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Hair Loss: Common Causes and Treatment T

Hair Loss: Common Causes and Treatment T

Hair Loss: Common Causes and Treatment T. GRANT PHILLIPS, MD; W. PAUL SLOMIANY, MD; and ROBERT ALLISON, DO Washington Health Systems Family Medicine Residency, Washington, Pennsylvania

Hair loss is often distressing and can have a significant effect on the patient’s quality of life. Patients may present to their family physician first with diffuse or patchy hair loss. Scarring alopecia is best evaluated by a dermatolo- gist. Nonscarring alopecias can be readily diagnosed and treated in the family physician’s office. Androgenetic alopecia can be diagnosed clinically and treated with . is diagnosed by typical patches of hair loss and is self-limited. causes patches of alopecia that may be erythematous and scaly and must be treated systemically. is a nonscarring, noninflammatory alopecia of relatively sudden onset caused by physiologic or emotional . Once the precipitating cause is removed, the hair typically will regrow. is an impulse-control disorder; treatment is aimed at controlling the underlying psychiatric condition. occurs when break secondary to trauma and is often a result of hair styling or overuse of hair products. is the abnormal diffuse loss of hair during the growth phase caused by an event that impairs the mitotic activity of the , most commonly . Physician support is especially important for patients in this situation. (Am Fam Physician. 2017;96(6):371-378. Copyright © 2017 American Academy of Family Physicians.)

CME This clinical content atients with hair loss will often Approach to the Patient conforms to AAFP criteria consult their family physician with Nonscarring Alopecia for continuing medical education (CME). See first. Hair loss is not life threaten- The history and physical examination are CME Quiz Questions on ing, but it is distressing and sig- often sufficient to determine a specific eti- page 360. Pnificantly affects the patient’s quality of ology for hair loss. It is convenient to divide Author disclosure: No rel- life. The pattern of hair loss may be obvi- the various causes into focal (patchy) and evant financial affiliations. ous, such as the bald patches that occur in diffuse etiologies, and proceed accordingly. ▲ Patient information: alopecia areata, or more subtle, such as the Patchy hair loss is often due to alopecia A handout on this topic is diffuse hair loss that occurs in telogen efflu- areata, tinea capitis, and trichotillomania. available at http://www. vium. As with most conditions, the physi- Diffuse hair loss is commonly due to telo- aafp.org/afp/2009/0815/ cian should begin the evaluation with a gen or anagen effluvium. Androgenetic alo- p373.html. detailed history and physical examination. pecia may be diffuse or in a specific pattern, It is helpful to determine whether the hair and may progress to complete baldness. loss is nonscarring (also called noncicatri- cial), which is reversible, or scarring (also HISTORY called cicatricial), which is permanent. Important clues to the etiology of differ- Scarring alopecia is rare and has various ent patterns and types of hair loss are listed etiologies, including autoimmune diseases in Tables 1 and 2. Hair that comes out in such as discoid erythematosus. If the clumps suggests telogen effluvium. Sys- follicular orifices are absent, the alopecia is temic symptoms such as fatigue and weight probably scarring; these patients should be gain suggest , whereas a referred to a dermatologist. This article will febrile illness, stressful event, or recent discuss approaches to nonscarring causes of may account for the diffuse hair alopecia. loss of telogen effluvium. The use of hair products such as straightening agents or Physiology of Hair Growth certain suggests a diagnosis of Hair grows in three phases: anagen (active trichorrhexis nodosa. A family history of growing, about 90% of hairs), catagen hypothyroidism may warrant laboratory (degeneration, less than 10% of hairs) and testing for this condition, whereas a family telogen (resting, 5% to 10% of hairs). Hair is history of hair loss supports the diagnosis shed during the telogen phase. of androgenetic alopecia.

SeptemberDownloaded 15, from 2017 the American◆ Volume Family 96, NumberPhysician website6 at www.aafp.org/afp.www.aafp.org/afp Copyright © 2017 American Academy of FamilyAmerican Physicians. Family For the Physician private, noncom 371- mercial use of one individual user of the website. All other rights reserved. Contact [email protected] for copyright questions and/or permission requests. Hair Loss SORT: KEY RECOMMENDATIONS FOR PRACTICE

Evidence Clinical recommendation rating References

Topical minoxidil is safe and effective for the B 5 PHYSICAL EXAMINATION treatment of androgenetic alopecia in women. The physical examination should focus Alopecia areata can be treated with intralesional B 11 on the hair and , but attention should . be given to physical signs of any comorbid Oral (Lamisil), itraconazole (Sporanox), B 2 (Diflucan), or griseofulvin is disease indicated by the review of systems. recommended for treatment of children with If only the scalp is involved, the physician tinea capitis caused by Trichophyton . should look for typical male or female pattern Cognitive behavior therapy is effective for the B 19 to determine the presence of androgenetic treatment of trichotillomania, and medical alopecia. Whole loss is consistent therapy may be more effective when combined with cognitive behavior therapy. with . Dry, broken hair sug- gests trichorrhexis nodosa, whereas scaling, A = consistent, good-quality patient-oriented evidence; B = inconsistent or limited- pustules, crusts, erosions, or and quality patient-oriented evidence; C = consensus, disease-oriented evidence, usual local adenopathy suggest . practice, expert opinion, or case series. For information about the SORT evidence rating system, go to http://www.aafp.org/afpsort. The pull test may be used to diagnose hair loss conditions.1 The examiner grasps

Table 1. Summary of Nonscarring Alopecia

Type Significant features Treatment and comments

Alopecia areata Acute, patchy hair loss; examination shows short, vellus Intralesional acetonide injected intradermally hairs, yellow or black dots, and broken hair shafts High rate of spontaneous remission

Anagen Diffuse hair loss days to weeks after exposure No pharmacologic intervention has been proven effective; effluvium to a chemotherapeutic agent; incidence after scalp cooling not recommended chemotherapy is estimated at 65% Minoxidil may help during regrowth period

Androgenetic Family history of hair loss; gradually progressive course Men: topical minoxidil (2% or 5% solution) alopecia Men: bitemporal thinning of the frontal and vertex Women: topical minoxidil (2% solution) scalp, complete hair loss with some hair at the Treatment should continue indefinitely because hair loss occiput and temporal fringes reoccurs when treatment is discontinued Women: diffuse hair thinning of the vertex with Adverse effects include (excessive hair growth sparing of the frontal hairline for age, sex, and race) and irritant or contact

Telogen Clumps of hair come out in the shower or in Treatment involves removing the underlying cause and effluvium ; associated with physiologic or emotional providing reassurance stress Condition is usually self-limited and resolves within two to six months

Tinea capitis infection of the hair shaft and follicles; Requires systemic treatment because topical antifungals patients present with patchy alopecia with or do not penetrate hair follicles without scaling Trichophyton species: oral terbinafine (Lamisil), itraconazole (Sporanox), fluconazole (Diflucan), or griseofulvin Microsporum species: griseofulvin

Trichorrhexis Hairs break secondary to trauma or because of fragile Stop offending actions nodosa hair (congenital or genetic); causative traumas include excessive brushing, heat application, that pull on hairs, and conditions that cause excessive scalp scratching

Trichotillomania Patches of alopecia, typically frontoparietal, that Optimal treatment is unknown; strong evidence is lacking progress backward and may include the for selective serotonin reuptake inhibitors; cognitive and behavior therapy with habit reversal and may be more effective than either approach alone Psychiatric referral may be indicated

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approximately 40 to 60 hairs at their base pulling force is not distributed uniformly using the thumb, index, and middle fingers and because it is difficult to approximate the and applies gentle traction away from the number of hairs grasped, thereby leading to scalp. A positive result is when more than false interpretations. 10% of hairs (four to six) are pulled from the scalp; this implies active hair shedding LABORATORY STUDIES and suggests a diagnosis of telogen efflu- Because many conditions can cause hair loss, vium, anagen effluvium, or alopecia areata. there are no routine tests to evaluate hair However, a negative test result does not nec- loss. Laboratory testing is indicated when essarily exclude those conditions. The pull the history or physical examination findings test is difficult to standardize because the suggest an underlying comorbidity.

Table 2. Common Findings, Related Diagnoses, and Workup for Hair Loss

Common findings Related diagnosis Diagnostic workup and comments

Abrupt onset of hair loss Telogen effluvium related to a specific event Inquire about inciting event

Gradual onset of hair loss Alopecia areata History and physical examination findings are diagnostic Pull test: increased telogen-to-anagen ratio (greater than the normal ratio of 1:10) Androgenetic alopecia Family history and specific patterns are important Scarring alopecias Refer if scarring is suspected

Diffuse hair loss Alopecia totalis if more than scalp Consider referral is involved (e.g., hypothyroidism, iron Laboratory testing depends on history and physical deficiency, other nutritional disorder) examination findings: complete blood count, - stimulating hormone level Telogen effluvium History and physical examination findings are diagnostic

Patchy hair loss Alopecia areata, trichotillomania History and physical examination findings are diagnostic Tinea capitis Obtain fungal cultures; itching, scaling, pustules, and lymphadenopathy may be present

Male or female pattern Androgenetic alopecia History and physical examination findings are diagnostic; scalp appears normal

History of or Trichotillomania Obtain psychiatric history; patient may not be forthcoming about psychiatric diseases pulling hair; pattern and appearance of hair are diagnostic

History of extensive use Trichorrhexis nodosa History and physical examination findings are diagnostic; of hair products or broken hairs seen on slight magnification tight hairstyles

Medication use Several types of hair loss, especially If a particular medicine is suspected, a discontinuation trial telogen effluvium is reasonable

Recent physical or Telogen effluvium History and physical examination findings are diagnostic; scalp emotional trauma appears normal; hair loss may not be obvious

Skin condition Scarring alopecia, tinea capitis; most History and physical examination findings are diagnostic nonscarring alopecias are associated with a relatively normal scalp

Systemic symptoms Related to systemic disease Laboratory testing depends on history and physical examination findings

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Specific Disorders ANDROGENETIC ALOPECIA Androgenetic alopecia is the most common form of hair loss in men and women and is a normal physiologic variant. It is most preva- lent in white men, with 30%, 40%, and 50% experiencing androgenetic alopecia at 30, 40, and 50 years of age, respectively 2 (Figure 1). Although this condition is less common in women, 38% of women older than 70 years Figure 1. Male . may be affected3 (Figure 2 4). Many patients with androgenetic alopecia have a family history of this condition. Hair thinning occurs in a sex-specific pat- tern. Men typically present with bitemporal thinning, thinning of the frontal and vertex scalp, or complete hair loss with residual hair at the occiput and temporal fringes.5 Women typically present with diffuse hair thinning of the vertex with sparing of the frontal hairline. Some women experience thinning over the lateral scalp. Common conditions that mimic androgenetic alopecia include thyroid disease, , and Figure 2. Female pattern hair loss. . Reprinted with permission from Mounsey AL, Reed SW. Treatment is based on patient preference. Diagnosing and treating hair loss. Am Fam Physician. Topical minoxidil (2% or 5% solution) is 2009;80(4):360. approved for the treatment of androgenetic alopecia in men. Hair regrowth is more robust at the vertex than in the frontal area, and will take six to 12 months to improve.5 Treatment should continue indefinitely because hair loss reoccurs when treatment is discontin- ued. Minoxidil 2% solution is recommended for the treatment of androgenetic alopecia in women.6 Adverse effects include irritant and . (Propecia), 1 mg per day orally, is approved to treat androgenetic alopecia in Figure 3. Alopecia areata. men for whom topical minoxidil has been texts, there is not good evidence to support ineffective. Adverse effects of finasteride their use.8 include decreased , erectile dysfunc- tion, and gynecomastia.7 ALOPECIA AREATA Minoxidil and oral finasteride are the Alopecia areata is an acute, patchy alope- only treatments currently approved by the cia that affects up to 2% of the population U.S. Food and Drug Administration for the with no difference between sexes 9 (Figure 3). treatment of androgenetic alopecia. Both of Approximately 20% of affected patients are these drugs stimulate hair regrowth in some children.10 The etiology is unknown, but the men, but are more effective in preventing pathogenesis is likely autoimmune. Patients progression of hair loss. Although there are a may have a single episode, or they may have number of other treatments listed in various remission and recurrence. The diagnosis can

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Distal shaft (normal caliber)

Proximal shaft (thinned)

Figure 5. Hair loss from tinea capitis. repeated every four to six weeks until resolu- tion or for a maximum of six months. Local Club-shaped adverse effects include transient atrophy and hair root telangiectasia. Other therapies for the treatment of alope- cia areata include topical mid- to high-potency corticosteroids, minoxidil, anthralin, immu- notherapy (diphenylcyclopropenone, squaric

ILLUSTRATION DAVID BY KLEMM acid dibutylester), and systemic corticoste- Figure 4. Exclamation point hair showing dis- roids.12 Currently available therapies often tal broken end of shaft and proximal club- yield unsatisfactory results, and some clini- shaped hair root. cians rely on the high rate of spontaneous Reprinted with permission from Mounsey AL, Reed SW. Diagnosing and treating hair loss. Am Fam Physician. remission or recommend a hairpiece or 2009;80(4):358. if remission does not occur.13

usually be made clinically. TINEA CAPITIS Hair loss in alopecia areata occurs in three Tinea capitis is a dermatophyte infection different patterns: patchy alopecia is circum- of the hair shaft and follicles that primarily scribed, oval-shaped, flesh-colored patches affects children (Figure 5). Risk factors include on any part of the body; alopecia totalis household exposure and exposure to contam- involves the entire scalp; and alopecia uni- inated hats, brushes, and instruments. versalis involves the whole body. Evaluation Trichophyton tonsurans is the most common of the scalp may reveal short vellus hairs, etiology in North America.14 Transmission yellow or black dots, and broken hair shafts occurs person-to-person or from asymptom- (which are not specific to alopecia areata). atic carriers. Infectious fungal particles may Microscopic examination of the hair follicles remain viable for many months; other vectors demonstrates exclamation mark hair (i.e., include fallen infected hairs, animals, and hairs that are narrower closer to the scalp and fomites. is commonly mimic an exclamation point; Figure 4 4). spread by dogs and cats. pitting is also associated with alopecia areata. Patients with tinea capitis typically present Treatment for adults with less than 50% of with patchy alopecia with or without scaling, scalp involvement is intralesional triamcino- although the entire scalp may be involved. lone acetonide injected intradermally using a Other findings include adenopathy and pruri- 0.5-inch, 30-gauge needle. Maximal volume tus. Children may have an associated kerion, is 3 mL per session.11 Treatment may be a painful erythematous boggy plaque, often

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with purulent drainage and regional lymph- adenopathy. Posterior auricular lymphade- nopathy may help differentiate tinea capitis from other inflammatory causes of alopecia. If the diagnosis is not clear from the history and physical examination, a skin scraping taken from the active border of the inflamed patch in a potassium hydroxide prepara- tion can be examined microscopically for the presence of hyphae. Skin scrapings can also be sent for fungal culture, but this is less helpful because the fungi can take up to six weeks to grow. Figure 6. Hair loss from trichotillomania. Tinea capitis requires systemic treat- ment; topical antifungal agents do not pen- symptoms of an underlying condition, but etrate hair follicles. If the causative agent is are often asymptomatic. They often notice a Trichophyton species, treatment options clumps of hair coming out in the shower include oral terbinafine (Lamisil), itracon- or in their hairbrush. They should be asked azole (Sporanox), fluconazole (Diflucan), to recall any potential trigger two to five and griseofulvin.15 These agents have similar months before the onset of the condition. efficacy rates and potential adverse effects, Examination of the scalp in patients with but griseofulvin requires a longer treatment telogen effluvium typically shows uniform course. Griseofulvin is the preferred treat- hair thinning. The presence of erythema, ment for infections caused by Microsporum scaling, or ; altered or uneven species, but definitive studies are lacking.15,16 hair distribution; or changes in shaft caliber, There are limited data about empiric treat- length, shape, or fragility may suggest other ment before culture results are available. diagnoses. Laboratory investigations are indi- Because griseofulvin may have lower cated if the history and physical examination rates in the treatment of T. tonsurans infec- findings suggest underlying systemic disor- tions, it may not be as effective when used ders (e.g., iron deficiency anemia, defi- empirically.15 All close contacts of patients ciency, renal or liver disease, thyroid disease). with tinea capitis should be examined for Telogen effluvium is usually self-limited signs of infection and treated, if necessary. and resolves within two to six months. Treat- ment involves eliminating the underlying TELOGEN EFFLUVIUM cause and providing reassurance. Potentially Telogen effluvium is a nonscarring, nonin- causative medications should be discontin- flammatory alopecia of relatively sudden ued, if possible. Telogen effluvium may last onset, with similar incidences between sexes for years if the underlying stress continues. and age groups. It occurs when large num- bers of hairs enter the telogen phase and fall TRICHOTILLOMANIA out three to five months after a physiologic Trichotillomania is an impulse-control dis- or emotional stressor. The list of inciting fac- order with a mean age of onset of approxi- tors is extensive and includes severe chronic mately 13 years (Figure 6). Patients with this illnesses, pregnancy, , high fever, mal- condition consciously or unconsciously pull, nutrition, severe infections, and endocrine twist, or twirl their hair. Trichotillomania is disorders. Causative medications include reported to affect as much as 4% of the pop- , anticoagulants, anticonvulsants, ulation, with the highest incidence in child- beta blockers, and antithyroid medications; hood and .18 discontinuation of oral contraceptive agents Trichotillomania may be difficult to diag- is another possible cause.17 nose if the patient is not forthcoming about Patients with telogen effluvium may have pulling at his or her hair. Patients typically

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present with frontoparietal patches of alope- conditions that may cause trichorrhexis cia that progress posteriorly and may include nodosa include the eyelashes and eyebrows. Bare patches are (bamboo hair), intussusception of the hair typical, and the hair may appear uneven, shaft at the keratinization zone, Menkes dis- with twisted or broken off hairs. Trichotil- ease, keratinization defects due to defective lomania may lead to problems with self- copper metabolism, and argininosuccinic esteem and social avoidance. Complications aciduria.22 Rarely, trichorrhexis nodosa can include infection, skin damage, and perma- be a manifestation of hypothyroidism.23 nent scarring.18 On examination, hairs appear to have The optimal treatment for this condition is white nodes; on closer inspection, these are not known, and psychiatric referral may be shown to be fracture sites along the shaft and indicated. Treatment options include cogni- cortex that have split into several strands. On tive behavior therapy 19 and selective sero- dermoscopy, hairs look like two brooms or tonin reuptake inhibitors, although strong paint brushes thrust together. evidence of a treatment effect has not been If the diagnosis is not clear, laboratory demonstrated. Preliminary evidence suggests testing should include a complete blood positive treatment effects with acetylcysteine, count, iron studies, copper level, liver func- olanzapine (Zyprexa), and tion testing, thyroid-stimulating hormone (Anafranil).19 A combination of cognitive level, and serum and urine amino acid levels. behavior therapy and medications may be Treatment includes avoiding or minimizing more effective than either approach alone.19 physical and chemical trauma.

TRICHORRHEXIS NODOSA ANAGEN EFFLUVIUM Trichorrhexis nodosa occurs when hairs Anagen effluvium is abnormal diffuse break secondary to trauma or because of frag- hair loss (usually abrupt) during the ana- ile hair (Figure 7). It affects the proximal hair gen phase due to an event that impairs the shaft, although the distal shaft may also be mitotic or metabolic activity of the hair folli- involved.20 Causative traumas include exces- cle. The incidence of anagen effluvium after sive brushing, heat application, tight hair- chemotherapy is approximately 65%24; it is styles, trichotillomania, and conditions that most commonly associated with cyclophos- cause excessive scalp scratching. Chemical phamide, nitrosoureas, and traumas include harsh hair treatments (e.g., (Adriamycin). Other causative medications excessive use of bleach, dye, , perms, include tamoxifen, allopurinol, levodopa, or relaxers21) and excessive exposure to salt bromocriptine (Parlodel), and toxins such water. Examples of congenital or genetic as bismuth, arsenic, and gold. Other medi- cal and inflammatory conditions, such as or vulgaris, can lead to anagen effluvium.25 Patients typically present with diffuse hair loss that begins days to weeks after exposure to a chemotherapeutic agent and is most apparent after one or two months.26 Approx- imately 50% of women with consider hair loss to be the most traumatic aspect of chemotherapy and nearly 10% would decline treatment for fear of hair loss.26,27 Anagen effluvium is usually reversible, with regrowth one to three months after ces- sation of the offending agent. Permanent alo- pecia is rare. A large meta-analysis of clinical Figure 7. Hair loss from trichorrhexis nodosa. trials concluded that scalp cooling was the

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only intervention that significantly reduced 11. Kumaresan M. Intralesional for alopecia areata. the risk of chemotherapy-induced anagen Int J Trichology. 2010;​2(1):63-65​ . 27 12. Gilhar A, Etzioni A, Paus R. Alopecia areata. N Engl effluvium. However, scalp cooling should be J Med. 2012;366(16):​ 1515-1525​ . discouraged because it may minimize deliv- 13. Delamere FM, Sladden MM, Dobbins HM, Leonardi-Bee ery of chemotherapeutic drugs to the scalp, J. Interventions for alopecia areata. Cochrane Database leading to cutaneous scalp metastases.27 Syst Rev. 2008;(2):​ CD004413.​ 14. Abdel-Rahman SM, Farrand N, Schuenemann E, et al. This article updates previous articles on this topic by The prevalence of infections with Trichophyton ton- Mounsey and Reed4; Springer, et al.28; and Thiedke.29 surans in schoolchildren: ​the CAPITIS study. Pediatrics. 2010;​125(5):​966-973. Data Sources: We searched PubMed using the key 15. Chen X, Jiang X, Yang M, et al. Systemic antifungal words alopecia areata, tinea capitis, trichotillomania, therapy for tinea capitis in children. Cochrane Database trichorrhexis nodosa, anagen effluvium, and telogen Syst Rev. 2016;​(5):​CD004685. effluvium. We also searched reference lists from relevant 16. Kakourou T, Uksal U;​ European Society for Pediat- articles and textbooks. ric . Guidelines for the management of Figures 1, 3, and 5 through 7 courtesy of Neil Fenske, MD, tinea capitis in children. Pediatr Dermatol. 2010;​27(3):​ University of South Florida Morsani College of Medicine. 226-228. 17. Goodheart HP. Goodheart’s Photoguide to Common Skin Disorders:​ Diagnosis and Management. 3d ed. Phil- The Authors adelphia, Pa.:​ Lippincott Williams & Wilkins;​ 2009:​323. 18. Franklin ME, Flessner CA, Woods DW, et al.;​ Trichotil- T. GRANT PHILLIPS, MD, is the associate director of resi- lomania Learning Center-Scientific Advisory Board. The dent education for the Washington (Pa.) Health Systems child and adolescent trichotillomania impact project:​ Family Medicine Residency Program. descriptive psychopathology, comorbidity, functional W. PAUL SLOMIANY, MD, is the associate program director impairment, and treatment utilization. J Dev Behav for the Washington Health Systems Family Medicine Resi- Pediatr. 2008;​29(6):​493-500. dency Program. 19. Ninan PT, Rothbaum BO, Marsteller FA, Knight BT, Eccard MB. A placebo-controlled trial of cognitive- ROBERT ALLISON, DO, is a clinical instructor for the behavioral therapy and clomipramine in trichotilloma- Washington Health Systems Family Medicine Residency nia. J Clin Psychiatry. 2000;61(1):​ ​47-50. Program. 20. James WD, Berger TG, Elston DM, Neuhaus IM, eds. Diseases of the skin appendages. In:​ Andrews’ Diseases Address correspondence to T. Grant Phillips, MD, Wash- of the Skin: ​Clinical Dermatology. 12th ed. Philadelphia, ington Health Systems Family Medicine Residency, 95 Pa.:​ Elsevier;​ 2016:747-788​ . Leonard Ave., Washington, PA 15304 (e-mail: tphillips@ 21. Mubki T, Rudnicka L, Olszewska M, Shapiro J. Evalua- whs.org). Reprints are not available from the authors. tion and diagnosis of the hair loss patient:​ part I. History and clinical examination. J Am Acad Dermatol. 2014;​ REFERENCES 71(3):​415.e1-415.e15. 22. Fichtel JC, Richards JA, Davis LS. Trichorrhexis nodosa 1. Dhurat R, Saraogi P. Hair evaluation methods:​ merits secondary to argininosuccinicaciduria. Pediatr Derma- and demerits. Int J Trichology. 2009;​1(2):​108-119. tol. 2007;​24(1):​25-27. 2. Wang TL, Zhou C, Shen YW, et al. Prevalence of andro- 23. Lurie R, Hodak E, Ginzburg A, David M. Trichorrhexis genetic alopecia in China:​ a community-based study in nodosa:​ a manifestation of hypothyroidism. Cutis. six cities. Br J Dermatol. 2010;​162(4):​843-847. 1996;​57(5):​358-359. 3. Shapiro J. Clinical practice. Hair loss in women. N Engl 24. Trüeb RM. Chemotherapy-induced alopecia. Semin J Med. 2007;357(16):​ ​1620-1630. Cutan Med Surg. 2009;28(1):​ 11-14​ . 4. Mounsey AL, Reed SW. Diagnosing and treating hair 25. Kanwar AJ, Narang T. Anagen effluvium.Indian J Der- loss. Am Fam Physician. 2009;​80(4):356-362​ . matol Venereol Leprol. 2013;79(5):​ ​604-612. 5. Price VH. Treatment of hair loss. N Engl J Med. 1999;​ 26. McGarvey EL, Baum LD, Pinkerton RC, Rogers LM. Psy- 341(13):​964-973. chological sequelae and alopecia among women with 6. van Zuuren EJ, Fedorowicz Z, Schoones J. Interventions cancer. Cancer Pract. 2001;​9(6):283-289​ . for female pattern hair loss. Cochrane Database Syst 27. Münstedt K, Manthey N, Sachsse S, Vahrson H. Changes Rev. 2016;​(5):​CD007628. in self-concept and during alopecia induced 7. Rittmaster RS. Finasteride. N Engl J Med. 1994;​330(2):​ cancer chemotherapy. Support Care Cancer. 1997;​5(2):​ 120-125. 139-143. 8. Banka N, Bunagan MJ, Shapiro J. Pattern hair loss in 28. Springer K, Brown M, Stulberg DL. 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