually non pigmented and unmedullated Terminal : are large, darkly pigmented and often medullated 90% of the hairs on the chest, trunk, shoulders, legs and arms of men are terminal, only 45% on women. Intermediate : occur on the scalp, their morphology falls between those of terminal and vellus and they are medullated and contain moderate amount of pigment.

16. ⦿ Dandruff is a skin condition that mainly affects the scalp . ⦿ Symptoms include flaking and sometimes mild itchiness. ⦿ It can result in social or self-esteem problems. A more severe form of the condition, which includes inflammation of the skin, and is known as seborrheic dermatitis . ⦿ Newborns and adults aged 30-60 are M ore likely to get seborrheic dermatitis ⦿ Physiological ⦿ Mild scaling of the scalp ⦿ Affects almost everyone during adult life ⦿ Manifestation of seborrheic dermatitis/psoriasis, allergic reaction.

17. ⦿ Stress ⦿ Your genes ⦿ A yeast that normally lives on the skin ⦿ Certain medical conditions and medicines ⦿ Cold, dry weather The factor contributing to Pityriasis Capitis Acne AIDS Alcoholism Depression Eating disorder Epilepsy Heart attack Parkinsons

18. ⦿ Adults with seborrheic dermatitis on their scalp can use over-the-counter dandruff (OTC dandruff) shampoo that contains one of these key ingredients : ⦿ Coal tar -It works by causing the skin to shed dead cells from its top layer and slow down the growth of skin cells. ⦿ Ketoconazole -Antifungal ⦿ Salicylic acid- Dry & scaly skin-for moisturizer, surface active agent ⦿ Selenium sulphide -Antidandruff ⦿ Zinc pyrithone- Control skin irritation

19. Other treatments include: ⦿ Antifungal products ⦿ Corticosteroid lotions ⦿ Prescription-strength medicated shampoos ⦿ Sulfur products ⦿ Often the best results come from a combination of treatments, both medication and lifestyle. ⦿ Work with your doctor or pediatrician if you're using a treatment other than shampoo , since there could be side effects, especially if you use it for longer or more often than prescribed . ⦿ If your seborrheic dermatitis doesn't get better, or if the area becomes painful, red, swollen, or starts to drain pus, see your doctor.

20. Excessive Growth Hypertrichosis Eg: Hirsutism Loss of Hair Eg : ( Alopecia ) ⦿ Reversibility Cicatricial (Scarring)- Non cicatricial (Non scarring) ⦿ P a tt ern Patchy- Alopecia areata Diffuse - Androgenetic alopecia Telogen effluvium

21. Growth of coarse terminal hair ⦿ Excessive for site /age of the patient ⦿ Involving non-androgen dependent follicles ⦿ G e n e r a li z e d h y p er t r i c h o s i s , which occurs over the entire body, ⦿ Localized hypertrichosis , which is restricted to a certain area. Causes: 1 . P o r p h y r i a c ut a ne a t a r da 2.Malnutrition D i e t o r a n e a ti n g d i s o r d e r l i k e a n o r e x ia nervosa Cancer Certain drugs androgenic steroids, Ha i r g r o w t h d r u g s M i n o x i d i l & c y c l o s p o r i n ( S a n d im m u n e – i s to prevent organ rejection)

22. Treatment Shaving Chemical epilation ( cosmetic preparation used to remove unwanted hair) ⦿ Waxing ⦿ Plucking ⦿ Hair bleaching ⦿ Long-term treatment includes electrolysis & laser surgery Electrolysis i s t h e d e s t r u c t i o n o f i n d i v i du a l h a ir follicles with small electrical charges . Laser surgery involve the application of special laser light over several hair at a one time. H a i r l o s s c a n b e p e r m a n e n t w i t h t h e s e t re a t m e n t , though you may need a few session to complete job.

23. Polycystic ovary disease A hormonal disorder causing enlarged ovaries with small cysts on the outer edges.--- (This hormone imbalance causes them to skip menstrual periods and makes it har d e r f o r t he m t o ge t pre g na n t ) ⦿ O v aria n t u m ors ⦿ Congenital adrenal hyperplasia - A pair of walnut-sized organs above your kidneys - (A person with CAH lacks one of the enzymes the adrenal glands use to produce hormones that help regulate metabolism, the immune system, blood pressure and o t he r e ss en t ial f un ct ion s )

24. ⦿ C u s hin g s s y ndro m e ⦿ Prolactinoma (A prolactinoma is a benign noncancerous tumor of the pituitary gland that produces a hormone called prolactin. Prolactinomas are the most common type of pituitary tumor. Symptoms of prolactinoma are caused by hyperprolactinemia—too much prolactin in the blood—or by pre ss ur e o f t h e t u m o r o n s urroundin g t i ss ue s ) ⦿ Idiopathic An idiopathic disease is  any disease with an unknown cause or mechanism of apparent spontaneous origin . From Greek ἴδιος idios "one's own" and π άθος pathos "suffering", idiopathy means approximately "a disease of its own kind".

25. Treatment of Hirsutism ⦿ C os m e t i c : ⦿ Depilatory creams ⦿ W a x i n g ⦿ P l u c k i n g ⦿ E l e c t r o l y s is ⦿ H o rm o na l : ⦿ C y p r o t er o n e a ce t a te ⦿ S p i r o n o lac t o n e ⦿ C o r t i c o s t e r o i d s

26. Mechanism of action Cyproterone is an anti-androgen . It suppresses the actions of testosterone (and its metabolite dihydrotestosterone) on tissues. ... The direct antiandrogenic effect of cyproterone is blockage of the binding of d i h y d r o t e s t o s t e r o n e t o t h e s p e c ifi c r e c e p t o r s in t h e p r o s t a t i c c a r c in o m a c e l l

27. Types Cicatricial: Permanent loss of hair N o n - c i c a t r i c i a l : A n d r o g e n e t i c a l o p e c i a . Telogen effluvium N e o n a t a l al o p e c ia Drug induced alopecia (anticoagulants, retinol (vitamin A) Alopecia areata (Patchy hair) Alopecia areata occurs when the immune system attacks hair follicles and may be brought on by severe stress .

28. Li c h e n p l a nus

29. A N D R O G E N E T IC A L OP E C IA ⦿ (Male pattern baldness) ⦿ Loss of hair : with increasing age ⦿ G e n eti c all y p r e d i s p o s e d i n d i v i d u al s ⦿ Response to circulating androgens Clinical Features ⦿ 16% men b/w 18-29 yr ⦿ 53% men b/w 40-49 yrs ⦿ 50% females below 50 yrs

30. A L OP E CI A AR E AT A Alopecia areata (AA) is a complex genetic, immune-mediated non-scarring disease that targets actively growing anagen hair follicles. The disease can affect all ethnic groups and both males and females at all ages. The lifetime risk is estimated to be approximately 2%. AA typically presents as one of four major patterns: Round or oval patches of hair loss „Loss of all scalp hair (alopecia totalis) „Loss of all body hair (alopecia universalis) „Ophiasis pattern alopecia areata

31. HAMILTON’s grading in males LUDWIG’s grading in females

32. Clinical Features... In addition to the common presentations of patchy or extensive hair loss, alopecia areata may present less commonly as reticular alopecia areata, diffuse scalp alopecia areata, or perinevoid alopecia areata. Patients who experience the reticular variant have ongoing disease activity with patches of non-scarring hair loss appearing and disappearing. When the AA process is active, hair-pull tests are positive and exclamation-mark hair fibers can frequently be found. These fibers have a broader distal segment than the proximal end and when these fibers grow they taper down proximally to a pencil point and may break easily, similar to what is seen with hair fibers experiencing anagen arrest as with chemotherapy

33. Nail abnormalities may precede, follow, or occur concurrently with hair-loss activity. Nail pitting as the most commonly reported nail abnormality. Other abnormalities include koilonychia, longitudinal ridging, brittle nails, onycholysis, onychomadesis, and periungual erythema . AA may occur in otherwise healthy individuals or it may occur associated with other diseases. Common disease associations include atopy (allergic rhinitis, asthma, and atopic dermatitis). Other common disease associations include thyroid disease and autoimmune diseases, such as thyroiditis and vitiligo. Though not a life-threatening disease, AA may have a significant psychological impact on patients, leading to a high lifetime rate of generalized anxiety disorders or even depression.

34. Pathophysiology of Alopecia areata: Histology: T-cell immunity plays a crucial role in the pathophysiology of AA. Histologically, a hallmark of AA has been the presence of a peribulbar lymphocytic infiltrate that consists primarily of activated T lymphocytes. These changes with disease activity and type are postulated to be associated with different therapeutic responses; for example, it may be that the use of steroids may be more effective in the acute phase as compared to the chronic phase of AA when the inflammatory infiltrate is less prominent.

35. If the diagnosis of AA is not straightforward, examination of a 4- mm scalp biopsy specimen may be useful in confirming the diagnosis. This biopsy specimen will typically show the characteristic peribulbar, inflammatory infiltrate, in both horizontal and vertical sections, as well as an increased percentage of follicles in telogen. Immunology: Normal anagen hair-bulb keratinocytes lack expression of major histocompatibility complex class I and class II antigens. However, in alopecia areata, human leukocyte antigen (HLA) A, HLA-B, HLA-C, and HLA-DR are all expressed on anagen hair bulbs.

36. These observations have led to the concept that immune privilege is lost in AA and that the disease involves Tcell interaction with aberrant HLA-DR antigens expressed by hair follicle keratinocytes. Increased, decreased, and normal peripheral blood T and B lymphocyte number and function have all been reported in AA patients. Genetics: The familial incidence of AA has been reported to range between 10% and 50% and it is now generally accepted that AA is a complex or multifactorial genetic trait. This is based on the following: --

37. Its prevalence in the population Concordance with twins (55%) A Gaussian distribution of severity A ten-fold increased risk of affected first-degree relatives The aggre g ation of a f fected in d i v i d uals i n f am i l ies, rat h er than showing a clear Mendelian pattern of inheritance. The major histocompatiblity complex class I chain-related gene A (MICA) was identified as both a potential candidate gene that could be associated with susceptibility as well as severe, extensive disease. Other disease associations described with disease severity include the IL-1 receptor antagonist

38. Nerves: Many AA patients experience occasional itching, tingling, formication, or slight local pain during combing, touching, or tension on their hair. Alterations in neuropeptide and neurotrophin expression in animal models of AA as well as humans have been reported, suggesting a role for the neurocutaneous immune system in AA . More recently, peripheral nerve function in the C2 and V1 dermatomes, both of which innervate scalp skin, was found to be abnormal as compared to controls. Stressful life events and psychiatric disorders have been studied as they relate to both the onset and the progression of alopecia areata.

39. Treatments .... There is no “best” treatment for AA and at this time there is no FDA-approved drug for the treatment of AA. It is believed that the available treatments at best only suppress the underlying process. Treatment for AA also needs to be considered in light of the normal course of the disease. Review of the literature indicates that in contrast to other treatments, contact sensitizers such as diphencyprone or squaric acid dibutylester have been used.

40. 1. Topical Sensitizers: Diphenycyprone is the most commonly used topical sensitizer. Patients are normally sensitized into a 2% solution within a two-week time period. The goal is to choose a concentration capable of producing a mild allergic contact dermatitis. Cosmetically acceptable hair regrowth may require up to two years of treatment. Sensitization, if usually performed on the scalp, and weekly applications are targeted to produce a mild eczematous reaction. Initial hair regrowth may be visible after 8–12 weeks and may be discontinued once hair regrowth occurs; likewise, treatment can be reinstituted if a relapse occurs.

41. 2. Steroids: Topical, Intralesional, Oral: The use of 0.05% betamethasone dipropionate cream, 0.05% clobetasol propionate, and 0.2% fluocinolone acetonide cream have all also been associated with hair regrowth with the time to regrowth averaging three months. Intralesional steroids, including triamcinolone acetonide or triamcinolone hexacetonide are commonly used to treat patients with less than 50% scalp involvement. Eyebrow regions may also be injected . Concentrations typically used range from 3 to 10 mg/cc.

42. Oral steroids may be of benefit to patients with active disease. An oral monthly pulse of 300 mg prednisolone for a minimum of four doses has also been reported to result in complete or cosmetically acceptable hair regrowth. Side effects of using oral or intravenous steroids for the treatment of AA deserve attention. Adverse e xperie n ces inclu d e weight gain, osteoporosis, hypertension, psychological changes, suppression of the adrenal cortical axis, striae, acne, hypertrichosis, and purpura. To counter the development of osteoporosis, calcium, vitamin D may be prescribed .

43. 3. Minoxidil: Topical and Oral: Patients with patchy AA have been reported to achieve cosmetically acceptable regrowth with 2% topical minoxidil and in one study it was suggested that patients with severe disease may benefit from 5 mg of oral minoxidil administered every 12 hours with a mean time of approximately 35 weeks to attain cosmetically acceptable hair regrowth. Topical minoxidil, either the 2% or 5% concentrations, can be beneficial in AA when the focus is on promoting follicle differentiation, early anagen to late anagen.

44. 4. Anthralin: Anthralin is postulated to target mitochondria and interact with the electron transport chain on the inner mitochondrial membrane, ultimately resulting in a decrease in adenosine triphophosphate synthesis. Concentrations used in the management of AA must be sufficient to elicit mild irritation and may range from 0.2% to 1.0% . However, just as with minoxidil, the use of this drug in published studied has not fulfilled the criteria of evidence-based treatment described earlier

45. 5. Light Therapy (UVA, NBUVB, UVB, Laser: The use of psoralen-ultraviolet A (PUVA) light has resulted in complete hair regrowth for some patients with either patchy or extensive AA. Although complete hair regrowth has been achieved with 50 to 80 treatment sessions, averaging three per week, hair loss is commonly seen following discontinuation. UVB light treatment has also resulted in complete hair and beard regrowth although hair loss may occur following discontinuation of treatment

46. 6. Combination Therapies: Topical minoxidil and oral prednisone: oral prednisone (starting at 40 mg/day) followed by 2% topical minoxidil applied daily for up to 14 weeks. Topical minoxidil and bethamethasone dipropionate: Patients applied 5% topical minoxidil twice daily, followed 30 minutes later by 0.05% beta-methasone dipropionate cream. Topical minoxidil and anthralin: patients applied 1 ml 5% topical minoxidil twice daily, followed by an overnight application of anthralin.

47. Androgenetic Alopecia Androgenetic alopecia describes a form of scalp-hair loss in which there is a decline in production of hair, which may eventually lead to balding. It affects both sexes and all ethnic groups although the severity and frequency are greater in men. The same is true of androgenetic alopecia in most women.

48. Clinical Features: Androgenic Alopecia Male Androgenetic Alopecia: Male androgenetic alopecia (male balding, male-pattern hair loss) is a common that can start at any age after puberty. In the majority of men balding is patterned of two major components are fronto-temporal recession and loss of hair over the vertex . Hairs become shorter. Ultimately this may lead to complete hair loss except at the lateral and posterior margins of the scalp where hair is retained.

49. Female Androgenetic Alopecia: Most women with androgenetic alopecia (also known as FPHL) present with a history of gradual thinning of scalp hair, often over a period of several years. The hair loss can start at any age from puberty onwards. In some women the hair loss may affect a quite small area of the frontal scalp whereas in others the entire scalp is involved .

50. Pathophysiology: Androgenic Alopecia The follicular changes in androgenetic alopecia, in both men and women, comprise a gradual reduction in the duration of anagen , prolongation of the “latent phase ” of the hair cycle. The l a tent phase, a lso ter m ed kenoge n , ref e rs between the telogen hair and reentry into anagen. t o t h e i n te r v a l Miniaturization may eventually lead to deletion of hair follicles. A modest degree of chronic inflammation around the upper part of hair follicles.

51. ETIOLOGY: Androgenic Alopecia Androgens: Male balding is an androgen-dependent. Testosterone is the major circulating androgen in men. However, there is compelling evidence that dihydrotestosterone (DHT), the 5α-reduced metabolite of testosterone, is responsible for hair loss. A role for androgens in the etiology of male balding is incontrovertible. The role of androgens in female androgenetic alopecia is less clear- than it is in men.

52. Prevalance: P o p u lation freq u en c y and severity o f an d roge n etic alo p ecia i n b o th sexes increase with age. A l m ost all m e n develop so m e of the fro n tal hairli n e a t the t e m ples during their teens. Hair loss progresses to a bald scalp in 50–60% of men by the age of 70. Balding is less common in Asian men. One early s t udy rep o rted that bal d ing is four times less comm o n in African American men than in Caucasians. The frequency and severity of androgenetic alopecia is lower in women than in men but it still affects a sizeable proportion of the population .

53. Diagnosis: The diagnosis of androgenetic alopecia in men rarely causes difficulties. In cases presenting with general thinning, other causes of diffuse hair loss should be considered, particularly when the hair loss progresses quickly. The diagnosis of female androgenetic alopecia may be more challenging. Rapidly progressive hair loss with a strongly positive “tug test” should raise the possibility of diffuse alopecia areata. Loss of body hair, eyebrows, or eyelashes, and nail changes will support the diagnosis but it is sometimes necessary to obtain histology

54. Treatments : Treatment for Male: At present only two medical treatments, minoxidil and finasteride are licensed for the treatment of male balding. Both drugs will stimulate some regrowth of hair in some men but are perhaps better regarded as preventative treatments. Neither will regrow hair on completely bald scalp and continued treatment is necessary to maintain the response. Both drugs have a good safety record, a consideration of paramount importance when treating hair-growth disorders.

55. Minoxidil Minoxidil was licensed as an oral drug to treat hypertension in the early 1970s. Because it significant hypertrichosis, this drug almost eliminated its use as an anti-hypertensive agent. Minoxidil solution were developed for topical application in the treatment of hair loss . A 2% formulation of minoxidil solution was subsequently licensed by the U. S. Food and Drug Administration for the treatment of male balding . A 5% formulation was marketed in 1993. The recommended dose is 1ml twice daily (for both 2% and 5% formulations).

56. Adverse effects of minoxidil are mainly dermatological . Constitue n ts of the ve h ic l e oc c asiona l ly c au s e scalp i r r i ta t ion, more commonly with the 5% formulation. Allergic reactions to minoxidil or propylene glycol (a component of the vehicle) are rare but necessitate stopping treatment. Some patients notice an increase in hair shedding 2–8 weeks after starting treatment. This is self-limiting and patients should be forewarned not to stop treatment if this happens

57. Finasteride Finasteride is a competitive inhibitor of type II 5α-reductase. Taken orally it reduces DHT levels in serum and in scalp by up to 70%’. The i m prove m ent pea k s a t a round 12 m onths and, on a vera g e, there is some decline after two years. Clinical trials have shown a small increase in sexual dysfunction (e.g., impotence) in men taking finasteride for male balding. These side effects resolve on discontinuation of the drug. Data from a long-term trial in 18,882 men aged over 54 taking 5mg Finasteride daily.

58. Surgery Surgical treatment of male balding involves the redistribution of terminal hair to cover balding scalp; the number of terminal hair follicles on the scalp remains the same. In most cases this means transplanting hair follicles from the occipital scalp to the balding areas. Surgical treatment can achieve very satisfactory results but careful patient selection and surgical skill allied to the aesthetics of scalp hair growth are essential .

59. Treatment for Women: For those who are keen to be treated there are two medical options: minoxidil solution and antiandrogens. In both cases it should be stressed that treatment will, at best, produce only a modest increase in hair density and that it is not possible to fully reverse hair loss. Furthermore, in those who respond, treatment has to be continued to maintain the response. A s in m en, su r gery is the o n ly m ethod c apa b l e o f res t o ri ng the appearance in the presence of severe hair loss

60. Minoxidil... Minoxidil solution 2% is licensed for the treatment of female androgenetic alopecia in most countries. The 5% formulation is not currently licensed for use in women. A more recent trial comparing 5% and 2% minoxidil solution found increases of 18% and 14% respectively in mean non-vellus hair counts after 48 weeks of treatment. Minoxidil is a safe treatment. Some patients complain that it leaves unsightly deposits on the hair. Occasionally it causes scalp irritation that may be severe enough to cause a temporary increase in hair shedding and patients should be warned about this. minoxidil solution is more reliably effective and better tolerated than anti-androgen treatment .

61. Antiand r ogens The antiandrogens cyproterone acetate, spironolactone and flutamide have all been used to treat female androgenetic alopecia, as has the 5α-reductase inhibitor finasteride, although none is licensed for this purpose. Cyproterone acetate acts by blocking androgen receptors. It also has progestational activity and suppresses the production of gonadotrophins. Spironolactone is a competitive inhibitor of aldosterone receptors. It also blocks androgen receptors and increases metabolic clearance of testosterone. It has been widely used to treat hirsutism.

62. Rep o rt sh o ws that wo m en t r e ated f or 1 2 m onths with spironolactone showed less hair loss than an untreated group. Flutamide is a pure androgen receptor blocker. A study shows that flutamide 250 mg daily with cyproterone acetate and finasteride in the treatment of 48 hyperandrogenic women with androgenetic alopecia. Those treated with flutamide showed a modest improvement in hair growth whereas those treated with cyproterone acetate or finasteride did not . Antiandrogen treatment is not without problems.

63. Women taking antiandrogens should not become pregnant because of the risks of feminizing a male fetus. Dose-related side effects of cyproterone acetate, including weight gain, fatigue, loss of libido, mastodynia, nausea, headaches and depression, are common. There is a significant risk of hepatotoxicity with flutamide and cyproterone acetate is also potentially hepatotoxic in high doses. Spironolactone may cause menstrual irregularities. Finasteride is well tolerated and is worth considering in post- menopausal and infertile women.

64. Surgery: Hair transplantation is less widely used in women than in men but can give good results in selected cases . It i s m ost a pprop r i a te i n wo m en wit h prono u nced h a ir l o ss of limited extent who retain good hair density in the donor site. Iron: The idea that body iron stores, usually measured as serum ferritin. Patients should be advised that iron treatment alone will not halt or reverse hair loss but it may improve the response to specific treatments.