Am Fam Physician. 2024;110(3):243-250
Author disclosure: No relevant financial relationships.
More than 80 million people in the United States are affected by hair loss, also known as alopecia. Nonscarring alopecias are categorized as diffuse, patterned, or focal. Diffuse alopecias include telogen and anagen effluvium, are usually self-limited, and depend on stopping the underlying cause (e.g., stress). Patterned hair loss, specifically androgenetic alopecia, is the most common form of alopecia; it is typically genetic, and first-line treatment is minoxidil. Oral finasteride is another treatment available for male patients. Focal hair loss includes alopecia areata, which is typically self-limited and treated with intralesional corticosteroid or oral immunosuppressant therapy; tinea capitis, which is treated with oral antifungals; and traction alopecia, which is treated by decreasing tension on the hair. Hair loss can be caused by several systemic diseases. A comprehensive history and physical examination, with targeted laboratory testing, may elucidate malnutrition, autoimmune diseases, and endocrine disease. Patients with moderate to severe hair loss are more likely to have accompanying anxiety, depression, and lower work productivity and quality-of-life scores. Educating patients about expected hair changes, treatment options, and realistic outcomes can help patients feel that they are being listened to and that their hair loss is being taken seriously.
More than 80 million people in the United States are affected by hair loss, also known as alopecia. Each year, an estimated $8.2 billion is spent on hair loss treatment globally.1 Patients typically report hair loss significantly beyond what can be appreciated on physical examination. Patients with moderate to severe hair loss are more likely to have accompanying anxiety, depression, and lower work productivity and quality-of-life scores.2 Educating patients about expected hair changes, treatment options, and realistic outcomes can help patients feel that they are being listened to and that their hair loss is being taken seriously.3
The body is covered with two types of hair-producing follicles: terminal and vellus. Terminal follicles grow long, thick hair, whereas vellus follicles produce hair that is short, fine, and nonpigmented. At birth, the scalp is covered by approximately 100,000 terminal follicles, and the rest of the body is covered with vellus follicles. During puberty, increased androgen levels cause vellus follicles in the axilla, chest, and genital areas to become terminal follicles; this leads to noticeable hair growth.4
Each follicle perpetually cycles through three phases. In normal physiology, approximately 90% to 95% of scalp follicles are in the anagen (growth) phase, which lasts 2 to 6 years. Follicles on other parts of the body have a shorter anagen phase, which is responsible for their shorter length. Less than 1% of scalp follicles are in the catagen (involution) phase, and 5% to 10% are in the telogen (resting) phase. At the end of telogen phase, the hair is shed; approximately 100 scalp hairs are lost each day. Normally, each follicle cycles independently, which prevents the mass shedding of hair.4
Scalp hair coverage is a combination of hair density and follicle diameter. The diameter of hair follicles peaks in female patients in their late 30s to mid-40s and decreases during and after menopause. In male patients, hair diameter peaks in the early to mid-20s. The decreasing diameter of hair fibers has the most significant impact on the overall perception of hair aging.5
DIAGNOSIS
It is useful to start by characterizing a patient's hair loss as diffuse, patterned, or focal.6 Diffuse alopecia is often caused by telogen or anagen effluvium. Androgenetic alopecia is the most common type of alopecia and is patterned.7 Focal alopecias include alopecia areata, tinea capitis, and traction alopecia. Most cases of alopecia are nonscarring. The workup and management of scarring alopecia are specialized; biopsy and referral to a dermatologist should be considered for these cases.
History
The onset of alopecia can be abrupt or gradual, and the scalp is usually involved. Determining whether the hair is being shed in large clumps is helpful. The physician should ask about associated factors like physical or emotional stress, use of chemotherapeutic drugs, and physical trauma such as tight braiding or hair pulling. Related systemic diseases may be suggested by a review of systems (e.g., thyroid disease, autoimmune disease, malnutrition). A family history of similar symptoms can help diagnose hereditary hair loss conditions (e.g., androgenetic alopecia). Any emotional distress that the alopecia has caused the patient should be addressed. The clinical features of many common causes of alopecia are noted in Table 1.6,8–28
| Type | Clinical features | Treatment |
|---|---|---|
| Diffuse alopecia | ||
| Anagen effluvium | Diffuse hair loss days to weeks after exposure to a chemotherapeutic agent; incidence after chemotherapy is estimated at 65%8 | Usually self-limited and resolves with stopping the offending agent; no pharmacologic intervention has been shown to be effective; minoxidil may help during regrowth period; scalp cooling can be effective in prevention, and newer studies do not show increased risk of metastases9,10 |
| Telogen effluvium | Clumps of hair come out in the shower or hairbrush; most often associated with physiologic or emotional stress; less likely implicated causes are medications, thyroid disease, and nutritional and vitamin D deficiencies; condition can also be idiopathic11 | Usually self-limited and resolves within 6 to 9 months; treatment consists of reassurance and removing the underlying cause; topical minoxidil can help during the regrowth period in patients with concomitant androgenic alopecia6,11 |
| Patterned alopecia | ||
| Androgenetic alopecia | Family history of hair loss; gradually progressive course; in male patients: bitemporal thinning of the frontal and vertex scalp, complete hair loss with some hair at the occiput and temporal fringes; in female patients: diffuse hair thinning of the vertex with sparing of the frontal hairline12–14 | Topical minoxidil 2% to 5% solution; hair loss will recur if treatment is discontinued; adverse effects include hypertrichosis (excessive hair growth) and irritant or contact dermatitis; adjuvant therapy with finasteride can be added15–19 |
| Focal alopecia | ||
| Alopecia areata | Acute, patchy hair loss; examination may show short vellus hairs, yellow or black dots, broken hair shafts, and exclamation point hairs, especially at the periphery of expanding patches20 | Intralesional triamcinolone acetonide; the condition has a high rate of spontaneous remission20; baricitinib (Olumiant) oral immunotherapy increases regrowth by more than 75% over placebo21,22; for children who cannot tolerate injections, high-potency topical corticosteroids may be used23 |
| Tinea capitis | Dermatophyte infection of hair shaft and follicles; patchy alopecia with or without scaling24 | Requires systemic treatment, because topical antifungals do not penetrate hair follicles; for Trichophytoninfections: oral terbinafine, itraconazole, fluconazole or griseofulvin; for Microsporuminfections: griseofulvin; a fungal culture should be obtained for diagnosis24 |
| Traction alopecia | Traction alopecia from styling:patches of alopecia along hairline25 Trichotillomania: patches of alopecia, typically frontoparietal, that progress backward and may include the eyelashes and eyebrows25 | Stop the offending traction on hair25; there is insufficient evidence for medications; for trichotillomania, behavioral therapy with habit reversal can be helpful; data regarding use of selective serotonin reuptake inhibitors are inconclusive26–28 |
| Trichorrhexis nodosa | Hair shaft weakness secondary to trauma or due to fragile hair (acquired or genetic); causative traumas include excessive brushing, heat or chemical applications, and scalp excoriation25 | Stop offending actions if the cause is trauma; correct nutritional deficiencies or endocrine abnormalities if the cause is acquired hair fragility 25 |
Physical Examination
Trichoscopy and dermoscopy of the scalp provide better visualization but are not commonly performed in the primary care office. The distribution of hair loss will point to different diagnoses. Alopecia areata is suggested by smooth, round lesions with hair shafts that thin toward the scalp, giving them an exclamation point shape (Figure 129). Scaly, erythematous lesions and occipital adenopathy with or without signs of secondary bacterial infection occur with tinea capitis. Bitemporal thinning that may include the vertex of the head occurs in androgenetic alopecia in male patients. Hair loss that is diffuse but concentrated at the vertex, sparing the frontal area, suggests androgenetic alopecia in female patients.30 Notable hair loss along the hairline can occur with traction alopecia from styling. Trichotillomania presents with irregularly shaped patches of hair loss with broken hairs of different lengths and coexistent new hair growth, which may include eyelashes and eyebrows.31
The hair pull test is typically performed at the vertex, both parietal regions, and the occiput. Hair should be at least 0.5 inches long, and it should not be pinned up. The test is performed by grasping 1 to 2 cm2 of hair (50 to 60 hairs) between the thumb, index finger, and middle finger and exerting gentle traction while sliding the fingers distally along the hair shaft to the end. Broken hairs are discarded. The test result is positive when more than two hairs are removed. Positive results in more than one region suggest telogen or anagen effluvium. If the test result is positive in only one region, alopecia areata should be considered.32 The hair follicles can then be further evaluated with microscopy to identify morphologies and assist with a final diagnosis.
Laboratory Examination
Laboratory evaluation can confirm diagnoses. Microscopic examination can help distinguish club-shaped (telogen) hairs— spherical white bulb at the base of the hair, as seen in telogen effluvium—from hairs in the anagen phase, which still have the inner root sheath attached.29
Evaluation for associated conditions such as hypothyroidism, iron deficiency or other causes of anemia, vitamin D deficiency, malnutrition, liver disease, autoimmune disease, or syphilis should be guided by the clinical evaluation.
DIFFUSE HAIR LOSS
Anagen Effluvium
Anagen effluvium occurs within 2 weeks of the administration of an offending agent. It is commonly referred to as chemotherapy-induced effluvium and is a nonscarring alopecia resulting from a toxic or inflammatory insult that is triggered by chemotherapeutic agents. Typically, the condition is self-limited, and hair growth resumes upon discontinuation of the offending agent. Toxin exposure, most commonly in the form of medications, causes damage to the hair shaft, which leads to breakage. If the bulb of the hair follicle is affected, hair loss occurs.8 Scalp cooling can help preserve hair during chemotherapy.9,10
Telogen Effluvium
Telogen effluvium is the most common cause of diffuse hair loss. At its peak, patients lose more than 200 scalp hairs per day. In normal physiology, each hair's telogen phase lasts 3 to 5 months before the hair is shed naturally. The pathophysiology of telogen effluvium is not completely understood, but it is thought that a stressor advances follicles into the telogen phase.11
Most cases of telogen effluvium are caused by stressors such as severe illness, childbirth, and major surgery. Evaluation should include testing for iron deficiency anemia, thyroid disease, malnutrition, and vitamin D deficiency. Medications such as lithium (most common medication cause), valproate, fluoxetine, warfarin, metoprolol, propranolol, retinoids, isoniazid, and the initiation or cessation of oral contraceptives may be implicated in telogen effluvium.
Telogen effluvium is usually self-limited. Hair loss begins 2 to 4 months after the inciting event and normalizes 6 to 9 months later if the inciting trigger is corrected. Patients with concomitant patterned hair loss may benefit from topical minoxidil.6
PATTERNED HAIR LOSS
Androgenetic Alopecia
In androgenetic alopecia, terminal follicles undergo a shortened anagen phase and become shorter, thinner vellus follicles, leading to the perception of hair thinning. Testosterone is converted to dihydrotestosterone by the enzyme 5 alpha-reductase, which binds to an androgen receptor on the follicle and activates genes responsible for transitioning terminal follicles to vellus follicles. Patients have increased 5 alpha-reductase activity and androgen receptor density or activity; this is thought to be related to genetics.14
Male patients present with asymptomatic hair loss involving the frontal-temporal regions and the vertex. Examination reveals miniaturization of follicles and hair loss in these areas. Female pattern androgenetic alopecia is characterized by diffuse thinning in predominantly the vertex.13
Although androgenetic alopecia is benign, cosmetic concerns lead patients to seek treatment. Studies demonstrate that topical minoxidil, which prolongs the duration of anagen phase, is an effective first-line treatment.15,16 There are multiple formulations; a randomized controlled trial in men found more hair growth with use of a 5% topical solution compared with a 2% topical solution or placebo.15 The medication should be applied to the scalp, not the hair, and can lead to the growth of new hair after several months. The medication must be used continuously; if it is stopped, hair regrowth will be lost over several months. The most common adverse effect is contact dermatitis.
For male patients, 1 mg of finasteride daily is an additional first-line therapy. Finasteride inhibits the conversion of testosterone to dihydrotestosterone. Two meta-analyses support the daily use of finasteride to improve hair counts compared with placebo.17,18 One year of use is needed to assess effectiveness. Notable adverse effects include sexual dysfunction, such as erectile dysfunction.19
In female patients, additional adjunctive therapies such as spironolactone or finasteride are commonly added to minoxidil or used on their own. However, evidence to support this practice is lacking. A recent Cochrane review called for additional randomized controlled trials to determine the effectiveness of these interventions.16 Figure 2 and Figure 3 are examples of patterned hair loss.
FOCAL HAIR LOSS
Alopecia Areata
Alopecia areata is an immune-mediated process in which follicles in the anagen phase are prematurely transitioned to the catagen and telogen phases, which leads to rapid hair loss. The most common presentation is a smooth, round, discrete area of complete hair loss on the scalp that developed over weeks. On examination, exclamation point hairs may be present. Focal hair loss can occur anywhere on the body, and the spectrum of disease includes total hair loss of the scalp (alopecia totalis) or the entire body (alopecia universalis). Patients may have co-occurring nail disorders, such as nail pitting. Diagnosis of focal hair loss is usually made clinically, with biopsy reserved for uncertain cases. Autoimmune disease, in particular thyroid disease, may be associated with alopecia areata, therefore screening for these disorders should be considered as clinically indicated.20,33
Alopecia areata spontaneously remits in most patients with a limited presentation, which is defined as affecting less than 50% of the scalp. Patients should be counseled on the course of the disease and possible adverse effects of treatment before initiating therapy. For limited cases, intralesional corticosteroids, repeated every 4 to 6 weeks until satisfactory regrowth, have been used as first-line treatment. However, a recent Cochrane review did not find evidence to support use of intralesional or systemic corticosteroids. Using systematic analysis of 63 studies, the review concluded that the oral immunosuppressant baricitinib (Olumiant) increases regrowth by more than 75% over placebo.21,22,34
Tinea Capitis
Tinea capitis is a common cause of hair loss in children. It is a dermatophyte infection that causes itchy and scaling hair loss. The most common presentation is one or more slowly enlarging scaly patches. Broken hair follicles appear as small black dots in the area of hair loss. Associated lymphadenopathy is a typical finding. Other presentations include diffuse scale with more subtle hair loss, or kerion, which is an immune reaction where crusted plaques and draining pustules form. The diagnosis of tinea capitis can be made clinically, but a fungal culture or a microscopic examination of a skin scraping using a potassium hydroxide preparation can be confirmatory. Oral antifungals are first-line treatment, because topical agents do not penetrate the scalp. Griseofulvin and terbinafine are well established; azoles are alternative options with less evidence supporting their use.24
Hair Fragility and Traction Alopecia
Traction alopecia occurs due to prolonged tension on the hair follicle. It is commonly caused by hair styling or hair pulling. The condition most commonly occurs in people who keep their hair in a traction hairstyle, such as braids or a tight pony-tail. The initial manifestation is erythematous papules, which can progress to hair loss. Initial treatment is to discontinue or modify the hairstyle causing the traction. Minoxidil has not been shown to promote hair regrowth in these patients. The treatment plan should also include cessation of chemical or heat treatments.
Trichorrhexis nodosa is a related condition in which hair is weakened by application of heat or chemicals, making it more susceptible to damage (Figure 4). Weakened hair shafts break because of trauma, leading to the appearance of thin, short, brittle hair. Less common etiologies that weaken the hair include genetic disorders, such as inborn errors of metabolism or systemic diseases like hypothyroidism. Presentation in infancy should prompt a workup for genetic etiology. In older patients who do not use chemical or heat treatments, evaluation should include a complete blood count, liver function tests, thyroid function tests, iron studies, and measurement of copper levels and serum and urine amino acids. The goal of treatment is to correct the underlying problem and avoid hair trauma.25
Trichotillomania is a traction alopecia in which a patient repeatedly pulls out their hair (Figure 5). This leads to hair loss and may cause significant stress. It is most common in children and adolescents and can be difficult to diagnose because patients may not be forthcoming about their hair pulling. Patients may have irregular patchy alopecia that may involve the scalp and other body sites including eyebrows and eyelashes. The remainder of the hair is usually normal, with a negative pull test. The base of the occiput tends to be spared because it is more difficult to reach and tends to be more tender.33 The patient's history can be compared with criteria in the Diagnostic and Statistical Manual of Mental Disorders, 5th ed., text revision to reach a final diagnosis.36 There is benefit from behavioral therapy, particularly habit reversal training.26,27 There is insufficient evidence of effectiveness for any medication to treat trichotillomania.26,28
This article updates previous articles on this topic by Phillips, et al.37; Mounsey and Reed29; Springer, et al.38; Thiedke39; and Scow, et al.40
Data Sources: A PubMed search was completed in Clinical Queries using the key terms: alopecia, androgenetic alopecia, nonscarring alopecia, and the various subtypes of alopecia discussed. The search included meta-analyses, randomized controlled trials, clinical trials, and reviews. Essential Evidence Plus and the Cochrane database were also searched. We critically reviewed studies that used patient categories such as race and/or gender but did not define how these categories were assigned, stating their limitations in the text. Search dates: May 5, 2023, and August 18, 2024.
