- Alopecia, or hair loss, has a broad spectrum of causes. In order to appropriately treat alopecia, the type of hair loss or pathophysiology must be clearly identified.
- The evaluation for hair loss requires a very thorough history and physical exam. Asking specific questions regarding the nature, duration, and anatomic involvement of hair loss is key, as well as detailed questions regarding medical comorbidities, past medical history, medications, supplements, diet, and cosmetic practices.
- After physical exam, diagnostic evaluation for hair loss may entail a hair sample mount, scalp biopsy, and/or blood tests to identify a diagnosis or underlying cause.
- There is not always an effective treatment for hair loss, but identifying the correct underlying process causing alopecia enables counseling and, possibly, treatment for patients.
Hair loss, or alopecia, is the result of increased shedding or breakage of hair and may be brought about by a broad spectrum of causes. Alopecia may result from primary disorders of hair or the hair follicle, and may be secondary to an underlying medical disease, skin inflammation, or an infection. The management of patients with alopecia is challenging for providers and patients alike, as alopecia commonly has a significant impact on a patient’s quality of life. Having a clear diagnostic algorithm enables expeditious diagnosis of clinical alopecia, and in some cases, avoids unnecessary diagnostic work-up and tests.
It is imperative to exclude secondary hair loss due to a medication or a medical condition, or due to skin inflammation or infection. A thorough history and physical exam is necessary. Scalp inflammation, the presence or absence of follicular openings, exclamation mark hairs, or hair tufting should be noted. If there is evidence of scalp inflammation in the area of hair loss and a diagnosis is not clear, a scalp biopsy and tissue culture is strongly indicated. Evidence of scarring should also prompt a scalp biopsy.
There are numerous pathophysiologic mechanisms that result in alopecia:
- hair shaft disorders
- an autoimmune disorder (such as alopecia areata)
- chemotherapy induced (such as anagen effluvium)
- scalp inflammation (leading to scarring alopecia, such as in lupus or lichen planus)
- hormonal (such as androgenetic alopecia men and women or hyperandrogenism in women)
- a medical illness (such as syphilis, thyroid disease, anemia, nutritional deficiency, vitamin D deficiency, iron deficiency, or due to shifts of hair from the growth phase to shedding phase, known as telogen effluvium)
- idiopathic (such as frontal fibrosing alopecia)
A biopsy may be helpful to discriminate between these entities, as many of these clinical syndromes give rise to either a diagnostic histopathologic picture or a specific histopathologic pattern (the distinction between neutrophilic versus lymphocytic scarring alopecia informs treatment directed at a particular immune cell-i.e., dapsone for neutrophils or mycophenolate mofetil for lymphocytes).
If a primary medical illness is suspected, or to rule out common causes of medically related hair loss or exacerbation of hair loss, consider ordering a complete blood count (to look for anemia), iron studies (iron level, transferring, ferritin, and iron saturation levels), thyroid-stimulating hormone, thyroxine, and vitamin D (25-hydroxy). See the Table, Primary Hair Disorders.
Primary Hair Disorders
|Diagnosis||Key clinical features||Pathophysiology||Diagnostic findings||Treatment|
|Androgenetic alopecia||Gradual hair loss on vertex and parietal scalp, typically spares the frontal hair line in women||Hormonal||No scarring present Miniaturized hairs||Minoxidil 5% solution, foam Finasteride 1 mg p.o. daily (for healthy men and in women who are not of child-bearing potential)|
|Alopecia areata||Coin-shaped (nummular) patches of non-inflammatory hair loss; exclamation hairs; may involve the entire scalp (totalis) or body (universalis)||Likely autoimmune; often associated with autoimmune or autoinflammatory medical conditions (such as autoimmune thyroid disease)||Lymphocytic non-scarring alopecia, with collections of lymphocytes at terminal hair follicles||Intralesional triamcinolone 10mg/cc for isolated lesions PUVA Anthralin Topical immunotherapy (such as DCNB)|
|Telogen effluvium||Rapid onset of diffuse, non-inflammatory hair loss, usually 2-3 months following medical illness, injury, giving birth, or stress||Metabolic||Shift in ratio to mostly telogen and catagen hairs with premature termination of anagen follicles||Spontaneous recovery over 6 months|
|Anagen effluvium||Rapid onset of non-inflammatory hair loss, usually <1 month following cancer chemotherapy or treatment with antimetabolites||Toxin-mediated due to anti-proliferative medications or anti-metabolites In rare cases associated with pemphigus vulgaris||Fragmented hair in hair follicle, tapered structure of hair shaft, damaged hair matrix||Spontaneous recovery over 6 months|
|Trichotillomania||Asymmetric, jagged, or scattered areas of inconsistent hair loss; eyelid margins are common site of involvement||Due to patient pulling out hair||Broken hairs, hair casts (trichomalacia), empty hair follicles, evidence of peri-follicular hemorrhage or inflammation||Discontinue hair pulling, counseling|
|Neutrophilic scarring alopecia||Due to scalp inflammation Types: tufted folliculitis, folliculitis decalvans, dissecting cellulitis of the scalp, dermatophytic folliculitis||Scalp inflammation by either neutrophils results in scarring and fibrosis, with elimination of hair follicles||Scarring and fibrosis accompanied by elimination of hair follicles and neutrophil-predominant inflammation||Neutrophilic: dapsone, colchicine, isotretinoin|
|Lymphocytic scarring alopecia||Due to scalp inflammation Types: lichen planus pilaris, lupus, pseudopelade, frontal fibrosing, central centrifugal cicatricial alopecia||Scalp inflammation by either neutrophils results in scarring and fibrosis, with elimination of hair follicles||Scarring and fibrosis accompanied by elimination of hair follicles and lymphocytic-predominant inflammation||Lymphocytic: hydroxychloroquine, cyclosporine, mycophenolate mofetil|
|Traction alopecia||Slightly controversial diagnosis, typically affects sites of hair in which hair-styling practices results in traction||May be due to prolonged, intense pulling on the hair due to hair styling practices||Typically no inflammation||Discontinue prolonged traction on hair|
|Hair shaft abnormality||Presents in childhood with inability to grow hair of significant length or at all; glistening or speckled hair shafts may be noted||Due to hair shaft abnormality||Hair mount is usually diagnostic, revealing abnormal hair shaft anatomy||None|
First-line treatment strongly depends on the type of hair loss. Specific pharmacologic treatments are discussed below for the two most common causes of alopecia: androgenetic alopecia and alopecia areata.
- In all cases of hair loss, no matter what the cause, the value of cosmetic camouflage of hair loss should not be underestimated. A number of highly cosmetically elegant camouflages for hair loss are now widely available, including wigs, hair extensions, and powder- or spray-based pigment to minimize the appearance of exposed scalp.
- Counseling regarding the natural history of the disease and treatment course, as well as acknowledgement of the significant impact of alopecia on quality of life are essential components to the therapeutic relationship between doctor and patient.
If the diagnosis is not clear or if not responding to treatment, consider a scalp biopsy.
- Topical minoxidil (2% solution or 5% solution or foam, such as generic minoxidil or Rogaine). Typically, 2% solution is used for females and 5% for males. Minoxidil should be applied daily or b.i.d. directly to dry scalp. An eczematous reaction or irritant dermatitis may complicate therapy and can be alleviated by application of a topical corticosteroid, such as triamcinolone 0.1% lotion. Hypertrichosis of other areas of the body, typically the face, may also occur but does not necessitate discontinuing the medication. In men with early vertex hair loss, acceptable cosmetic hair growth occurs in only one-third to one-half of patients by 4-8 months. Frontal-bitemporal recession often fails to respond. Therapy must be continued or hair loss recurs.
- Finasteride (1 mg tablet taken daily, such as Propecia), 1 mg tablet daily. In male patients, a family or personal history of prostate cancer should prompt further discussion and possible urologic consultation. Prostate-specific antigen levels are significantly reduced (up to 50%) by the administration of finasteride. This medication may also result in loss of libido, impotence, or ejaculation failure, and patients should be appropriately warned of this potential, reversible side effect. Finasteride should only be used in healthy males and in women who are not of childbearing potential.
- Hair transplantation is an excellent therapy in appropriate patients and can often be combined with surgical scalp reduction. Although simultaneous minoxidil therapy to prevent future hair loss is recommended by some, it is not of proven benefit.
- Rule out androgen excess syndromes in women. The patient may have adrenal or ovarian cysts or tumors.
Limited hair loss
- No treatment may be required, as spontaneous regrowth is common in 2-6 months.
- If treatment is instituted, an intralesional injection of corticosteroids may be of value. Inject lesions with triamcinolone 2.5-10 mg/cc and if necessary repeat treatment every 4-6 weeks. Corticosteroid injections may cause focal reversible scalp depressions.
- Intralesional corticosteroid injections are not practical for patients with alopecia totalis, but may be used in this setting to induce hair growth in cosmetically important areas, such as the eyebrows.
Extensive hair loss
- A reliable, standard therapy is not available.
- Application of minoxidil 2% or 5% solution or foam q.d. or b.i.d. may be attempted, but efficacy has not been ascertained.
- Anthralin-induced irritant dermatitis or contact allergen application may be efficacious. The most frequently studied contact allergen sensitizer is dichloronitrobenzene (DCNB); squaric acid dibutyl ester, another potent topical allergen that may be used and has the theoretical advantage that it is not a mutagen. Referral to a dermatology provider or a person experienced in anthralin or contact allergen application protocols is strongly recommended.
- Corticosteroid injections may cause focal reversible scalp depressions, and has been reported to cause blindness in rare cases.
- Systemic steroids induce hair growth in patients with extensive alopecia areata, but such therapy is not recommended. High doses are usually required, and hair loss recurs after steroid discontinuation. The complications of long-term, high-dose steroid therapy are not justified.
- Alopecia areata is infrequently associated with other autoimmune disorders, including thyroid disease, vitiligo, pernicious anemia, and Addison’s disease.
- Contact dermatitis therapy may cause widespread dermatitis and lymphadenopathy.
When to refer to a dermatologist
- When the diagnosis of alopecia or its underlying cause is not clear.
- When a scalp biopsy is necessary.
- When alopecia is not responding to standard first-line therapy.
- For anthralin-induced irritant dermatitis or contact allergen based therapies for treatment of widespread alopecia areata.
- 8-year-old healthy girl with a two-year history of hair loss
- Irregular, jagged and scattered patches of hair loss on the scalp; no eyelashes
- Parents note that hair loss started when the family moved to a new state and describe a difficult, ongoing transition to their new home
- No biopsy is indicated; on further questioning, the parents admit that they have noticed their daughter pulling at her hair, especially the eyelashes, when stressed; a diagnosis of trichotillomania is highly likely
- Reassurance is given; the hair growth is likely fully reversible; a long discussion regarding strategies to modify hair-pulling triggered by stressors; patient and family are given referral to family counseling
- Follow-up in 3 months
- Hair-pulling is ongoing, but several areas of prior alopecia now have full regrowth
- Reassurance is emphasized; continuation of family counseling is encouraged
- 16-year-old healthy boy with sudden onset of asymptomatic hair loss in patchy areas on the scalp vertex
- No family history of autoimmune disease, including vitiligo or autoimmune thyroiditis
- Review of systems does not reveal evidence of hair-pulling, nutritional deficiency, infection, or endocrine disease
- Physical exam reveals perfectly round (nummular) patches of complete, non-scarring hair loss; no evidence of scalp erythema or inflammation; a hair-pull test, pulling 20 hairs from the base of the hair, reveals 12 hairs
- No biopsy is necessary; a clinical diagnosis of alopecia areata is given
- After discussion of treatment options, the patient decides to proceed with intralesional corticosteroid injections and triamcinolone 10 mg/cc is injected in 0.1 cc bolus to the dermis in affected areas (3 injections given to each approximately 2×2 cm patch); the procedure is well tolerated
1-month follow-up evaluation
- Partial regrowth of hair in the injected areas
- No new lesions noted on full body exam
- Additional intralesional triamcinolone 10 mg/cc is given to areas of persistent alopecia
- Follow-up in 1 month (resolved, no new lesions)
- 54-year-old perimenopausal woman with a 6-month history of gradual hair loss at parietal scalp
- A full history is performed; no other medical problems or medications
- Review of systems does not reveal any evidence of hyperandrogenism or virilization, endocrine disease, nutritional deficiency, or anemia
- A family history is notable for “male pattern baldness” in several male siblings, her father, and her mother
- A scalp examination is performed; there is almost 50% reduction in hair density in the frontal and parietal scalp, with relative preservation of the frontal hairline and no evidence of scalp inflammation or scarring; a hair-pull test of 20 hairs reveals 5 terminal hairs.
- A diagnosis of androgenetic alopecia is likely, supported by her history, family history, and physical exam.
- It is not clear whether there are additional medical comorbidities that may be exacerbating disease; a complete blood count (for anemia), iron studies, TSH, T4, and 25-OH vitamin D are tested; diagnostic evaluation for hyperandrogenism is not warranted given that she does not endorse any other manifestations of hyperandrogenism or virilization
- A skin biopsy is offered to the patient, which she accepts; she is highly-motivated to confirm the diagnosis of androgenetic alopecia; a 4 mm punch biopsy of the affected area of alopecia is performed
- Follow-up evaluation and suture removal in 2 weeks
2-week follow-up evaluation
- A scalp biopsy demonstrates miniaturization of hair follicles consistent with androgenetic alopecia, without any other evidence of inflammation
- The natural history of androgenetic alopecia, treatment options, and expectations for treatment is discussed; cosmetic camouflage strategies are also discussed
- Patient decides to start minoxidil 2% solution daily application
- All lab testing was normal
6-month follow-up evaluation
- Significant hair regrowth is noted in previously affected areas
- No adverse side effects are noted
- The patient is encouraged to continue ongoing application of minoxidil
Alkhalifah, A et al (2010) Alopecia Areata update: part I and II. J Am Acad Derm, 62: 177-202.
Hillmann, K and Blume-Peytavi, U (2009) Diagnosis of hair disorders. Semin Cutan Med Surg, 28:33-38.
Mirmirani, P, Huang, KP, and Price, VH (2011) A practical, algorithmic approach to diagnosing hair shaft disorders, Int J Dermatol, 50:1-12.
Rulon, E and Safranek, S (2009) What is the best diagnostic approach to alopecia in women? J Fam Prac, 58:378-379.