Cicatricial and Noncicatricial Alopecias
Paul Curtiss
Kumar Sukhdeo
Kristen I. Lo Sicco
Jerry Shapiro
OVERVIEW
Alopecia refers to a reduction or complete loss of hair in an otherwise hair-bearing area. As discussed later, the etiology of alopecia is primarily divided between nonscarring (noncicatricial) and scarring (cicatricial) processes. These diagnoses are non-mutually exclusive, and multiple patterns may evolve in the same patient. Careful history taking and examination by an informed practitioner is essential in establishing the correct diagnosis and dictating management. Particular attention should be maintained in evaluating for cicatricial alopecias because permanent hair loss may occur if misdiagnosed or delayed. Although alopecias are not life-threatening, a profound link exists between hair growth and patients’ self-perception. To this end, alterations in normal hair patterns drive many clinic visits and can have devastating psychological impact on patients’ quality of life.
NONCICATRICIAL ALOPECIAS: ALOPECIA AREATA
BACKGROUND
Alopecia areata (AA) is a common, nonscarring alopecia characterized by an autoimmune attack on the hair follicle. It affects approximately 0.1% to 0.2% (1.7% lifetime
risk) of individuals in the United States, with a spectrum of hair loss ranging from a small isolated patch of hair loss, multiple focal patches of hair loss (patchy alopecia), complete scalp hair loss (alopecia totalis [AT]) to universal body hair loss (alopecia universalis [AU]).1
risk) of individuals in the United States, with a spectrum of hair loss ranging from a small isolated patch of hair loss, multiple focal patches of hair loss (patchy alopecia), complete scalp hair loss (alopecia totalis [AT]) to universal body hair loss (alopecia universalis [AU]).1
PRESENTATION
Patients present with a history of the recent sudden appearance of patches of hair loss on the scalp or beard.
DIAGNOSIS
Clinical Diagnosis
Classic scalp lesions in AA are well demarcated, circular, completely smooth patches in heterogeneous distribution. This seemingly haphazard organization can produce a cosmetically unacceptable phenotype for the patient causing significant psychosocial distress. Clinical features include exclamation hairs (ie, hair shafts with proximal tapering and distal widening), preferential sparing of graying hairs early on in the disease, and nail pitting.
AA disease course is variable, with 5% of patients progressing to AT or AU. A rare variant with bandlike alopecia extending across the posterior and inferior scalp is termed an ophiasis pattern. Many patients with milder disease experience periods of spontaneous remission even in the absence of treatment.2 AA also presents frequently in the pediatric population, with 20% of patients experiencing their first patch of hair loss before the age of 18 years, which is a critical period in the development of patients’ identity. In these patients it may be a substantial psychosocial cause of stress for both children and families, and higher rates of suicide are noted in adolescent populations. Therefore, mental health screening should be conducted on new and established cases of AA.
Histopathology
Terminal follicle with necrosis of matrix cells in the bulb is an early finding in the acute stage of AA. Cross section of AA at the dermohypodermal transition level reveals the presence of many miniaturized follicles and telogen germinal units. Telogen germinal units are distorted with melanophages. Miniaturized hair follicles in AA also demonstrate lymphocytes within the bulb.
Subtypes
Alopecia areata (localized patches)
Alopecia totalis (entire scalp)
Alopecia universalis (all body hair)
Differential Diagnosis
Androgenetic alopecia
Telogen effluvium
Lichen planopilaris
Anagen effluvium
PATHOGENESIS
AA is an autoimmune disease with a strong genetic component; there is 50% concordance in monozygotic twins and one-third of patients having an affected family member. Several pathoetiologic mechanisms have been implicated, including loss of immune privilege of the follicle site, T-cell overactivation, and inappropriate antigen presentation by HLA/MHC complex subtypes.3 Hashimoto hypothyroidism is the most frequently associated autoimmune disease, occurring between 8% and 24% of patients with AA. Less commonly AA has also been associated with vitiligo, Down syndrome, Addison disease, and autoimmune recessive polyglandular syndrome (APS-1).4
TREATMENT
It is challenging to conduct clinical studies on AA for several reasons. Great variety exists in the severity of disease ranging from self-limiting illness to permanent total hair loss. Mild patchy alopecia often remits spontaneously, whereas those with severe, longstanding phenotypes (AU, AT, ophiasis pattern) may not experience meaningful recovery regardless of treatment modality. Unfortunately, no universally accepted metric of hair regrowth exists, which makes comparison between different trials and treatments challenging.
A 2008 Cochrane review of 17 trials including 540 patients with various treatments, including topical corticosteroids, intralesional corticosteroids, oral corticosteroids, and phototherapies, concluded that there was insufficient evidence to support any agent in the treatment of AA.5
 ALGORITHM 7.1.1 Treatment algorithm for alopecia areata. DPCP, diphenylcyclopropenone; IL-TAC, intralesional triamcinolone acetonide; JAK, Janus kinase; SADBE, squaric acid dibutylester. |
Nonetheless, many smaller studies show efficacy of different treatments and a variety of treatment modalities can be attempted over time. Several split-scalp trials of individuals with AT/AU, although not conventionally blinded or randomized, showed promising results but were not included. In general, clinicians should employ a progressive approach escalating from better tolerated in office and topical treatments to more involved treatments (Algorithm 7.1.1).
Medical
Topical
Many different formulations of topical corticosteroids have been used to treat AA with mixed results. They are an excellent treatment choice in the young pediatric population where intralesional therapies and contact irritants are not well tolerated and risks of systemic medications are not well studied.
Clobetasol under occlusion has been tried in patients with severe phenotypes in both randomized and split scalp studies. One method has been to apply clobetasol 0.05% ointment nightly for 6 of 7 nights of the week. A split-scalp trial showed significant regrowth in 17.8% of patients, whereas no growth was seen on the control (vehicle-only) portion of scalp.6 Folliculitis is not an uncommon side effect but can be minimized by using clobetasol foam formulations. We recommend a trial of high-potency topical steroids in patients with significant hair loss who fail to respond to topical immunomodulators.
Anthralin is a contact irritant that can be effective and well tolerated, particularly in the pediatric population if topical corticosteroids fail to achieve satisfactory results. Anthralin 0.5% or 1% cream should be applied for 20 minutes daily. The duration should be increased by 10 minutes at 2-week intervals up to an hour until a low-grade dermatitis develops and then maintained at that dose. If a dermatitis reaction does not develop, there is a low probability that a cosmetic outcome will be achieved and therapy can be discontinued.
Topical immunotherapies should be considered as first-line agents in patients with greater than 50% scalp involvement where intralesional therapies may be less
desirable or tolerated. The most widely studied medications in this class of agents include diphenylcyclopropenone (DPCP) and squaric acid dibutylester (SADBE).7 DPCP treatment should begin with application of 2% concentration for sensitization, applied to a 4 × 4 cm area of the scalp. Two weeks later, DPCP should be applied at a lower concentration (0.0001%) for 48 hours. The concentration should be incrementally increased until a low-grade tolerable eczematous dermatitis reaction is observed. If after 6 months of therapy there is no improvement in disease severity, it should be considered a failure and another agent or class of medication should be considered.
desirable or tolerated. The most widely studied medications in this class of agents include diphenylcyclopropenone (DPCP) and squaric acid dibutylester (SADBE).7 DPCP treatment should begin with application of 2% concentration for sensitization, applied to a 4 × 4 cm area of the scalp. Two weeks later, DPCP should be applied at a lower concentration (0.0001%) for 48 hours. The concentration should be incrementally increased until a low-grade tolerable eczematous dermatitis reaction is observed. If after 6 months of therapy there is no improvement in disease severity, it should be considered a failure and another agent or class of medication should be considered.
Systemic
Corticosteroids. Systemic corticosteroids should not be used as a first-line treatment in the management of AA or as part of a long-term treatment strategy. Because of their extensive side-effect profile and the propensity of AA to relapse, great care should be taken in selecting appropriate patients who can benefit from shorter courses (1-6 months) of oral steroids.
An approach to minimize side effects has been weekly or biweekly pulse-dose steroids. One randomized, placebo-controlled clinical trial showed some benefit of a weekly dose of 200 mg for 3 months in 8 of 23 patients in the treatment arm with none of the 20 patients in the placebo arm.8 Given the short follow-up period of studies and the long-term deleterious effects of steroids (eg, osteoporosis), it is unclear to what degree steroid-related morbidity is decreased. Furthermore, steroids often provide transient results and disease activity resumes after discontinuation of therapy. Clinicians should maintain an exit strategy when embarking on any regimen involving a trial of systemic steroids, regardless of response. In those who do not experience a robust treatment response, corticosteroids should be discontinued.
Tacrolimus and cyclosporine are potent T-cell inhibitors explored as treatment for patients with particularly severe disease phenotypes. These treatments have some favorable success rates reaching as high as 78% with cyclosporine when combined with oral prednisone, but given the high rates of side effects, including permanent nephrotoxicity, hepatotoxicity, hypertension, gingival hyperplasia, increased risk for opportunistic pathogens, and neoplasia, their practicality is limited and should be considered only in severe phenotypes after careful discussion of risks and benefits with patients.9 As with steroids, clinical trials have demonstrated that short courses are unlikely to produce durable, long-lasting results after medications are discontinued.
More recently, systemic Janus kinase (JAK) inhibitors, such as tofacitinib and ruxolitinib, have been used in the treatment of AA.10 The mechanism of action of these medications in AA is inhibition of T-cell activation. Small prospective studies have shown response rates up to 75% with ruxolitinib in patients with moderate and severe phenotypes where spontaneous remission is unlikely.11,12 Although this class of medications has undeniable therapeutic promise, it should be noticed that results are often lost after discontinuation of medication. Despite this, it may represent a safer long-term systemic option in patients with severe phenotypes who experience a robust treatment response.
Cosmetic
Topical
Minoxidil is a widely used adjuvant to other therapies, particularly other intralesional and systemic therapies. Its primary mechanism of action is promoting hair growth rather than treating the underlying AA. The authors recommend that 5% minoxidil should be applied twice daily to the scalp and is a reasonable addition to most therapeutic regimens particularly intralesional and topical corticosteroids.
Intralesional
For adult patients presenting with less than half total scalp involvement, intralesional corticosteroids should be considered first-line therapy. Many small trials support the efficacy of intralesional steroids in the management of AA. One randomized study evaluating the relative efficacy of isotonic saline vs intradermal corticosteroids showed 71% response in the steroid arm when compared with 7%% in the saline treatment group.13 We recommend 2.5 mg/mL concentration for the eyebrows, anterior hairline, and face that is equally effective as higher concentrations but with decreased risk of atrophy.14 Injections should be done every 4 to 6 weeks for up to 6 month to evaluate treatment response (Figure 7.1.1). Additionally, low-volume injections (up to 80) of intralesional corticosteroids may be used as an alternative to DPCP/SADBE in patients with greater than 50% hair loss with favorable response rates.15 A topical anesthetic can be applied before injection to minimize
discomfort, especially in pediatric patients. This therapy should be paired with topical minoxidil and topical corticosteroids for more rapid, effective results. Local skin atrophy, telangiectasia, and hypopigmentation are common side effects with intralesional therapies but are usually transient and well tolerated.
discomfort, especially in pediatric patients. This therapy should be paired with topical minoxidil and topical corticosteroids for more rapid, effective results. Local skin atrophy, telangiectasia, and hypopigmentation are common side effects with intralesional therapies but are usually transient and well tolerated.
 FIGURE 7.1.1 Alopecia areata before (A), during (B), and after (C) treatment. Patient was treated with multiple small-volume injections of intralesional triamcinolone, topical clobetasol solution, and minoxidil 5% solution. |
NONCICATRICIAL ALOPECIAS: ANAGEN EFFLUVIUM
BACKGROUND
Anagen effluvium (AE) is a common nonscarring alopecia in the United States. AE is characterized by the abrupt halt in the follicular growth phase, which results in fragility, hair shaft breakage, and massive shedding. This condition is most commonly triggered by chemotherapeutics but can also be caused by various exogenous toxins as well as autoimmune disease. Alopecia in this form is often a cause of extreme stress on behalf of the patient related to receiving chemotherapy, and its anticipated occurrence can affect decisions to receive cancer treatment.16,17
PRESENTATION
AE typically begins within the first 2 weeks of exposure to an offending chemotherapeutic agent. Because chemotherapy preferentially targets the proliferating cells, quiescent stem cells are generally spared and patients typically regrow hair within several months after final exposure.
DIAGNOSIS
Clinical Diagnosis
The history of chemotherapy several weeks to months before the onset of nonscarring diffuse hair loss is the basis for the diagnosis of AE.
Histopathology
The proximal end of the hair shafts fracture under minimal strain, which produces the characteristic proximally tapered, fractured hair shaft. Less mitotically active areas and telogen hairs are relatively spared.
PATHOGENESIS
A variety of chemotherapeutics have been implicated in AE. Chemotherapeutics and certain toxins often exert a great effect on rapidly dividing cells in the human body. Hair follicle matrix keratinocytes and associated pigment machinery are in a state of continuous rapid mitotic activity during the anagen phase, rendering these cellular populations vulnerable to antimitotic agents.18 When exposed to toxins or chemotherapeutics, mitotically active cells undergo apoptosis, resulting in a point of weakness at the proximal end of the elongating anagen hair shaft, which fractures under minimal strain (Table 7.1.1).
Less common causes of AE include connective tissue disease, severe protein malnutrition, and toxin exposure (boron, mercury, and thallium).
TABLE 7.1.1 Causes of Chemotherapy-Induced Anagen Effluvium | |||||||||||||||||||||||||||||||||
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TREATMENT
Medical
AE is generally a self-limiting disease that resolves when the insulting agent is removed. In cases of chemotherapy-induced AE, no additional diagnostic workup is needed. In patients not receiving chemotherapeutics who present with AE it is critical to identify the offending toxin and treat appropriately. In many cases of chemotherapy-induced AE there are no treatments that will prevent or ameliorate the disease process. Anticipatory counseling and making plans for hair loss, including exploring head coverings, is most appropriate. Patients should be counseled that hair loss is a transient effect of the medication that should resolve following completion of their medical regimen. Algorithm 7.1.2 illustrates the treatment for AE.
Topical
Bimatoprost. Bimatoprost is a prostaglandin analogue that promotes eyelash growth. A randomized, double-blinded study showed qualitative improvement in eyelash density for 37.5% of postchemotherapy patients in the treatment arm versus 18.2% of patients in the vehicle arm.19 There are no studies showing efficacy in the prevention of chemotherapy-induced hypotrichosis of the eyelash. We recommend patients use 0.03% bimatoprost solution after conclusion of their chemotherapy regimen if eyelash hypotrichosis is a significant complaint.
Minoxidil. Minoxidil has been studied in the treatment of chemotherapy-induced AE with conflicting results. Two small studies showed no evidence that minoxidil prevents AE; however, one suggested that it may improve recovery rate.20,21 In patients who wish to promote hair growth after completion of their chemotherapy we recommend minoxidil 5% solution applied to affected areas of scalp twice daily.
Cosmetic
Devices
Scalp cooling devices have been extensively explored as a method of preventing chemotherapy-induced alopecia.
After significant safety data from Europe as well as clinical studies within the United States, there are now scalp cooling devices cleared by the US Food and Drug Administration (FDA). They are safe and efficacious in reducing hair loss in patients receiving taxanes or anthracyclines for breast cancer.22,23,24 Patients with prolonged infusion times or those receiving high doses of anthracyclines are likely to receive smaller benefit.
After significant safety data from Europe as well as clinical studies within the United States, there are now scalp cooling devices cleared by the US Food and Drug Administration (FDA). They are safe and efficacious in reducing hair loss in patients receiving taxanes or anthracyclines for breast cancer.22,23,24 Patients with prolonged infusion times or those receiving high doses of anthracyclines are likely to receive smaller benefit.
 ALGORITHM 7.1.2 Treatment algorithm for anagen effluvium. |
Importantly, safety data for other malignancies is more limited. It is not recommended to use scalp cooling devices in patients with significant circulating tumor burden, including hematologic neoplasms. Scalp cooling devices should not be used in patients with cold sensitivity, including cold agglutinin disease and cryoglobulinemia, or those with significant liver disease. The decision to use a scalp cooling device should be made only after a careful discussion with the patient’s oncology team as these devices are not universally recommended.
NONCICATRICIAL ALOPECIAS: ANDROGENETIC ALOPECIA
BACKGROUND
Androgenetic alopecia, also referred to as female-pattern hair loss (FPHL) or male-pattern hair loss (MPHL), is the most common cause of hair loss that affects 70% of men and 50% of women by age 80 years.25 Although patients should be reassured of its benign nature, pattern hair loss is often a cause of psychosocial distress and there exist high-quality, evidence-based treatments for the condition in both men and women.
PRESENTATION
Patients present with a history of insidious thinning of hair. They report a widening of their part, loss of volume to the hair, the gradual exposure of scalp visibility and increased hair in the shower, bed pillow, or on their hairbrush.
DIAGNOSIS
Clinical Diagnosis
Clinically, pattern hair loss is characterized by progressive shortening of the anagen phase and decrease in anagen to telogen ratio, causing follicle miniaturization, the clinical hallmark of androgenetic alopecia. Eventually, the miniaturized hairs become too short to reach the surface of the scalp, resulting in increased visibility of the scalp, referred to as balding.26 In men the natural history of the MPHL occurs bitemporally, frontal, mid scalp, and vertex; typically falling within the Hamilton-Norwood
classification patterns.27 In contrast, FPHL manifests as diffuse central thinning or more prominent frontal thinning in a “Christmas tree” pattern with preservation of the anterior hairline.
classification patterns.27 In contrast, FPHL manifests as diffuse central thinning or more prominent frontal thinning in a “Christmas tree” pattern with preservation of the anterior hairline.
Histopathology
When in a classic presentation, androgenetic alopecia is often a clinical diagnosis. However, biopsy of the involved scalp in androgenetic alopecia will show miniaturized hairs, dramatically increased number of vellus hairs with a normal total number of hair follicles. There is little to no inflammation, and uninvolved scalp is normal. Deeper sections will reveal stellae where the hair bulb and dermal papilla had been, and the bulb will be found on more superficial sections because of miniaturization. Biopsy specimens should ideally be 4-mm punches, and the practitioner should indicate on the requisition that the sample should be sectioned horizontally to evaluate the hair follicles.28
Subtypes
MPHL typically presents with bifrontotemporal recession and vertex thinning, whereas FPHL presents more commonly as thinning in the crown or frontal area only, and less commonly with a MPHL-like pattern. Androgenetic alopecia occurs very rarely in prepubertal children and more commonly presents with an FPHL pattern.
Differential Diagnosis
Telogen effluvium
Diffuse alopecia areata
Trichotillomania
Traction alopecia
Pressure-induced alopecia
PATHOGENESIS
The mechanism of MPHL is well characterized as an androgen-dependent polygenic trait with strong paternal and maternal hereditary components. Hair loss is mediated primarily by local 5 alpha-dihydrotestosterone (DHT) levels. Testosterone is converted to DHT by the enzyme 5α-reductase. Concentrations of DHT, 5α-reductase, and androgen receptor have been demonstrated to be increased in the balding scalp.26
Women with FPHL characteristically undergo a similar process of miniaturization as men, but the role of androgens is less clearly understood. Hyperandrogenism will result in FPHL; however, the majority of patients with FPHL will not show signs of androgen excess. Importantly, underlying or exacerbating conditions should be ruled out by examination and serological studies. All women should receive appropriate blood work, including complete blood count, ferritin, and thyroid stimulating hormone (TSH). Additional laboratory tests should be considered if there is evidence of endocrine abnormalities.
TREATMENT
Approaches to treatment in both men and women diagnosed with patterned hair loss can differ significantly, and will be discussed separately. Validated FDA-approved treatments should be employed before attempting nonconventional approaches. Importantly, many treatment regimens require multimodal therapy.
Male-Pattern Hair Loss
Algorithm 7.1.3 describes the treatment for MPHL.
Medical
Topical
Minoxidil. Topical minoxidil is a well-studied therapy in MPHL, which carries FDA approval. Minoxidil is available over the counter in 2% and 5% formulations as either a solution or foam. The 5% formulation is more efficacious and is well tolerated without a significant increase in the side-effect profile. For these reasons, 5% minoxidil should be considered a first-line agent. The mechanism of action is not entirely understood, but the drug presumably lengthens the anagen phase resulting in prolonged growth.
Within 3 to 6 weeks of initiating therapy, topical minoxidil frequently results in a form of telogen effluvium (TE) that persists for 2 to 8 weeks. This occurs as telogen hairs shed and new anagen hair growth begins. Patients should be counseled on this expected hair loss and to continue treatment through this phase. Further
discussion should emphasize the lengthy period of time required for visible changes in hair patterns, as some patients may be discouraged by the initial lack of effect. Patients should be evaluated at 6 months after starting treatment before a decision is made on patient response. Few clinical studies directly compare the efficacy of minoxidil vs finasteride or combination therapy, but small comparative trials suggest that combination therapy is more efficacious and should be attempted as long as medications are tolerated29 (Figure 7.1.2).
discussion should emphasize the lengthy period of time required for visible changes in hair patterns, as some patients may be discouraged by the initial lack of effect. Patients should be evaluated at 6 months after starting treatment before a decision is made on patient response. Few clinical studies directly compare the efficacy of minoxidil vs finasteride or combination therapy, but small comparative trials suggest that combination therapy is more efficacious and should be attempted as long as medications are tolerated29 (Figure 7.1.2).
 ALGORITHM 7.1.3 Treatment algorithm for male-pattern hair loss. PRP, platelet-rich plasma. |
Systemic
Finasteride. Finasteride is an inhibitor of 5α-reductase that inhibits conversion of testosterone to DHT. This oral therapy has FDA indications for androgenetic alopecia at 1 mg daily and should be considered a first-line agent in the treatment of MPHL.
Long-term randomized trials suggest that approximately two-thirds of men will have a cosmetic improvement when compared with 7% of placebo patients.30 Importantly, therapy often takes longer than 6 months to yield cosmetic improvement and patients should be maintained on medication for at least 1 year to assess efficacy.
Some patients taking finasteride experience deleterious sexual side effects, including erectile dysfunction, decreased libido, and decreased ejaculatory volumes. In clinical trials, these were seen in 1.8% of men aged 18 to 41 years vs 1.1% of patients who received placebo.30 Side effects generally resolve with discontinuation of treatment. prostate-specific antigen is often used in the screening for prostate cancer and is reduced in men taking finasteride and should be interpreted of twice the true value in men taking the medication.31 For this reason, a baseline PSA should be obtained before starting finasteride therapy in those men over 40 years of age.
Dutasteride. Dutasteride is a more potent inhibitor of 5α-reductase than finasteride and more commonly used in the treatment of benign prostatic hypertrophy (BPH) than MPHL. Dutasteride reduces DHT levels by 93% to 94% at 0.5 mg when compared with 70% by finasteride at 5 mg daily.32 This therapy is efficacious in phase 3 clinical studies at 0.5 mg daily, the dose typically prescribed for BPH, when compared with
placebo.33 The relative benefit of 5α-reductase inhibitors was studied in a randomized, placebo-controlled clinical trial conducted comparing dutasteride at increasing doses with finasteride 5 mg. Dutasteride exhibited dose-dependent changes with the greatest response achieved at 2.5 mg daily.34 As expected, there was an associated increase in patients experiencing decreased libido with 12.5% in the 2.5-mg dutasteride group versus 1.5% in the 0.5-mg dutasteride group. Side-effect rates in the 0.5-mg dutasteride group were similar to those in the 5-mg finasteride group. The long-term safety data for dutasteride are more limited than for finasteride, and more data are needed to evaluate its long-term efficacy. A trial of dutasteride is most reasonable in patients who are dissatisfied with finasteride results and do not wish to explore follicular transplantation.
placebo.33 The relative benefit of 5α-reductase inhibitors was studied in a randomized, placebo-controlled clinical trial conducted comparing dutasteride at increasing doses with finasteride 5 mg. Dutasteride exhibited dose-dependent changes with the greatest response achieved at 2.5 mg daily.34 As expected, there was an associated increase in patients experiencing decreased libido with 12.5% in the 2.5-mg dutasteride group versus 1.5% in the 0.5-mg dutasteride group. Side-effect rates in the 0.5-mg dutasteride group were similar to those in the 5-mg finasteride group. The long-term safety data for dutasteride are more limited than for finasteride, and more data are needed to evaluate its long-term efficacy. A trial of dutasteride is most reasonable in patients who are dissatisfied with finasteride results and do not wish to explore follicular transplantation.
 FIGURE 7.1.2 Male-pattern hair loss before (A) and after/(B) treatment with topical minoxidil 5% solution and 1 mg oral finasteride. |
Cosmetic
Platelet-Rich Plasma. Platelet-rich plasma (PRP) is an evolving procedure for androgenetic alopecia showing some benefit in individuals. This modality employs venipuncture to draw between 10 to 60 mL of the patient’s own whole blood, which is then is centrifuged to fractionate red blood cells, leukocytes, platelets, and serum. The platelet-rich portion is harvested, typically enriched in platelet concentration by 3- to 10-fold, which is then injected into the scalp at regularly spaced intervals. Although PRP has undeniable therapeutic promise shown by several studies with trichologic examination, this treatment option is vexed by interoperator differences in preparation method, yield, and injection technique. Standardized protocols along with additional data with randomized controlled studies will help in determining more precisely its efficacy and role in the management of androgenetic alopecia.35,36
Phototherapy
Low-Level Laser Light Therapy. Low-level laser light therapy (LLLT) has been studied in the treatment of MPHL. Multiple randomized, blinded, sham-controlled studies have shown a statistically significant increase in terminal hair density.37,38 There
are no studies comparing efficacy over FDA-approved medications (eg, minoxidil, finasteride) or improved efficacy as an adjuvant therapy. Other critiques of LLLT have pointed out that there are limited long-term studies showing growth beyond 6 months.39 Generally, LLLT is not considered a first-line therapy and should not be selected over current FDA-approved medications.
are no studies comparing efficacy over FDA-approved medications (eg, minoxidil, finasteride) or improved efficacy as an adjuvant therapy. Other critiques of LLLT have pointed out that there are limited long-term studies showing growth beyond 6 months.39 Generally, LLLT is not considered a first-line therapy and should not be selected over current FDA-approved medications.
Surgical
Hair Transplantation. Permanent improvement of MPHL can be achieved through hair transplantation. For patients with more significant hair loss or those who are dissatisfied with the level of response to finasteride and minoxidil, transplantation represents an excellent treatment, which undeniably can produce a significant cosmetic improvement over a short period of time. The principle of “donor dominance” causes transplanted hairs from the occipital region to maintain their characteristics and not undergo follicular miniaturization. Patients will continue to lose nontransplanted hairs in a progressive pattern and should continue their medical regimen if they do not have a stable pattern of hair loss before transplantation.
The traditional method of hair transplantation, follicular unit transplantation (FUT), involves harvesting an ˜2-cm full-thickness donor strip from the occipital scalp in a horizontal ellipse followed by manual dissection and transplantation of individual follicular units. The resultant scar is thin and generally obscured from sight in the majority of hairstyles.
Follicular unit extraction (FUE) is an alternative to the traditional method of hair transplantation. FUE eliminates the horizontal elliptical scar by removing individual follicular units without strip harvesting. For individuals who prefer to maintain very short or “buzzed” posterior hair styles this technique provides less cosmetically appreciable scarring. However, the FUE method is dramatically more time intensive and costly than FUT.
Recently, innovative technologies in robotics have led to the adoption of robotic FUE technique. Using continuous imaging feedback, robots are able to harvest large amounts of individual follicular units with low rates (6%) of follicular transection and accomplish the procedure in significantly less time than standard FUE.40 The currently available ARTAS robot has a large upfront cost but may ultimately be more cost and time efficient than traditional FUE.
Female-Pattern Hair Loss
Algorithm 7.1.4 shows the treatment for FPHL.
Medical
Topical. Although multiple treatment modalities have been proposed for the treatment of FPHL, minoxidil is the only treatment with FDA approval and has the strongest level of evidence to support its efficacy. Multiple clinical trials and large meta-analyses have validated benefit in hair number, shaft diameter, appearance, and patient satisfaction at 1%, 2%, and 5% concentrations and in several vehicle formulations.41
Currently, only the 2% minoxidil solution has FDA approval; however, clinical trials suggest that 5% is more efficacious.42 There is a slightly higher risk of hypertrichosis in the 5% formulation, which is generally tolerated or easily treated with various depilatory techniques. Patients should begin with 5% formulations and can decrease concentration to 2% if adverse side effects are not well tolerated (Figure 7.1.3).
As with men, shedding should be expected in the first 2 to 8 weeks of therapy and patients should be counseled to continue treatment. Patients typically required 6 to 12 months to realize benefits of minoxidil. As with men, benefits are lost within several weeks upon discontinuation.
Oral Medications
Spironolactone. Spironolactone is an aldosterone antagonist with antiandrogenic properties. Several case reports and one randomized, placebo-controlled trial compared spironolactone with cyproterone acetate with evidence to support its use in the management of FPHL.43,44,45 Patients should start with 50 mg daily and increase monthly to reach a target of 200 mg daily.
Clinicians should obtain serum metabolic and kidney panels before initiation of treatment. Ongoing checks of metabolic panels at least every 6 months is recommended by the authors.46 Spironolactone can cause feminization of the male fetus, and premenopausal women should receive appropriate contraception and counseling.
Finasteride. There is less evidence to support the use of finasteride in women than in men. One randomized trial using 1 mg finasteride daily in postmenopausal women failed to show benefit.47 Premenopausal women with hyperandrogenism have responded discordantly in clinical trials obviating a conclusion on its use in these patients.48,49 In hyperandrogenic patients, a
trial of finasteride 1 mg orally daily is reasonable. This medication is generally well tolerated in women but is teratogenic and considered an X class medication, and therefore women of childbearing age should receive appropriate contraception and counseling.
trial of finasteride 1 mg orally daily is reasonable. This medication is generally well tolerated in women but is teratogenic and considered an X class medication, and therefore women of childbearing age should receive appropriate contraception and counseling.
 ALGORITHM 7.1.4 Treatment algorithm for female-pattern hair loss. PRP, platelet rich plasma. |
Surgical
Care must be taken in selecting ideal female candidates who will receive significant cosmetic benefit. Women with mild FPHL are less likely to notice as significant a cosmetic benefit. Women with less patterned distribution may achieve no benefit if the donor site shows evidence of hair loss. Surgical candidates who will maximize benefit are those with high-density donor hair sites and extensive focal thinning in the frontal scalp. Patients should continue to use minoxidil after recovery from transplantation to minimize future loss.
 FIGURE 7.1.3 Female-pattern hair loss before (A), during (B), and after (C) treatment with 5% topical minoxidil solution. |
NONCICATRICIAL ALOPECIAS: TELOGEN EFFLUVIUM
BACKGROUND
TE is a leading cause of diffuse acute hair loss and, less commonly, responsible for chronic hair loss. TE has a higher incidence in women, occurs at any age, and does not exhibit predilection for any specific ethnic or racial group.50 Common causes of TE include medications, pregnancy (telogen gravidarum), major surgery or illness, and significant emotional stress. TE is generally a self-limiting illness that tapers within 2 to 3 months of increased hair shedding and resolves spontaneously if no secondary cause is identified. Rarely, individuals will develop a chronic TE whereby no inciting cause is identified and the illness persists greater than 4 months.
PRESENTATION
Patients typically present with an acute increase in hair shedding in the shower or from combing their hair 2 to 4 months after the instigating insult.
DIAGNOSIS
Clinical Diagnosis
Physical examination of the scalp not shampooed in the past 24 hours reveals a positive hair pull test, with hair shafts capped with telogen bulbs. AE also demonstrates diffuse hair shedding, but pulled hairs lack root sheaths.
Importantly, effort should be made to distinguish chronic TE from FPHL, which may mimic the disease. TE is distinguished often by the absence of patterned hair loss and no evidence of increased ratio of miniaturized hairs to terminal hairs, a hallmark of FPHL. When the clinical picture is unclear, a scalp biopsy should be performed that may help guide management. TE may unveil alternative chronic forms of hair loss such as FPHL and it is not a mutually exclusive diagnosis.
Histopathology
The total number of hair follicles is preserved in TE, and there is no inflammation. The main histologic finding in TE is an increase in the number of telogen hair follicles and follicular stellae in the deeper layers. Follicle size is also preserved, which differentiates TE from androgenetic alopecia, in which follicular miniaturization is characteristic.28
Subtypes
Classic TE (typically resolves within a few months)
Chronic TE (lasting >4 months)
Differential Diagnosis
Androgenetic alopecia
Anagen effluvium
Diffuse alopecia areata
PATHOGENESIS
The mechanism that triggers TE is not well understood. A variety of causes may result in TE, including systemic illness, acute febrile illness, endocrine (thyroid) causes, collagen vascular disease, rapid weight loss, extreme protein malnutrition, and zinc deficiency. It is theorized that these triggers lead to disturbance of the normal hair cycle leading to transition to telogen phase and then shedding of the hair shaft.
TREATMENT
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