Alopecia - Different Forms and Treatments

The importance of human hair in view of social communication and sexual attraction is enormous. Thus, diseases that lead to hair loss (alopecia), structural hair shaft defects or excessive hair growth on the body are often accompanied by a diminished sense of personal well-being and self-esteem, leading to depressive moods and withdrawal from social interims.

Following are the main types of alopecia:

ANDROGENETIC ALOPECIA: AGA or pattern hair loss is by far the most common type of hair loss in men and women. Male pattern hair loss (MPHL) (also known as male AGA, male balding) is a hormone (androgen) dependent, genetically determined trait. Female pattern hair loss (FPHL) (or female androgenetic alopecia) is believed to be the same entity. However, the requirement of androgens is less clear cut than in men and the distribution of hair loss is generally different. In both, men and women, AGA is characterized by a progressive decline in the duration of anagen (active growth phase), an increase in the duration of telogen (terminal phase) and miniaturization of scalp hair follicles.

Epidemiology:

Men: Estimates of the prevalence of AGA vary widely. Most men will develop some degree of a recession of the hairline during their lifetime. Some hair loss is seen in around 50% of men and women beyond 40 years of age. The risk of male pattern baldness depends on the family history in the father, the mother, or the maternal grandfather. Men whose father had hair loss were twice as likely to have hair loss as men whose father showed no hair loss. Ethnic variation in the incidence of AGA has been reported. AGA seems to be four times less frequent in men of African ancestry, around three times less frequent in Korean men and approximately 1.5 times less frequent in men originating from China, Japan or Thailand.

Women: Female Pattern Hair Loss (FPHL) is less common than Male Pattern Hair Loss (MPHL) but shows a similar age-related increase in frequency and severity. However, the condition can start as early as the prepubertal period both in men and women. Around 40% of Caucasian women have developed some degree of FPHL at age 70. FPHL seems to be less frequent in Asian women.

Pathophysiology: The underlying causes of patterned hair loss have yet to be determined. In men, MPHL appears to result from a combination of androgen (mainly testosterone) hyperactivity, a genetic predisposition to hair loss-related sensitivity to androgen action as well as an androgen-independent genetic predisposition. For females, the condition known as female pattern hair loss (FPHL) may have a more complex etiology. However, androgen action combined with genetic sensitivity to those actions seems to play a dominant role in most cases, and indeed these factors may be present generally in FPHL. In AGA, large, pigmented hairs, called terminal hairs, are gradually replaced by fine (nearly invisible) colorless vellus hairs. This transformation follows a progressive course with each hair cycle in the following manner. Scalp hair develops in three phases: (1) a growth phase, or anagen, of approximately 2–6 years; (2) a short (2–3 weeks) phase, catagen, which actually represents the termination of anagen; and (3) transition to the telogen phase. A telogen hair does not grow and is shed from the follicle after about 12 weeks. MPHL and FPHL exhibit a progressive decrease in anagen duration with each cycle, producing shorter, thinner hairs. Finally, the interval between late telogen hair shedding (exogen) and new hair growth with initiation of anagen increases, resulting in more follicles without hair and an apparent reduction in scalp hair density.

TELOGEN EFFLUVIUM

Epidemiology: The second most common cause of hair loss in women after FPHL is TE. The latter presents as a nonpatterned increase in shedding of terminal hairs, diffusely over the entire scalp, and can produce an apparent thinning of hair in severe cases. While both genders can experience TE, attitudes toward hair loss result in a greater proportion of females who complain. TE can co-present with AGA, particularly in early-onset situations, and this can complicate diagnosis and treatment. TE differs from AGA in that it is not androgen-sensitive and does not appear to be inherited. TE also tends to be related to external causes and is often reversed when the exogenous stimuli are removed.

Pathophysiology:

Acute Telogen Effluvium: The pathophysiology underlying TE is best characterized as a premature shift of hairs from the anagen (growth) phase into the catagen (resting) and telogen (terminal) phases. However, there are variants: anagen may be prolonged, or telogen may instead be shortened or prolonged. Which type of shift occurs depends on the stimulus producing the shift, with the main clinical difference being the latency of effluvial onset following the stimulus. The hair loss that commonly occurs following pregnancy is generally seen 2 or 3 months after birth, although some individuals can exhibit longer times to onset. While this is classic TE, the mechanism has been shown to involve a delayed transition from anagen to catagen/telogen, which results in a simultaneous shedding of large numbers of terminal hairs. This hair does eventually regrow; however, the returning hair may show changes in texture, color, and curliness, and may not attain its previous length. As such, pregnancy (parturition or abortion) may in some cases produce permanent changes in anagen length. Other perturbations can produce TE, usually involving premature termination of the anagen phase. Some women experience transient TE 2–3 months after discontinuing or changing oral contraceptive medication; the delayed onset of TE in these cases distinguishes it from the anagen effluvium (AE) initiated by certain drugs. In the 1970s, the popularity of fad “crash” diets resulted in many cases TE about 3 months after initiation of these spartan regimens, depending on the severity of weight loss. Sudden deprivation of amino acids and other dietary factors most likely produced the condition, and the hair tended to regrow following cessation of the diets. Surgical procedures, psychological traumas, and febrile illness have all been reported to produce TE events. Drugs are widely reported to produce temporary hair loss. This is usually, but not necessarily, of the AE variety, since, depending on the causal agent, the time course and severity may suggest a diagnosis of TE to be appropriate. Agents producing TE include cimetidine, enalapril and captopril, propranolol, and lithium among others. Finally, hair loss occurring following environmental contamination or poisoning, for example with selenium, arsenic, thallium, mercury, and lead, displays an AE-like rapid onset.

Chronic Telogen Effluvium: Chronic Telogen Effluvium (CTE) is used in distinguishing the abrupt-onset, short-acting type TE, usually caused by exogenous triggers or parturition, from a more durable condition (CTE) that may not be so clearly related to any external event. While “crash” diets have been pinpointed as potential triggers for acute TE, chronic malnutrition can analogously lead to CTE. Protein deficiency is the likely mechanism in this type of balding. It is less clear whether zinc or biotin deficiencies are also correlated with chronic diffuse hair loss. Although controversial, iron deficiency, as evidenced by decreased serum ferritin and anemia, may be a trigger for CTE. Hypothyroidism has also been associated with CTE.

ALOPECIA AREATA

Epidemiology: At any given time, approximately 0.2% of the world population is suffering from alopecia areata with an estimated lifetime risk of 1.7%. It is a common cause of abrupt-onset hair loss but occurs less frequently than androgenic alopecia or TE. Both sexes are affected equally. Although it may occur at any age, incidence at a younger age is higher. Alopecia areata is the most common form of alopecia seen in children. The familial occurrence is around 15% but the expression of the disorder is variable among different family members. 5% of patients suffering from alopecia areata develop hair loss of their entire scalp hair (alopecia totalis), and 1% of patients develop loss of total body hair (alopecia universalis) at some point.

Pathophysiology: Alopecia areata is a chronic, organ-specific autoimmune disease, which affects hair follicles and sometimes nails. Alopecia areata is thought to be an autoimmune disease with inappropriate immune- response to hair follicle associated proteins. A collapse of the normal immune privilege of the anagen hair bulb may play a key role in the pathogenesis of this disease. There is a high frequency of a positive family history of alopecia areata in affected individuals, ranging from 10% up to 42% of cases, and a much higher incidence of positive family history in early-onset alopecia areata. Many patients report the experience of major emotional stress prior to the onset of alopecia.

ANAGEN EFFLUVIUM

Pathophysiology: AE is a result of a disturbance of hair follicle matrix cells. The anagen phase is interrupted and the hair falls out 7–14 days after the initiating event without entering catagen or telogen. Drugs used in chemotherapy quickly produce severe hair loss and even total baldness. A rapid onset undoubtedly indicates an immediate release from anagen hair. Immediate anagen hair release is characterized by an easy release of anagen hairs after gentle pulling.

TEMPORAL TRIANGULAR ALOPECIA

Epidemiology: Lesions can be present at birth or first appear before school age. Temporal triangular alopecia (TTA) has been reported in Asian and Caucasian patients with no sexual predilection. TTA is often misdiagnosed as alopecia areata.

ANDROGENETIC ALOPECIA (AGA): The identification of AGA is usually not difficult if the alopecia occurs in a classical clinical pattern. In 1951, the first grading scale for MPHL was produced. The Hamilton scale ranges from type I to VIII. Whereas type I represents the prepubertal scalp with terminal hair growth on the forehead and all over the scalp, type II and III show gradual, mostly M-shaped frontal recession of the hairline, type IV, V, and VI show additional gradual thinning at the top, type VII and VIII show a confluence of the balding areas and leave hair only around the back and the sides of the head. In 1977, classification for the pattern of AGA in women was introduced, characterized by a diffuse loss of hair on the crown and persistence of the frontal hairline. It was then noted that AGA did not necessarily present with diffuse hair loss over the entire top but rather may have increased hair loss towards the front, called frontal accentuation or Christmas tree pattern. Women can also show a male pattern of distribution, as well as men can show a more female pattern.

TELOGEN EFFLUVIUM: Acute telogen effluvium is characterized by a fairly sudden onset of massive shedding. Anagen hairs are prematurely shifted into telogen hairs and the normal anagen/telogen ratio of 90:10 can switch to 70:10. Women often present with the “bag sign”: bringing in bags with hair that they have collected every day or over a couple of days. More than 300 telogen hairs can be shed every day. Chronic Telogen Effluvium can most commonly be seen in women. Patients report ongoing massive shedding or recurrent episodes of shedding. As a rule of thumb, any diffuse hair shedding lasting longer than 6 months after any triggering event, or after withdrawal from suspected causal drugs, should be considered CTE. Both acute and CTE usually resolve once trigger factors are eliminated. However, CTE triggers may be difficult to identify. Women with TE are often most concerned about complete baldness. The patient has to be reassured that the condition does not lead to complete baldness and that the hair likely grows back around 6 months after the removal of the initiating trigger. The patient should understand that the condition is reversible, but that the shedding may persist for a few weeks or months once the initiation factor is eliminated.

ALOPECIA AREATA: Alopecia areata is characterized by an acute onset. It typically presents with oval or round, well-circumscribed, bald patches with a smooth surface in a diffuse distribution. Alopecia totalis results in the loss of the entire scalp hair and may occur suddenly or follow partial alopecia. Partial alopecia may be observed in other areas of the body as well. Loss of total body hair is called alopecia universalis and may also occur suddenly or follow long-standing partial alopecia. Characteristic hallmarks of alopecia areata are “black dots” (cadaver hairs, point noir), resulting from hair that breaks before it reaches the skin surface. Exclamation point hairs, with a blunt distal end and taper proximally, appear when the broken hairs (black dots) are pushed out of the follicle. Localization of the initial patch is most frequently on the scalp but may occur on any hair-bearing part of the body. Patches are usually without further symptoms but may show mild itching and erythema in some cases. Alopecia areata can less commonly present in a diffuse generalized pattern that resembles androgenic alopecia or TE. In the acute stages, gentle pulling from the periphery of bald areas will yield more than 10 hairs. The involvement of nails is common with nail pitting and a sandpaper-like appearance. The disease has been described in association with a variety of other disorders, such as cataracts, thyroid disease, vitiligo, psoriasis, and Down syndromes. The course of the disease is very variable and characterized by an irregular relapsing course, with about 25% of affected individuals having a solitary episode. Spontaneous regrowth of hair is common. Different body areas appear to regrowth independently. About 60% of patients have at least a partial regrowth by 1 year, but this is often followed by repeated episodes of hair loss. About 40% of the relapses occur within the first year, but a large percentage of patients may relapse after 5 years. Hair can regrow white but may change to the patient’s natural color over time. Poor prognosis is linked to the involvement of the backside of the head and/or hairline (called the ophiasis pattern if sweeping around the periphery of the scalp), a chronic relapsing course, the presence of nail changes, and onset during childhood. The number of patients progressing to alopecia totalis also higher in patients with hair loss from the trunk and extremities. Complications of Alopecia Areata can be a relapsing course and progression of hair loss to severe forms of alopecia totalis or universalis are dreaded complications. Missing hair on the scalp and face, including nose hair and eyelashes/brows can increase the incidence of sunburn and skin cancer, as well as inflammation of nose, pharynx, and eyes. Although the condition is not life threatening, changes in appearance frequently cause a diminished sense of personal well-being and self-esteem, leading to severe depression and withdrawal from social situations.

ANAGEN EFFLUVIUM: The anagen hair has a broom-shaped, pigmented bulb. Two different types of AE can be distinguished: Dystrophic AE and Immediate anagen release. Dystrophic AE can be caused by chemotherapy, radiation, toxins or alopecia areata. Microscopic investigation of the hair bulbs, obtained from a hair pull test or trichogram, usually shows a tapered tip with the weakened hair shaft broken shortly above the bulb (“dystrophic hair”). Normal appearing anagen hair with inner and outer root sheath can be found to some extent in every AE.

TEMPORAL TRIANGULAR ALOPECIA:  TTA is nonscarring, noninflammatory alopecia that presents with one or more roughly triangular, oval, or lancet-shaped alopecic patches in the front and temple areas. A few terminal hairs or vellus-like hairs can often be found in the periphery of the affected area and the scalp is normal. The lesions are usually asymptomatic and the hair elsewhere on the scalp is of normal density. The patches are mostly unilateral (80%) but can occur on both temples as well (20%). A strip of hair of normal density can be seen between the affected patch and the forehead.

Diagnosing various forms of Alopecia

Global Assessment and Imaging: The global examination of the scalp includes an assessment of the overall pattern of the hair problem. It is important to determine density and distribution and if the hair loss is focal or global. Furthermore, the presence of scaling, erythema, erosions, crust or pus-filled swellings is noted. The clinical examination also involves the nails, since some disorders, for example, alopecia areata, lichen planopilaris (LPP), or ectodermal dysplasia can also affect finger and toenails.

Pull test: The pull test is a useful ancillary, qualitative test for the assessment of the ongoing activity of hair loss. The examiner grasps approximately 50–60 hairs and tugs at them from proximal to the distal end. Removal of six hairs indicates a positive pull test and active shedding. However, the test can be considered positive if three hairs can be pulled out in several different areas of the scalp. The proximal ends are examined against a white (for dark hair) or black (for light hair) background. A blunt tip indicates hair breakage; a tapered tip can indicate regrowth or miniaturized hairs. The proximal end of the hair shafts may also be examined with a light microscope to determine if the hairs break off (blunt ends) or came out as club hairs (telogen hair).

Biopsy: A scalp biopsy is necessary, particularly when confirming the diagnosis of scarring alopecia. A scalp biopsy should also be considered for the differential diagnosis of Telogen Effluvium, diffuse alopecia areata, and AGA. One 4-mm punch biopsy is taken from a clinically active area, processed for horizontal sections. A second 4-mm punch biopsy from a clinically active disease affected area is cut vertically into two equal pieces. One-half provides tissue for transversely cut routine histological sections; the other half is used for direct immunofluorescence (DIF) studies. Usually, only one biopsy from the affected area is necessary for the diagnosis of nonscarring alopecia; the samples are preferably processed with horizontal sections.

Trichogram: This technique is a simple method of quantifying hair loss by comparing the proportion of anagen to catagen and telogen hairs. For accurate measurement, patients are asked to avoid washing their hair 3–4 days prior to the test. Also, perms, dyes, or straightening of hair can alter results and have to be avoided at least 6 weeks prior. A group of about 25–50 hairs is grasped with a needle holder close to the scalp and plucked sharply in the direction of the hair. The proximal ends of the hair shafts are placed on a glass slide in a drop of water and covered with a coverslip and stained. The roots are then examined by light microscopy with 100-fold magnification. Ten to twenty percent of telogen hair can be regarded as normal (the percentage of anagen hairs is slightly higher in women and children compared to men); a telogen count over 35% is highly suspicious for a Telogen Effluvium. By repeating the Trichogram over a time period, a hair loss condition can be followed and treatment results can be measured.

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ANDROGENIC ALOPECIA: AGA is a progressive condition with a decrease in hair density of approximately 6% of hair fiber per year. However, increased shedding can occur periodically and the extent of hair loss depends on the genetic predisposition.

Minoxidil: Minoxidil is a biologic response modifier, which has been shown to halt AGA in many patients and regrow hair to a certain extent. It is now used as a 2% and a 5% topical treatment in a lotion or foam preparation. The mechanism of action is not fully understood. A direct effect on the hair follicle cells may be responsible for the effects of minoxidil. Several clinical trials have shown the efficacy of topical minoxidil. An increase in hair counts probably reflects a reversal of miniaturized hairs to thicker, more highly visible terminal hairs. Although studies have been performed on the top of the scalp, the drug also works on the frontal scalp, especially if hairs have not completely miniaturized to vellus-like hairs. Moderate to dense regrowth could be seen in up 30%–45% of patients. Some patients experience an increased shedding in the first 4–6 weeks of application. This positive sign seems to indicate anagen induction with earlier “molting” of telogen hairs from the follicles. The patient should be educated and prepared for this possible side effect to improve compliance. Observed side effects include contact dermatitis in 6.5% of patients and increased facial hair in 3%–5% of women. Most patients do not have a true contact allergy to minoxidil but irritation from propylene glycol. The 2% lotion with less propylene glycol, other vehicles with butylene glycol or the foam may then be used. To discriminate, which component causes dermatitis, a patch test or testing the product on the forearm is helpful. Only minimal amounts of minoxidil are systemically absorbed and serum levels are too low to have hemodynamic effects in normotensive or hypertensive patients. Nevertheless, less than one in thousand patients may experience increased heart rate and decreased blood pressure. Patients with decreased blood pressure or heart problems should be cautious and use the medication with approval from their cardiologist. The cardiac effects suggested in earlier studies could not definitely be linked to minoxidil and may be due to increased incidence of coronary artery disease in subsets of men with AGA. Topical minoxidil solution is used twice daily (1ml or 25 drops bid). It is also available in a 5% foam. If the hair has been shampooed, the hair and scalp should be at least towel-dry. The lotion or foam should stay on the scalp for at least 4 hours before the next shampoo. The patient should be informed that this is a lifelong treatment. It takes 4–6 months before the medication starts working and that the maximum effect can be expected after 1 year.

5-Alpha Reductase Inhibitor Drugs: The main drugs included in this category are:

Finasteride: Finasteride is a synthetic steroid that has been used for the treatment of AGA in men since 1997. It is a potent and highly sensitive selective 5α-reductase type-2 inhibitor. The administration of 1 mg finasteride daily reduces the concentration of the active component of Testosterone in scalp skin by 64%, serum Testosterone is reduced by 68%. The dose-response curve is nonlinear and therefore higher doses do not lead to significantly increased suppression of the hormone or greater clinical benefits. In studies, a significant hair count increase in men with alopecia or frontal AGA could be shown after 6 and 12 months. Finasteride stabilizes hair loss in 80% of patients with top of the scalp hair loss and 70% of patients with frontal hair loss. The chance of mild to moderate regrowth is 61% on the top and 37% on the frontal scalp. After 24 months of continuous use, 66% of the patients experienced a certain amount of hair regrowth at the top (approximately 10%–25% of the hair the patient lost previously). Most of the patients showed no further hair loss and only a few patients continued to lose hair. Continued use beyond 2 years does not promote continued hair regrowth. Instead, the hair density stabilizes with the retention of the newly acquired hair. If successful, the treatment should be continued indefinitely because the balding process continues once treatment ceases. Finasteride was found to be well tolerated with side effects occurring in fewer than 2% of patients. The side effects included decreased libido in 1.8%, erectile dysfunction in 1.3%, and decreased ejaculate volume in 0.8% of the recipients. Finasteride 1 mg daily does not affect semen production in men aged 19–41 years of age. The effect on prostate volume and serum prostate-specific antigen (PSA) in younger men was small and reversible after discontinuation of the drug. Finasteride can decrease PSA levels by 50% in older men. Therefore, a baseline prostate test is taken in men over 40. Long term side effects of 1 mg finasteride daily are yet unknown. Finasteride is not approved for use in women and its efficacy in FPHL is still controversial. A study of finasteride 1 mg/day in postmenopausal women with FPHL showed no differences in anagen: telogen ratio and the terminal hair: miniaturized hair ratio.

Dutasteride: Dutasteride is an inhibitor of type I and II 5α-reductase. It is approved at a dose of 0.5 mg daily for the treatment of symptomatic benign prostatic hyperplasia. Some studies have shown great efficacy in the treatment of MPHL and FPHL. However, dutasteride is not FDA approved for use in androgenetic alopecia.

Cyproterone Acetate: The antiandrogen cyproterone acetate (CPA) is a synthetic drug. CPA is available in Europe, Canada, and South America. It is usually combined with Ethinyl estradiol as a birth control pill. CPA is not approved by the FDA for the treatment of AGA. For the treatment of FPHL, a regimen with CPA daily on days 5–15 of the menstrual cycle and Ethinyl estradiol on days 5–25 or CPA daily on days 1–10 of the cycle and Ethinyl estradiol on days 1–21 have been suggested. In a study of 66 women, 33 women with FPHL used topical minoxidil 2% plus combined oral contraceptive whereas 33 women received CPA 52 mg daily plus Ethinyl estradiol 35 for 20 days of the cycle. The later combination result in greater hair density. Side effects from CPA are irregular menstrual cycles, weight gain, breast tenderness, loss of libido, depression, nausea. Since CPA is an antiandrogen, its use in men is obsolete, unless a gender change is desired.

Spironolactone: Spironolactone is a synthetic drug. The maximum androgen suppression is reached after 4–12 months; dosages of 200 mg daily are required. Spironolactone may have a preventative effect in FPHL and may reduce shedding in individuals without hyperandrogenism. However, Spironolactone is not approved by the FDA for the treatment of FPHL and should not be used in men. The main side effect is menstrual irregularities, which may be mitigated by decreasing the dose to 50–75 mg/day and adding oral contraceptives or after 2–3 months of therapy. Spironolactone is contraindicated in patients with renal insufficiency, increased serum potassium, pregnancy, abnormal uterine bleeding, and women with a genetic predisposition of breast cancer.

17- Alpha and Beta Estradiol: In Europe, topical 17α- or 17β-estradiol are commercially available for the treatment of FPHL. Studies have shown an increase in anagen and decrease telogen rates after topical treatment compared with placebo treatment. The underlying pathways of 17α-estradiol-induced hair regrowth are unknown. Research showed that 17α-estradiol is able to diminish the amount of DHT formed by human hair follicles after incubation with testosterone while increasing the concentration of weaker steroids. Since estradiol is absorbed through the scalp skin, systemic side effects must be considered, and it cannot be used in men.

Low Level Light Therapy: Laser sources have become very popular in medical and nonmedical areas. Manufacturers and suppliers often guarantee hair regrowth and various devices are available without a prescription. The only FDA approved low-fluence laser light device is the Hair Max Laser Comb® (FDA approval as a medical device). Paradoxical hair growth has occurred in patients undergoing laser hair removal when relatively low energy fluences were used. The mechanism of action of this phenomenon is unknown. Low-level laser light sources appear to be safe to use in the treatment of hair loss.

Hair Restoration Therapy: Hair restoration is the most successful and permanent treatment for AGA in suitable candidates. It includes hair transplantation (HT) and, in skillful hands, scalp-reduction surgery. Suitable candidates for HT are those with reasonable expectations, a donor supply that is adequate to cosmetically improve the recipient area coverage and those without contraindications for surgery. The most dramatic change in cosmetic appearance is achieved in patients with stages VI and VII. With recent advancements in technique and combination with medical treatment, more patients may benefit from the surgical option. Larger numbers of smaller grafts are moved per session, and results have thus become very natural. It is possible and advisable to distribute small grafts in between preexisting hairs and thus account for future hair loss. Rational use of the donor area with the strip harvesting or FU extraction makes several sessions possible in many patients if they experience progressive hair loss. HT is based on the principle of donor dominance as shown by androgen-independent follicles retaining their properties when they are transplanted into androgen-dependent areas. The donor supply is limited by the area of the strip (size of the “safe zone,” scalp elasticity) and the density of the donor's hair. HT is an outpatient procedure and may take up to 10 hours, depending on various factors, especially the number of grafts. Tumescence anesthesia is used for the donor and recipient areas, sometimes combined with nerve blocks. The most commonly used technique is strip harvesting. It allows for a relatively fast removal of large numbers of hairs leaving a fine line as a scar, which can be minimized with special harvesting and wound closure techniques. The strip is dissected into FUs (“families” of hairs growing together in one connective tissue sheath) under magnification these grafts are then carefully and strategically placed in the balding areas. The recipient side is prepared with small needles or spears, according to the size of the graft. A recent technique involves separately harvesting individual FUs using very small blunt punches (follicular unit extraction (FUE). This procedure is usually more time consuming but avoid a long scar in the back of the scalp. Follicular unit extraction is indicated in patients who desire to wear a very short hairstyle.

Wigs and Hairpieces: Scalp prostheses are practical for patients who are not candidates for hair restoration surgery, women with extensive hair loss and/or patients without satisfying improvement after using medical therapy. Wigs and hairpieces can provide excellent cosmetic results, especially when they are custom made. It is usually easier to overcome the reluctance to wear a scalp prosthesis if the hairpiece blends in nicely with the preexisting hair and is comfortable to wear. Women tend to be less reluctant to wear a wig or hairpiece, especially if the patient is exposing her natural hairline.

TELOGEN EFFLUVIUM: The removal of the cause is the major goal in the treatment of TE. Iron supplementation is recommended if the ferritin level is less than 70 ng/mL. Borderline hypothyroidism can be difficult to identify. Women, who complain about hair loss, depression, lack of energy, mental fatigue, cold intolerance, weight gain or/and constipation are suspicious for the diagnosis of hypothyroidism. Thyroid Stimulating Hormone (TSH) levels may fluctuate but are usually elevated, with normal or reduced thyroid hormone levels. If a thyroid dysfunction is suspected, the patient should be closely followed by an endocrinologist. Topical 2% or 5% minoxidil solution 1 mL twice daily can be helpful, especially in women with prolonged hair loss with unknown triggers or in patients with drug-related hair loss who are unable to discontinue the initiating medication.

ALOPECIA AREATA: At this time all available treatments for alopecia areata are palliative, only controlling the ongoing episode of hair loss and not curing the condition itself.

Conservative Treatment: Alopecia areata shows a high rate of spontaneous remission, especially in those patients with a short history and limited scalp involvement. On the other hand, in alopecia totalis and universalis, treatments have a high failure rate. After the discussion of possible risks and benefits of all options, “no treatment” may be a legitimate option for some patients.

Topical Steroids: Super-potent (class I) and potent (class II) topical steroids are widely used to treat alopecia areata. Evidence of efficacy has been proven for class I steroids when applied under occlusion and for class II steroids when used in combination with minoxidil.

Intralesional Steroids: Intralesional steroid (triamcinolone acetonide or triamcinolone hexacetonide) injection is first-line therapy for adult patients with less than 50% scalp involvement. Treatment is repeated every 4 to 6 weeks, and the total amount injected per session varies from 15–40 mg. An initial response is often seen after 4–8 weeks. Some patients experience indentation of the scalp skin in the injection sites due to nonpermanent atrophy of the subcutaneous fat. Permanent skin atrophy can occur if the same skin area is injected repeatedly over months and years. If no regrowth can be seen after 4 months of treatment, other treatment options should be considered. Intralesional steroid injections are usually used on the scalp, eyebrows and beard area and can be combined with topical treatment.

Oral Steroids: Oral steroids are effective in the treatment of alopecia areata. However, the regrown hair frequently falls out again when the treatment is discontinued. The use of oral steroids is controversial and largely used on a short-term basis with rapidly advancing hair loss. They should not be used as routine treatments because they do not alter the long-term prognosis and can cause side effects such as striae, acne, obesity, cataracts, and hypertension.

Topical Minoxidil: There is some evidence of clinically acceptable hair regrowth using topical minoxidil 5% solution. Better results can be achieved when minoxidil is used in combination with class II topical corticosteroids or anthralin. Minoxidil shows little efficacy in alopecia totalis and universalis.

Anthralin: Anthralin is an irritant and is primarily used in the treatment of psoriasis. It is also efficient in the treatment of alopecia areata with cosmetically acceptable improvement varying from 20% to 25% for patchy alopecia areata. Anthralin is used as a 0.2%–1.0% cream or ointment. It is usually applied daily to the affected scalp areas and left on for 20–30 minutes for the first 2 weeks, and then 45 minutes daily for 2 weeks, up to a maximum of 1 hour daily. Some patients may tolerate overnight therapy. When therapy is effective, new hair growth can usually be seen after 2–3 months of treatment. Because of its good safety profile, anthralin can be used safely in affected children. Side effects of anthralin are irritation, scaling, inflammation of the follicles and enlarged lymph nodes. Anthralin is not suitable for the treatment of eyebrows and beard area. Patients should be cautious not to get anthralin in the eyes and to protect the treated skin areas from UV irradiation. Brown discoloration of the treated skin and brown staining of clothes and linen may occur. The patient should be advised to rinse off the anthralin with cool or luke-warm water since hot water increases the likelihood of brown stains of tiles and bathtub.

Topical Immunotherapy: Although not yet approved by the FDA, topical immunotherapy seems to be the most effective therapeutic option with the best safety profile in the treatment of chronic severe alopecia areata. The desired effect of the treatment is the creation of contact dermatitis. Diphenylcyclopropenone (DPCP) and squaric acid dibutyl ester (SADBE) are the most commonly used contact sensitizers. Applying a small amount of a 2% solution to a small scalp or other areas (often the arm) one week prior to treatment initiation sensitizes the patient. The DPCP or SADBE solution is then applied weekly to the scalp, starting at a concentration of 0.0001%. The scalp should not be washed for 48h post-treatment and should be protected from UV radiation. Every week the concentration is carefully increased until the patient develops a mild reddening and mild itching. The treatment is continued with this concentration; the highest concentration used is 2%. Success rates vary from 17%–75% with the lowest success rates in patients with alopecia totalis and universalis. Side effects include lymph node enlargement in 100% of patients, severe contact inflammation of the skin, discoloration of the skin and increased pigmentation on the scalp and other parts of the body. Greater caution is indicated in patients with atopic dermatitis and dark skin types.

Photochemotherapy: Ultraviolet B light is found to be useful in some patients with alopecia areata. Further therapeutic options include both oral and topical administration of psoralen followed by UVA irradiation (PUVA-therapy). Photo(chemo)therapy shows a very high relapse rate especially after tapering the treatment. The major concern about long term UV irradiation of any kind is its promotion of all types of skin cancer, including melanoma. Therefore, phototherapy should only be considered in exceptional cases.

Cyclosporine: Oral cyclosporine has been shown to have a beneficial effect on some patients with alopecia areata. The side effects of oral cyclosporine include elevated cholesterol levels, as well as headaches, painful sensations, fatigue, diarrhea, gingival hyperplasia, flushing, and muscle pains. Cyclosporine can be combined with low dose oral prednisone and may be considered in patients with severe atopic dermatitis and alopecia areata. However, due to its side effect profile and the high recurrence rate observed after discontinuation, cyclosporine seems to be a relatively impractical treatment for alopecia areata.

Camouflage, Wigs, and Hairpieces: When alopecia is progressive despite treatment and sometimes during treatment for improved cosmesis, extensive alopecia areata of the scalp can be camouflaged with wigs. In women with alopecia areata of the eyebrows, permanent makeup may be considered. Local and national alopecia areata support groups (National Alopecia Areata Foundation, www.naaf.org) can be very helpful for patients and their relatives.

ANAGEN EFFLUVIUM: Once the initiating trigger is removed, the hair usually regrows after around 120 days. Cases of incomplete recovery following multiagent chemotherapy are sometimes noted. Patients should be advised about scalp prostheses and other forms of head covering.

TEMPORAL TRIANGULAR ALOPECIA: TTA seems to be unresponsive to medical treatment. Hair transplantation or excision are reasonable therapeutic approaches.

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