COMPLETE HOW TO TREAT QUIZZES ONLINE ( to earn CPD or PDP points.

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1 HowtoTreat PULL-OUT SECTION COMPLETE HOW TO TREAT QUIZZES ONLINE ( to earn CPD or PDP points. inside The normal hair cycle Non-scarring alopecias Scarring alopecias The author DR KENG-EE THAI, consultant dermatologist, department of dermatology, Prince of Wales Hospital, Randwick; Eastern Suburbs Dermatology, Bondi Junction; and Nepean Dermatology, Kingswood, NSW. Background HAIR loss is a common presentation to the general dermatologist, and though unlikely to be life threatening, can result in considerable distress. Although alopecia (Greek for hair loss ) can occur on any hairbearing skin, it is scalp and facial loss for which patients seek help. There are several types, which are broadly divided into scarring (cicatricial) or non-scarring, though diseases within these arbitrary groups are not necessarily related. The emphasis of this review is on nonscarring alopecias. These tend to be more common and have more management options available to the GP. It is impractical to provide an exhaustive review of all forms of hair loss; therefore rarer types are not discussed. The normal hair cycle An understanding of the normal hair cycle provides a perspective on hair diseases. Hair shaft synthesis is a tightly controlled event, with the hair phenotype being predetermined by the nature of the hair follicle. The follicle has physical and biochemical interactions with the underlying dermal papilla which it envelops. Each hair follicle grows in a cyclical fashion, consisting of several stages. Anagen is the growth phase where a hair shaft is actively being produced by the underlying follicle. At the end of this period, hair shaft synthesis ceases; this telogen part of the cycle lasts three months. Catagen is a transitional stage that lasts several days, in between anagen and telogen. At the end of telogen, exogen describes the release of the old hair shaft, which allows the next anagen to commence. During anagen the scalp hair shaft grows at approximately 1cm per month. With a hair cycle varying between three and five years, a hair shaft of about 36-60cm is achievable. Of the approximately 100,000 hair follicles on the scalp, about 80% are in anagen at any time. These anagen follicles are distributed throughout the scalp. They are growing asynchronously, each hair being in a different phase of its own cycle. Humans normally lose about hairs daily as a minority of hairs transition between telogen and the next anagen. Hair loss disorders typically result from a disruption of the hair cycling, destruction of the hair follicle, or damage to the hair shaft. cont d next page

2 HOW TO TREAT Hair loss Non-scarring alopecias Acute telogen effluvium THE typical patient with acute telogen effluvium (ATE) presents with diffuse hair loss from all parts of the scalp, approximately three months after a physiological or psychological insult. This hair fall continues for up to six months, after which hair density normalises. ATE is a very common cause of non-scarring hair loss. Many different triggers may provoke it: chronic or acute systemic illness, surgery, infections, sudden weight loss, accidental trauma, parturition, blood loss and various emotional stressors. The pathogenesis is unclear and may well be due to a large number of hairs being forced into premature telogen by the triggering event. Three months later the scalp hairs go into anagen, where the longer telogen hairs are lost, initially being replaced by cosmetically insignificant, smaller anagen hairs. As the hairs lengthen, overall scalp density recovers. Patients present with acute onset of diffuse scalp hair loss (figure 1 and figure 2). There is no obvious patterned loss, no widening of the central part (as with androgenetic alopecia, see below) and hairs can be easily extracted. However, in the early stages telogen effluvium and androgenetic alopecia can be indistinguishable. The clinician should enquire about any triggering events around three months prior to the hair loss. Cases with a classic history need no further diagnostic investigations. Apart from managing the original trigger, repeated reassurance is the standard management. Most cases will resolve within six months. However, if the loss continues then a scalp biopsy may be required to rule out androgenetic alopecia. Topical minoxidil can be used by those who want an active role in their hair regrowth. Chronic telogen effluvium This form of telogen effluvium persists beyond six months, may not have a specific trigger, and almost exclusively occurs in women. Most patients experience acute, distressing hair fall and a marked decrease in scalp hair density. Examination finds a normal-looking scalp with some bitemporal recession, but no obvious widening of the hair part. The main differential diagnosis is early androgenetic alopecia. A scalp biopsy is often required to differentiate between the two, as chronic telogen effluvium (CTE) requires only reassurance, while androgenetic alopecia is amenable to pharmacological therapy. Metabolic and drug causes of alopecia Figure 1 and Figure 2: Acute telogen effluvium. Note the diffuse loss with no specific pattern. Hairs are sparse both at the vertex and the parietal scalp. should also be suspected and appropriate investigations performed (see below). CTE typically resolves over 3-4 years, with periods of increased as well as decreased hair density. Once female pattern baldness has been ruled out, constant reassurance is all that is required. Patients need to be aware that a return to the premorbid density of hairs may not always occur. Once again, topical minoxidil can be used. Androgenetic alopecia Androgenetic alopecia occurs in both genders. Half of all men are balding by age 50 and half of all women by age 60. Most individuals will develop a degree of androgenetic alopecia over time, thus this condition may well be seen as a variant of normal. A polygenetic inherited tendency is likely and, in conjunction with circulating androgens, leads to progressive miniaturisation of terminal scalp follicles. This occurs in a stepwise fashion; with each hair cycle there is progressive reduction in follicle size (thus decreased hair shaft diameter) and duration of anagen (thus shorter hairs). Long, thick terminal hairs are ultimately converted to small vellus hairs that make no cosmetic impact. Contrary to popular belief, the number of follicles is not reduced. Not all hair follicles are affected equally, as body and pubic hairs are not under the same influence. Occipital hairs are also relatively spared from miniaturisation. Men and women bald differently. Males have a receding hairline and bald patch. A minor degree of temporal recession marks the onset of androgenetic alopecia and occurs in the majority of men. This often occurs in the late teens, but may be delayed until the fourth decade. Balding of the vertex follows. There is then progressive frontal recession and expansion of the vertical bald patch until all that is left is an occipital rim. Women maintain their frontal hairline and occipital scalp hair, and lose density over the crown (figure 3). This progressively thins out, with an obvious widening of the central hair part-line (figure 4). With careful styling, women can quite effectively disguise early female pattern balding. In men and in well-established disease in women, the pattern is well recognised and investigations are unnecessary. In women with early-onset hair loss, CTE is the most likely differential diagnosis. Patients are often quite distressed about their degree of hair fall. A scalp biopsy provides diagnostic certainty and gives confidence for definitive therapy. Three, 4mm punch biopsies from the crown should be sent in formalin for horizontal sections. The specimen should be read by a pathologist experienced in hair disorders. A quantifiable increase in the number of miniaturised vellus hairs relative to larger terminal hairs confirms the diagnosis. (When performing biopsies for inflammatory hair loss, vertical sections should be requested, as this provides the classical morphological view of scalp skin. Terminal-tovellus ratios are less important.) If CTE is in the differential diagnosis, screen for iron deficiency, thyroid disease, antinuclear antibody and any other metabolic syndrome revealed on history. Menstrual irregularities should raise the suspicion of polycystic ovary syndrome and be investigated for accordingly. Any signs of virilisation (deepening voice, muscular growth, hirsutism, clitoromegaly, male pattern hair loss in a female) should also prompt screening for an androgen-dependent tumour: testosterone, free androgen index and imaging if required. Figure 3: Female pattern androgenetic alopecia showing significant decrease in vertex hair density but preservation of frontal hair line. Medical treatment Minoxidil is a vasodilating antihypertensive. When used as a topical lotion it induces and maintains anagen. It is most effective for early disease and for vertical thinning. Solutions of 1% and 2% are available, with the higher concentration giving faster and better results. One millilitre of lotion should be applied twice daily to a dry scalp before styling. Response to treatment is unpredictable, and disappointing for those who only regrow cosmetically insufficient indeterminant or vellus hairs. Up to 50% of patients experience stabilisation of loss and 10% achieve regrowth. Treatment needs to continue long term, as cessation will result in loss of all new hairs. Note that the miniaturisation process of androgenetic alopecia continues, thus the overall density will continue to fall after an initial regrowth of about 18 months, albeit with the added benefit of minoxidil-supported hairs. Adverse effects are uncommon, but the lotion can cause an irritant dermatitis and can make hairs tacky and difficult to style. There are reports of overuse leading to hypotensive episodes. Finasteride is the only oral agent approved for the treatment of androgenetic alopecia in Australia, but it is only approved for male pattern balding. This is a selective inhibitor of the type II isoenzyme of 5α-reductase, an enzyme required in the conversion of testosterone to dihydrotestosterone. It is marketed in Australia as a 1mg tablet specifically for androgenetic alopecia. Exceeding the 1mg per day dosage does not appear to give additional benefit. It works better for vertex loss but also helps bitemporal and frontal loss. Five-year studies demonstrated increased hair counts in more than 90% of patients, though the majority of the increase occurred within the first two years. Continued use of finasteride is required to maintain scalp hair density, as cessation results in resumption of the natural rate of loss. Adverse effects are minimal and occur only marginally more frequently than in the placebo group: decreased libido, retrograde ejaculation and erectile dysfunction. There are no known drug interactions. However there are two pertinent issues. When monitoring PSA in patients on finasteride, the numerical value needs to be doubled, as finasteride tends to halve the measured PSA. Though patients on finasteride have a lower incidence of prostate cancer, those who do develop it have lesions with higher Gleason scores. Patients need to be made aware of this possibility and regular PSA measurements should be performed. As finasteride is a potent teratogen, it should not be used in fertile women and is not approved for female pattern balding in Australia. However, there is good evidence to show that a higher dose of finasteride (2.5mg daily) may be useful in post-menopausal women with female pattern balding. 1 Though there are no approved treatments available for female pattern balding, spironolactone and cyproterone acetate have been used for some time. Both serve as competitive inhibitors of the androgen receptor, blocking testosterone-induced miniaturisation of hair follicles. Therapeutic effect takes six months to two years; cessation of hair loss rather than regrowth is considered successful treatment. Cessation of treatment results in recommencement of hair follicle miniaturisation. Both treatments require a reliable form of contraception, as feminisation of a male fetus can result. The oral contraceptive pill may be required to regulate menstrual irregularities that can occur with either agent. Spironolactone is primarily used as a potassium-sparing diuretic. Apart from its androgen blockade effect, it also inhibits ovarian androgen synthesis. The literature for spironolactone is mainly for the management of hirsutism, though there is adequate empirical experience for its use in female pattern androgenetic alopecia. Effective doses vary between 50mg and 200mg daily, with higher doses being more efficacious. I typically initiate therapy at 100mg daily for one month then increase it to 200mg daily. Postural hypotension and urinary frequency can occur early during treatment and settle quickly. Serum potassium assays should be performed every few months to monitor for hyperkalaemia. Cyproterone acetate is used at relatively high doses for 30 Australian Doctor 13 February

3 Figure 4: Female pattern androgenetic alopecia with an obviously widened central hair part. female androgenetic alopecia. Premenopausal women should use 100mg daily between days 5 and 15 of the menstrual cycle, while postmenopausal patients can use 50mg daily continuously. Menstrual irregularities are common, as are distinct mood changes. I prefer to rely on oral therapies rather than minoxidil. Tablets are easier to take and halt the balding process. Minoxidil is expensive, bothersome to apply and only has a slight benefit whilst the patient continues to bald unabated. Other therapies Camouflage is really only useful for early androgenetic alopecia. Various sprays or sprinkle-on powders are available, which are held onto the hairs/scalp by electrostatic charge. These need reapplication daily and take some discipline to use, as the camouflage can rub onto clothing, bedding and hands. Getting the hair wet can result in the dye material running. Wigs and hair extensions are useful for those in whom medical treatments are not appropriate or no longer appropriate, or for those who want to augment their current density. It is said that only bad wigs are noticeable, thus patients need to attend a good wigmaker and be willing to invest in a good hairpiece. Wigs can be synthetic or natural, complete or partial. Human hair wigs are more expensive, but look better, last longer and can be styled more easily. Female patients who are starting to thin often use hair extensions to increase their distal hair density. Hair transplantation is a well-established treatment option for androgenetic alopecia in both sexes. Transplantation exploits the fact that hairs from the occipital scalp are typically preserved in androgenetic alopecia and when transplanted to a remote site continue to grow according to their original programming. A strip of occipital scalp is harvested and the defect closed directly. The donor skin is then dissected into individual follicular units Wigs and hair extensions are useful for those in whom medical treatments are not appropriate or no longer appropriate. containing one to three hairs and transplanted into the recipient vertical or frontotemporal scalp. The process is labour intensive and quite specialized: several sessions of several hundred transplants each time are required. There is a redistribution of the follicles on the scalp, which achieves coverage of bald areas, rather than an increase in overall follicular density. Thus hair transplantation is more useful in early balding. The transplanted follicles are often placed among native hairs in the crown and frontoparietal scalp. As the balding process miniaturises the original hairs, not only do these areas become sparsely covered, but the transplants become obvious. This trees left standing appearance can appear embarrassingly unsightly. To avoid this, it is important to advise patients that continued medical treatment is usually required posttransplant to preserve the original hairs. Alopecia areata Alopecia areata (AA) is a common autoimmune, nonscarring alopecia that classically results in patchy hair loss. It is a disease of unknown cause, with a definite genetic predisposition manifesting as an autosomal dominant trait with variable penetrance. The familial risk is up to 30%. The disease is most common at about five and 30 years of age. Poorer prognosis and more extensive disease are associated with childhood onset, trisomy 21, atopy, initially severe disease (alopecia totalis/universalis), as well as a coincident endocrine disorder, alopecia oophiasis (see below), and a poor response to treatment. AA is associated with various other autoimmune diseases such as thyroid disease, vitiligo, Addison s disease, pernicious anaemia, rheumatoid arthritis, lupus erythematosus, scleroderma, ulcerative colitis, myasthenia gravis and diabetes. Screening for these may be performed if there is adequate clinical suspicion. Histopathology shows a peribulbar and intrafollicular lymphocytic infiltrate. Anagen follicles are affected by the infiltrate, leading to weakening of the hair shaft at the keratogenous zone. The hair fractures when the damaged area reaches the surface. The hair follicle is then forced into telogen, with a resultant reduction in follicle diameter. Thus affected hairs have a relatively wider, fractured distal portion with a tapering of the shaft more proximally, giving the characteristic exclamation mark appearance. These exclamation-mark hairs are in telogen and thus easily extracted. In most cases, the first patch of hair loss occurs on the scalp. Patches of AA on other hair-bearing areas may simply go unnoticed. Eyebrows and eyelashes as well as pubic and other body hair may be lost. Early pigmented hairs are typically lost first and any regrowth tends to be depigmented. Hairs are easily extracted from the edge of any patch. Exclamation-mark hairs measure about 3-4mm in length and are not necessarily found, but are diagnostic if present. Singular patches are often followed by other patches. Spontaneous resolution will likely occur, but relapse is virtually guaranteed in all patients. Several patterns are recognised. The singular patch is typical, as shown in figure 5. It may coalesce with other patches to form an irregular pattern. Alopecia oophiasis describes a pattern of loss at the margins of the scalp. Alopecia totalis is loss of all scalp Figure 5: Alopecia areata. hairs, while alopecia universalis is loss of all body hairs. Diffuse AA is a rare finding where there is diffuse hair loss throughout the scalp rather than a discrete patch, but biopsy confirms peribulbar inflammation. A peri-naevoid form is described with hair loss around benign naevi. Diagnosis is usually straightforward, with a singular, smooth patch of hair loss with characteristic exclamation-mark hairs. Differential diagnoses for AA include tinea capitis, trichotillomania and a mild scarring alopecia. However, these usually have their own characteristic findings. A scalp biopsy is only needed if the pattern is atypical or there is a suspicion of diffuse AA. The clinician should also consider screening for other autoimmune conditions, as guided by clinical findings. It is important for both patients and clinicians to realise that multiple treatment options exist for AA, none of which alters the long-term natural history of the disease. In two-thirds of patients, hair regrows within a year of the first episode of hair loss, while the other third of patients never recover and may progress to alopecia totalis. Though distressing, the disease is not life threatening, and available treatment options offer no guarantees of success. Partial regrowth is often just as unacceptable as the original bare patches. Indeed, conservative treatment is often an option and careful styling or use of wigs may be appropriate. A potent topical corticosteroid is a logical first-line option for young children and recent-onset disease. Twice-daily therapy for three months is needed, with regular review to observe for signs of dermal atrophy. Use of topical steroids can be somewhat disappointing, with intralesional steroids being more effective. Up to two-thirds of patients experience regrowth with intradermal injections of triamcinolone acetonide (10mg/mL). Enough should be injected to blanch and create palpable infiltration. Regrowth is obvious by about six weeks. Temporary dermal atrophy occurs after one injection; repeated injections lead to permanent atrophy. Singular patches are effectively treated with intralesional injections. However, if too many patches are injected, not only is this uncomfortable, but an appreciable dose of steroids is delivered and may have systemic implications. No more than 4mL should be injected within a month. Dilute intralesional steroids are also useful for eyebrows (at 5mg/mL); the risk for atrophy is greater. Topical dithranol can be used for patchy disease. It is an alternative to steroids and two-thirds of patients may respond. The mechanism of action is unclear. It is used in a similar manner to the treatment of psoriasis and should be trialled for three months. Irritation and staining will occur but are temporary. Widespread disease presents a greater management challenge. Those who have alopecia totalis or universalis may well become resigned to their condition. Men get used to the bald look. Patients of either gender who want coverage will sometimes elect to invest in a good hairpiece and may pencil in the eyebrows. Functionally eyebrows are important to keep sweat from running down to the eyes and eyelashes function to keep debris out. A short course of oral corticosteroids can induce regrowth in up to three-quarters of patients. A relatively high dose is required (up to 0.8mg/kg/day of prednisone) for several weeks. The effect is often not durable and some patients relapse during treatment. Once regrowth is established, introduction of alternative therapy is important. For many dermatologists, topical immunotherapy in the form of diphencyclopropenone (DCP) is the mainstay of treatment of widespread disease. Its mechanism of action is still unclear but may have to do with immune diversion. This synthetic allergen causes an allergic contact dermatitis on the scalp surface, which presumably then frees the deeper hairs from their immune attack. Patients are initially sensitised to a 2% solution applied under an occlusive dressing for 24 hours. They are then taught to apply a dilute solution to the affected areas (or the entire scalp) on a weekly basis. Most will have a starting dose of a 0.001% solution. Patients are advised to expect erythema, itch and discomfort for several days. Lymphadenopathy is also common. Those without a reaction after one month can have the dose titrated upwards. Those with severe reactions (blistering, burning, etc) should have the DCP concentration reduced. Irritation does not always occur, but is a surrogate marker of an adequate dose. Patients should self-apply or have a family member apply the agent, initially under the direct supervision of their doctor. Contact with any other part of the skin will result in a reaction there. Helpers should also take adequate precautions to prevent themselves from being sensitised. It is not possible to identify responders, and the agent needs to be trialled for at least six months before abandoning it. Other rare adverse events include vitiligo and urticaria. There is varying opinion as to the duration of therapy. Some recommend cessation once full regrowth has occurred, but others advocate continuous long-term treatment. Other third-line therapies are available, but have their limitations. Oral or topical PUVA (psoralen and ultraviolet A) therapy can be used in those not wanting a systemic agent. It requires a significant time commitment and has long-term risks of skin cancer induction; ultraviolet A-emitting phototherapy units are rapidly becoming obsolete. Systemic cyclosporin, azathioprine and oral zinc have been reported to be useful, as have topical nitrogen mustard and cryotherapy. The excimer laser system has been tried with variable success. Topical tacrolimus and pimecrolimus have not shown any benefit to date. Anagen effluvium Acute hair loss that occurs with chemotherapy and radiotherapy is well recognised. Anagen effluvium results from acute toxicity suffered by the hair follicle matrix keratinocytes, leading to growth arrest and then fracture of the pathologically narrowed anagen hairs. In chemotherapy, all anagen hairs are affected, and rapidly cont d page February 2009 Australian Doctor 31

4 HOW TO TREAT Hair loss from page 31 shed within days of the insult. As the hairs are still in anagen, they can continue to grow once chemotherapy ceases. It is important to reassure patients that hairs will regrow after therapy. Radiation-induced anagen effluvium tends to last longer, and at high doses may induce permanent alopecia. Anagen effluvium can also occur with heavy metal poisoning such as arsenic and thallium, as well as graftversus-host disease. Traction alopecia Traction alopecia is a result of chronic, low-grade mechanical tension on hairs resulting in their fracture or extraction from the follicles. The classic patient is the black African woman who wears her hair in tightly braided corn-rows after chemical straightening. However, any tight styling can result in hair loss: ponytails, tight buns, or even regular vigorous combing/ grooming. There will be a peculiar pattern of alopecia that makes sense when the direction of hair shaft tension is considered. The logical management is to advise a change in grooming behaviour, ie, to stop the traction. But patients can be quite resistant to changing their styling habits, and may not be accepting of the diagnosis. A biopsy may be required if there is a possibility of coexistent androgenetic alopecia. Trichotillomania should also be considered. Trichotillomania Trichotillomania (TTM) is a self-inflicted form of traumatic alopecia. Patients pick and pluck their hairs resulting in unnatural or bizarre patterns of hair loss. Several patient groups are classically described Figure 6: Trichotillomania. Note the off-centre alopecia and unruly hairs. in this relatively common disorder. Young children often develop a hair-pulling habit that has no long-term behavioural sequelae. A furry or fluffy toy is a good substitute for their scalp to divert plucking behaviour. A similar group involves adolescent and young adult women who have what amounts to a habit tic; they pluck hairs as they would bite their nails. True TTM is classified under the American Psychiatric Association Diagnostic and Statistical Manual (DSM- IV) as an impulse control disorder. There is an association with anxiety, depression, substance abuse and various personality disorders. Patients have a build-up of tension that is rapidly but temporarily relieved by the oftensurreptitious plucking behaviour. Clinically early patches are ill defined, with a normal scalp and a stubble of broken hairs of irregular lengths. There is no complete alopecia. Multiple sites are common, as is alopecia from eyebrows and eyelashes. More established cases can have a bizarre and irregular pattern of loss (figure 6). The tonsural pattern spares the scalp margins and has a very poor prognosis. Management of true TTM can be extremely complex. There is often complete denial of the plucking behaviour, and a scalp biopsy may be needed to rule out other disorders. A multidisciplinary approach is required, but effective treatment can only be instituted when the patient concedes to the diagnosis. There are no established effective therapies and typically a combination of behavioural modification therapy and pharmacotherapy is required. Referral to a psychodermatology clinic is useful, if available and the patient is agreeable. Though there are many case reports of various psychotropic and mood-stabilising drugs being useful, clomipramine may be the only agent found to be effective in controlled trials. Other metabolic causes The most common systemic causes of diffuse alopecia would include thyroid disease and iron deficiency. Thyroid function tests and iron studies should be routinely performed in patients with diffuse hair loss. Secondary syphilis, chronic renal failure, hepatic failure, SLE, zinc deficiency, malignancy, drugs, and malnutrition or malabsorption may also induce various patterns of hair loss. Hair loss in these conditions may well overlap with ATE. Loose anagen syndrome This relatively common syndrome is due to poor adhesion between the hair shaft cuticle and the inner root sheath of the follicle, leading to easily extractible anagen hairs. There is often a familial tendency and it tends to affect young blonde females more often. Figure 7: Loose anagen syndrome. A patch of hair loss with easily extractable hairs; no exclamation mark hairs are seen. The disease presents in early childhood and can persist to the mid-to-late teens. Affected girls have somewhat unruly hair of different lengths. Focal areas of alopecia can be found in some. The hairs are easily extracted without pain and the child only needs infrequent haircuts (figure 7). Hairs should be examined under light microscopy where anagen hair roots are seen with a characteristic ruffling of the cuticle just distal to the root. No treatment is required except advice to style gently, as spontaneous resolution eventually occurs. Tinea capitis Though not strictly a hair loss condition, tinea capitis should always be considered with a patch of alopecia. Of the many types of tinea capitis, the small-spore ectothrix infection is the most common, with a well-demarcated patch of broken hairs that have a grey, fuzzy coating due to fungal spores on the shafts surface. There is minimal inflammation and several patches may be seen. Hairs are often extracted easily and these classically fluoresce under Wood s lamp illumination. The kerion is an inflammatory, boggy and purulent mass often mistaken for a scalp abscess. Hairs can be painlessly extracted and incisional drainage will yield no discharge (something to be avoided!). There is often a coexistent bacterial infection. Plucked hairs and skin scrapings should be sent for fungal microscopy and culture. A swab for bacterial microscopy and culture may be helpful for kerions. Griseofulvin at a dose of 500mg/day in adults (child: 10-15mg/kg/day up to a maximum of 500mg/day) should be used for at least six weeks. An antifungal shampoo should also be used daily to reduce fungal spore shedding. Cultures should be repeated at regular intervals if there is suspicion of continued tinea, and therapy should continue for two weeks after mycological and clinical cure. Griseofulvin is lipid-soluble and is best taken with a fatty meal. Children often tolerate it better when tablets are crushed and mixed with ice cream (or another soft, fatty food). Terbinafine is also effective at a dose of 4-5mg/kg/day. An alternative dosing regimen is to use 62.5mg/day (onequarter of a tablet) for children weighing 10-20kg, 125mg/day (half a tablet) for those weighing 20-40kg and the full adult dose of 250mg/day for those weighing more than 40kg. A broadspectrum antibiotic is useful for secondary bacterial infection. Scarring alopecias Lichen planopilaris LICHEN planus is a common cutaneous eruption characterised by violaceous, polygonal, flat-topped papules on the skin. It can also affect the scalp, causing a scarring alopecia termed lichen planopilaris (LPP). LPP starts as classic papules but quickly evolves into perifollicular erythema, follicular plugs, alopecia and formation of a scar. As the area of involvement spreads, a bald patch forms with a smooth white scar lacking follicular ostia in the centre, and the expanding edges feature follicular plugs and perifollicular erythema. It is important to examine the rest of the patient for lichen planus. Scalp biopsies should always sample multiple sites within a patch, as histopathology of a scarred area may be non-specific. Punch biopsies should include the scar, the active periphery where there is inflammation, and any other interesting feature. The lichenoid inflammation is characteristically perifollicular, with sparing of intrafollicular skin. Treatment should be multimodal and is aimed at stopping the disease rather than reversing the hair loss. Small areas affected or the inflammatory front will benefit from intralesional or potent topical corticosteroids. A short course of oral corticosteroids may help settle acute disease and should then be substituted with a steroid-sparing agent. There is no consensus as to what works best for LPP. Oral acitretin (25-75mg/day) is the current standard for cutaneous lichen planus and should be considered first line in LPP; diffuse hair loss is a common adverse effect. Acitretin is a potent teratogen and fertile women require a reliable contraceptive during therapy and for three years after cessation. Hydroxychloroquine ( mg/ day) has also been used with some success. Cyclosporin, methotrexate and azathioprine are useful in some cases. Griseofulvin, minocycline, tetracycline, thalidomide and PUVA have been used in isolated cases. A variant of LPP is frontal fibrosing alopecia (FFA). This rare disorder occurs in women and can mimic androgenetic alopecia, with frontal hair loss and recession. It is important to note that a substantial minority of women with non-scarring female pattern balding can have some frontal recession. Close inspection will find the perifollicular erythema and loss of follicular ostia in scarred skin. Unfortunately, FFA is said to be unresponsive to therapy, however conventional therapy should be tried. Figure 8: Discoid lupus erythematosus. Discoid lupus erythematosus Discoid lupus erythematosus (DLE) is a variant of cutaneous lupus erythematosus (LE) that causes scarring. One-third of SLE patients will have DLE lesions during the course of their illness, but most patients who only have DLE do not evolve into SLE. The typical plaque of DLE has erythema, adherent scale, follicular plugging, and an irregular mix of atrophy, scarring and dyspigmentation. When on the scalp, DLE leads to an inflammatory destruction of hair follicles. Scarring alopecia is found in one-third of patients with DLE; the typical DLE features are seen with obvious follicular plugging and pigmentary disturbance. The plaques can spread irregularly across the scalp, resulting in extensive alopecia (figure 8). 34 Australian Doctor 13 February

5 Figure 9 : Acne keloidalis nuchae. Note the keloidal nodules and associated scarring hair loss. Figure 10: Tufted folliculitis. Multiple hair shafts emerging from a large ostium surrounded by scarring. Active folliculitis decalvans is the cause. Figure 11: Dissecting cellulitis of the scalp. Large interconnecting abscesses with overlying hair loss. Figure 12: A: Erosive pustular dermatosis. Large crusted areas of dried purulent crusts. Wiping away reveals pool of pus. B: After several weeks of potent topical steroids. Resolution of purulent areas replaced by granulation tissue. A important in directing therapy. If a fungal kerion is suspected, then fungal microscopy and culture should be performed. A scalp biopsy is mandatory for diagnosis. Treatment is aimed at staphylococcus eradication, but there is no consensus. Various combinations of beta-lactam antibiotics, tetracyclines, cotrimoxazole, rifampicin, clindamycin, fusidic acid and fluoroquinolones have been used. Short courses of single agents can be effective, but relapse is common after cessation. Combination therapy is often more effective with severe disease, for example, rifampicin and fusidic acid together with clindamycin or oral zinc for several months. The histopathology of DLE of the scalp has all the typical features of cutaneous LE, which is a lichenoid-type inflammation. One feature that distinguishes DLE from LPP is interfollicular inflammation, which is not found in LPP. It is important to distinguish hair loss from DLE and the diffuse non-scarring alopecia that occurs with SLE and subacute cutaneous LE. A check of the American Rheumatological Association diagnostic criteria for SLE should always be performed to rule out systemic involvement. Once SLE has been ruled out, a multimodal approach should be used. Topical and intralesional steroids will help individual lesions. Oral prednisone is useful for rapidly progressive disease, while hydroxychloroquine up to 400mg daily can induce remission within months. Once the disease settles, the patient can slowly be weaned off all drugs. Alternative therapies include topical tacrolimus, topical imiquimod, chloroquine, acitretin, dapsone, methotrexate, thalidomide, cyclosporin, mycophenolate mofetil and cyclophosphamide. Acne keloidalis nuchae Though not a true scarring alopecia, this chronic inflammatory folliculitis of the occipital scalp can lead to nodular scars and keloids that destroy hair follicles (figure 9). The aetiology is unclear, but it tends to occur more in black men and is thought to Erosive pustular dermatosis is not uncommonly found in older men with partially bald and sun-damaged scalps. B be a race-related peculiarity of the pilosebaceous unit, with mechanical trauma being a precipitant. Inflammatory papules within the occipital scalp progressively worsen and extend upwards. Papules and pustules may coalesce, forming plaques and ridges which evolve into a scar eventually replacing hairs. The area may be irritated or itchy and there is often a history of significant acne vulgaris at some time. It is neither a true acne nor is there true keloid formation. Swabs should be taken to rule out secondary infection. A potent topical steroid cream (at night) and topical clindamycin lotion (twice daily) should be used for several weeks to months in early disease, reducing inflammation and secondary infection. More severe disease may benefit from the addition of oral tetracyclinetype drugs as for acne. Intralesional steroids are useful for larger nodules and itchy scars. Laser ablation and surgical excision of the scarred or inflamed area are also described. There are also case reports of imiquimod and topical pimecrolimus being useful. Folliculitis decalvans Folliculitis decalvans is likely to be an abnormal inflammatory host-response to chronic staphylococcal folliculitis. It is most common on the scalp, but can occur in other hair-bearing areas. Inflammatory folliculitis is followed by a scarred patch of hair loss. There is continued pustular activity at the edge and with each successive wave of folliculitis the scarring expands. Linear areas of erythema, crusting and pustulation can occur, as well as tufting of the follicles. This last feature describes multiple hair shafts emerging from one follicular ostia surrounded by scars (figure 10). Swabs should be taken for bacterial microscopy and culture; Staphylococcus aureus is typically found. Sensitivities are Dissecting cellulitis of the scalp This inflammatory disease manifests as multiple interconnecting abscesses on the scalp that eventually result in widespread scarring alopecia (figure 11). It is classically described as being part of the follicular occlusion triad, with acne conglobata and hidradenitis suppurativa. Dissecting cellulitis of the scalp is rare but important to recognise as the treatment is not antibiotics but rather systemic isotretinoin. The treatment course is similar to that for severe acne; prednisone and erythromycin may be added at the beginning for their antiinflammatory effect. Early effective treatment may result in significant regrowth of hairs. Erosive pustular dermatosis Erosive pustular dermatosis is not uncommonly found in older men with partially bald and sun-damaged scalps. Areas of crusting and discharge may be wiped away to reveal a lake of pus or a crop of pustules (figure 12). Scarring alopecia is produced with the expansion of the affected area; this can occur for years before presentation. A malignancy is often suspected with a heaped-up area of crusting and dried pus. Wiping away the purulent material may reveal erosions or granulation tissue. A potent topical steroid is the primary treatment. This can be used under wet dressings twice daily to improve efficacy and to soak off the excess crusting. Two to three weeks of therapy produces a favourable effect, but maintenance therapy may be required. Oral antibiotics can also be used as an adjunct. It is important to continue monitoring these patients, as cutaneous malignancies are also common on a sun-damaged scalp. A biopsy should be performed if steroids are not helping. Conclusion HAIR loss is a relatively complex problem. The clinician needs to understand the potent psychological impact that alopecia has on their patient. A thorough search for a diagnosis is important, as treatment is often possible and there may be systemic implications that warrant further therapy. The presence or otherwise of scarring initially guides the work-up; a scalp biopsy is often important in clinching the diagnosis. Reference 1. Trüeb RM. Finasteride treatment of patterned hair loss in normoandrogenic postmenopausal women. Dermatology 2004; 209: Online resources Australasian College of Dermatologists: New Zealand Dermatological Society: American Academy of Dermatology: National Alopecia Areata Foundation (USA): cont d next page 13 February 2009 Australian Doctor 35

6 HOW TO TREAT Hair loss GP s contribution DR MATILDA METLEDGE Sydney, NSW Case study MISS N, 29, has had slow, diffuse progressive hair loss since her late teens. She was diagnosed with androgenetic alopecia and was trialled over some years with various combinations of cyproterone, spironolactone and antidepressants with no success. She commenced topical minoxidil but quickly developed a severe irritant dermatitis whenever she applied it, requiring cessation of therapy. Although she has largely come to terms with her cosmetic appearance, any mention of it by family or friends quickly reduces her to tears. She has now completed her family and would like to discuss finasteride or other treatments. Questions for the author As she has not used minoxidil for many years now, is it likely that she will react in a similar way on retrial? Is there any way to reduce the reaction? Minoxidil lotion often produces pruritus and an irritant contact dermatitis. Very occasionally an allergic contact dermatitis can occur. A severe reaction may represent overuse of the agent, or a true allergic contact dermatitis (ACD). Only 1mL should be applied each time, distributed evenly throughout the entire scalp. If an ACD is suspected, then a Repeat Open Application Test (ROAT) should be attempted: a small amount of minoxidil should be applied to the medial epicondyle twice daily for one week to observe for a dermatitic reaction. If there is no reaction, the patient can try it on the scalp carefully and sparingly. Various alternative practitioners have recommended hair food products consisting of many different ingredients, silica featuring in most. Is there any evidence that any of these (very expensive) products make any difference? Are there any which you would recommend? There is scant evidence for any of these supplements being useful. Indeed there are some older studies that specifically show no benefit. Patients should be discouraged from using these agents, which really only have placebo value. However, if a deficiency was discovered on routine screening, then supplementation may be appropriate. This may well be how some of these supplements have come to be seen as useful, as certain deficiency states have hair loss as part of the syndrome. What would be your approach to trialling finasteride in this case? In Australia oral finasteride is approved for androgenetic alopecia in males only. There are some data that show finasteride to be useful in post-menopausal women, but this is strictly an off-label indication. Currently finasteride is not approved for use in fertile women and cannot be routinely recommended. Any use in young women is also off-label and both clinician and patient bear all responsibility for its use. However, given that the patient above is greatly distressed by her hair loss and has not had success with the traditional antiandrogens, finasteride may be tried. The patient would have to be strictly counselled that the drug is not approved for use in her situation and that there is no evidence that it is useful at male doses. She would need to have a reliable contraception (prefably a permanent form, otherwise two reversible forms), and be reminded that finasteride is a teratogen (but so are cyproterone and spironolactone). However, the patient can be reassured that the medication is generally otherwise quite safe and has virtually no known drug interactions. The 2.5mg daily dose is preferred simply because past trials at 1mg daily showed no efficacy. Many cosmetic clinics advertise laser treatment for hair loss. What is the likely result of these treatments, some of which are advertised by impressive before and after pictures even with advanced hair loss? There is an old fallacy that heating the scalp increases scalp blood flow, which in turn encourages hair growth. In the past various scalp-heating devices have been peddled, and as each contraption falls out of favour, a new one takes its place. These so-called laser devices are simply a 21st century permutation of the same. Most of these are no more than a bank of lowenergy light-emitting diodes (LEDs) on a handle, rather than a true laser. As far as I am aware, there is no evidence that they are useful. As the old saying goes, If it looks too good to be true, it usually is. How to Treat Quiz Hair loss 13 February 2009 INSTRUCTIONS Complete this quiz online and fill in the GP evaluation form to earn 2 CPD or PDP points. We no longer accept quizzes by post or fax. The mark required to obtain points is 80%. Please note that some questions have more than one correct answer. ONLINE ONLY for immediate feedback 1. Which TWO statements regarding the normal hair cycle are correct? a) Anagen is the growth phase where a hair shaft is actively being produced by the underlying follicle b) Exogen is a transitional stage occurring at the end of anagen, before the next telogen c) About 40% of the hair follicles on the scalp are in anagen at any time d) Humans normally lose about between 50 and 200 hairs daily 2. Heather, 45, presents with a three-month history of diffuse hair loss. She is otherwise well and takes no medication. On examination there is no obvious patterned loss and no widening of the central part. Further history reveals she was in a car accident three months ago. You suspect she may have acute telogen effluvium (ATE). Which TWO statements are correct? a) In ATE the hairs are usually difficult to extract from the scalp b) In the early stages telogen effluvium and androgenetic alopecia can be indistinguishable c) All cases of suspected ATE need confirmation with scalp biopsy d) Most cases of ATE will resolve within six months 3. Which THREE statements regarding androgenetic alopecia are correct? a) Half of men are balding by age 50 and half of women by age 60 b) In androgenetic alopecia the number of hair follicles is reduced c) In androgenetic alopecia there is a progressive reduction in follicle size and duration of anagen d) If a scalp biopsy is required to confirm the diagnosis of androgenetic alopecia, samples should be sent for horizontal sections 4. Rosalind, 55, presents with progressive hair thinning over many years. She is otherwise well. Her frontal hairline is normal, but the hair is less dense over the crown. She asks if any topical treatments might help. Which TWO statements regarding topical minoxidil for androgenetic alopecia are correct? a) Minoxidil is most effective for early disease and for vertical thinning b) Up to 90% of patients experience stabilization of loss and 50% achieve regrowth with minoxidil c) Treatment with minoxidil needs to continue long term d) If started in early disease, minoxidil can delay the miniaturisation process of androgenetic alopecia 5. Terence, 50, presents with a long history of hair loss, with progressive frontal recession and an expanding vertical bald patch. He tried minoxidil but developed an irritant dermatitis and asks about other treatments. Which TWO statements regarding oral therapy for androgenetic alopecia in men are correct? a) Finasteride acts by inhibiting conversion of dihydrotestosterone to testosterone b) Five-year studies of finasteride use demonstrated increased hair counts in over 90% of men c) When monitoring PSA in patients on finasteride, the numerical value needs to be halved as finasteride tends to double the measured PSA d) Patients on finasteride have a lower incidence of prostate cancer, but those who do develop it have lesions with higher Gleason scores 6. Which THREE of the following conditions may cause hair loss? a) Thyroid disease b) Iron overload c) Chronic renal failure d) Zinc deficiency 7. Which TWO statements regarding the aetiology and pathogenesis of alopecia areata (AA) are correct? a) AA is a common autoimmune non-scarring alopecia b) AA has a genetic predisposition manifesting as an autosomal recessive trait c) There is no association between AA and other autoimmune diseases d) Affected hairs have a characteristic exclamation mark appearance 8. Which TWO statements regarding the clinical features and diagnosis of AA are correct? a) In most cases of AA, the first patch of hair loss occurs on the scalp b) Alopecia totalis is the term for loss of all body hairs c) Exclamation mark hairs must be present in order for a diagnosis of AA to be made d) A scalp biopsy is only needed if the pattern is atypical or there is a suspicion of diffuse AA 9. Which THREE statements regarding the management of AA are correct? a) Two-thirds of patients regrow from their first episode of AA within a year b) While multiple treatment options exist for AA, none of these alters the long-term natural history of the disease c) A potent topical corticosteroid is a first-line option for recent onset disease d) Topical dithranol has not been found to be effective in AA 10. Which TWO statements regarding lichen planopilaris (LPP) are correct? a) LPP is a common, non-scarring alopecia b) In patients with suspected LPP, it is important to examine the rest of the patient for lichen planus c) A single punch biopsy sample of the scalp is adequate for diagnosis of LPP d) Treatment is aimed at stopping the disease rather reversing the hair loss CPD QUIZ UPDATE The RACGP now requires that a brief GP evaluation form be completed with every quiz to obtain category 2 CPD or PDP points for the triennium. You can complete this online along with the quiz at Because this is a requirement, we are no longer able to accept the quiz by post or fax. However, we have included the quiz questions here for those who like to prepare the answers before completing the quiz online. HOW TO TREAT Editor: Dr Wendy Morgan Co-ordinator: Julian McAllan NEXT WEEK The next How to Treat examines domestic violence, a major public health problem in Australia. The author is Associate Professor Kelsey Hegarty, primary care research unit, department of general practice, University of Melbourne, Victoria. 36 Australian Doctor 13 February