Hair loss is a common complaint — usually benign, sometimes serious, and invariably distressing. Even if the loss is minimal, patients are afraid they’ll go bald. The differential is full of obscure entities that only a dermatologist can diagnose, but the most common causes can be identified in primary care.
Begin with two main distinguishers:
- Examine the scalp — Is there skin disease or not?
- Is the hair loss diffuse or focal?
HAIR LOSS — DIFFERENTIAL DIAGNOSIS
No Scalp Disease
Scalp Involvement Present
Click link for a few Pictures; then you can toggle back & forth as you read.
NORMAL SCALP (Non-Scarring Hair Loss)
Most patients with hair loss do not have scalp conditions. Their skin is completely normal. This is also called “non-cicatricial alopecia” in contrast to “cicatricial” (i.e “scarring” or involvement of skin).
First Step — Determine if the loss is diffuse or not, by seeking focal patches of complete (or nearly-complete) baldness. Ask the patient where they’re losing hair. If it’s all coming from one spot, they can often show you.
Focal Hair Loss
** Alopecia Areata — Presents as one or more patches of complete baldness surrounded by normal hair. This is usually a stand-alone autoimmune disease, but may be a manifestation of Lupus (SLE). Inquire about other possible SLE symptoms. Order an ANA and an RPR.
A positive RPR might mean patchy hair loss due to 2° Syphilis, but might be a biologic false-positive common in SLE. The treponemal confirmatory test usually distinguishes, unless the person had syphilis in the past. Biologic false-positives are usually low-titer (≤1:8); 2° Syphilis titers are very high (see posting on labs for Syphilis).
Send Alopecia Areata to Derm, unless you know how to inject the area with steroids & follow progression. Focal disease can advance to Alopecia Totalis (complete baldness), or rarely even Alopecia Universalis (loss of all body hair).
Other conditions cause focal hair in specific areas.
** Male-Pattern Hair Loss begins at the temples, mid-frontal area, or the vertex. A receding hairline might progress, but often won’t. We speak of male-pattern hair loss as focal, in that the entire scalp isn’t affected all at once. Actually, the more politically-correct term is “androgenetic alopecia,” but then you have to specify “in men,” since androgenetic alopecia presents more diffusely in women (see below).
** Traction Alopecia — Hair loss caused by specific styling that requires traction, including ponytails and other. This is usually evident from exam, as long as you think about it. Treatment means changing one’s hair style; I always apologize when I discuss this, since I don’t like intruding on another beholder’s sense of beauty. But it’s important to educate as to bare facts, since long-standing traction alopecia can become permanent.
Heat and chemicals can break hairs, which patients sometimes incorrectly perceive as hair loss. Education here is the same.
** Tricotillomania — A nervous tic leading persons to twist or yank at their hair. The pattern of loss can be patchy, diffuse, or simply weird. Some sufferers have insight, and endorse the “bad habit.” Others are oblivious, deny, or conceal, which makes diagnosis harder. Patches of hair loss aren’t completely bald (as in Alopecia Areata), and hairs are broken off at different lengths. Hair loss can become permanent. Treatment ranges from education to cognitive behavioral therapy to SSRI’s.
Diffuse Hair Loss
** Telogen Effluvium — This is the most common cause of hair loss. It may involve from 5% to 15% of hairs. Upon close examination, the patient’s overall hair seems to be thinning. Casual observers rarely notice. Patients themselves see large quantities of hair falling when they comb or brush, & are scared to death.
Activity of each hair follicle progresses through 2 main phases:
- Anagen: Hair strand grows continuously for 3-6 years (~90% of hairs)
- Telogen: Resting phase lasting 1-6 months (~10% of hairs)
The hair is shed at the end of Telogen, and Anagen resumes with a new strand. At birth, follicles gradually begin their activity, cycles are not synchronous, so Telogen hairs don’t all fall out together. However, various physical or psychological stressors can cause many follicles to suddenly enter Telogen at once.
Inciting events can include significant illness, surgery, injury, labor and delivery, severe weight loss, and major psychological trauma. I’ve had two friends experienced this upon leaving home. New medications may be another possibility; there’s no good data, but those implicated have included beta-blockers, anticoagulants, retinoids, propylthiouracil, carbamazepine, and immunizations.
Telogen Effluvium occurs 1 to 6 months after its cause. It usually resolves within 6 months. A chronic form of the condition can persist longer, manifested by ongoing diffuse hair thinning, but not total baldness. This is much less common.
Diagnosis is clinical: Diffuse, non-focal hair loss without any evidence of scalp disease. It’s nice if you can identify an inciting event. Dermatologists have a variety of diagnostic tricks involving pulling out hairs, but I don’t refer these patients. I might order a TSH, CBC, and ferritin, & rule out other possibilities by history.
Even if I can’t pinpoint the trigger, I reassure patients that:
- Most people aren’t able to notice;
- Nobody becomes totally bald; and
- Hair will grow back normally within 6 months. If not, I send to Derm [have never had to].
The main condition mimicking Telogen Effluvium is Female-Pattern Hair Loss.
** Female Pattern Hair Loss — Physiologic hair loss, presumably with some level of genetic etiology, is not uncommon among Caucasian women. It manifests as gradual progression of diffuse hair thinning, that doesn’t advance to baldness as in men. The hairline and occiput are usually less affected. Primarily begins after menopause, though not necessarily. The condition is also termed “androgenetic alopecia in women,” which sounds fancier but contributes little understanding since hormones are not convincingly causal.
Female-Pattern [physiologic] hair loss is distinguished primarily from Telogen Effluvium by a more insidious onset, & no history of inciting event several months prior. Sometimes an episode of the latter unmasks the former. Rule out more focal causes of hair loss noted above by their locations. Scalp skin is of course normal.
The main reason to refer to dermatology is for psychological reasons. Women in our society are much more impacted by physiologic hair loss than men. If hair loss is affecting quality of life, dermatologists begin with a trial of topical minoxidil. Just be sure it’s applied to scalp (not the hair), and at least 2 hours before bedtime so it dries in time to not spread during sleep (& induce unwanted hair growth elsewhere).
** Other — Rarely will any other occult condition be responsible for diffuse, non-scarring hair loss. Thyroid diseases invariably present with other symptoms. Vitamin A toxicity can be suspected by history of dietary extreme (particularly excessive carrot juice, which also turns skin orange-color). Iron deficiency as a cause of hair loss is controversial. Selenium toxicity only occurs in the setting of pharmacologic overdosing [vitamin faddists].
Zinc deficiency might be considered in the debilitated, perhaps the elderly without adequate food access, and persons with cirrhosis or chronic pancreatitis. It can be exacerbated by diuretics and ACE-Inhibitors. Diagnose by empiric supplementation; serum zinc testing is unreliable.
Acute thallium poisoning causes immediate GI symptoms, then rapidly progressive hair loss at 2-3 weeks after ingestion, with associated painful ascending peripheral neuropathy. Call poison control if suspicious. Diagnose this, & you’ll get hired as consultant for TV crime shows.
We often order a CBC, TSH, and serum ferritin in the work-up. Patients are pleased. The yield is invariable zero.
Various cancer chemotherapies cause arrest of anagen hair growth, resulting in rapid massive hair loss. Diagnosis should be obvious from history. If this occurs on its own, consider thallium, boron, or arsenic poisoning. Consult dermatology, local Poison Control, or police.
SCALP DISEASE PRESENT (Scarring Alopecia)
** Tinea Capitus — In developed countries, this is virtually only seen in children; doubt the diagnosis if you entertain it for an adult. Scalp lesions are round with scaly plaque. Tinea’s typical “leading edge” confirms the diagnosis. Sometimes black dots can be seen in the empty hair follicles. Occipital nodes are not uncommon. When it presents as a soft, boggy nodule covered with exudate, it’s called a kerion.
** Seborrheic Dermatitis & Psoriasis — Both these conditions involve the hairline, and may extend further backwards into the scalp. Both are scaly. Distinguish them as follows:
- Seborrheic Derm is greasy / Psoriatic scales are silvery-white
- Seborrheic Derm often descends to the eyebrows & cheeks
- Psoriasis may be found elsewhere, typically extensor elbows, knees, heels, sacrum
Though both may be treated with topical steroids, Seb Derm is often responsive to topical anti-fungals. Also, anybody with extensive Seborrheic Dermatitis (more than simple dandruff) should be tested for HIV.
** Folliculitis / Cellulitis — Bacterial scalp infections can certainly cause hair loss. Treatment is for Staph aureus, which nowadays means MRSA in many parts of the country. Since many unusual dermatologic conditions resemble Staph to the non-specialist, if resolution isn’t apparent within a few days, stop the antibiotic and refer to Dermatology.
** Discoid Lupus — An autoimmune condition that may be stand-alone, or less-commonly as a manifestation of Systemic Lupus (SLE). It presents as patchy hair loss with reddish, scaly scalp plaques. It’s easily differentiated from Alopecia Areata and 2° Syphilis, because neither of the latter cause skin changes. If I suspect Discoid Lupus, I usually query about other symptoms of SLE, draw an ANA, and send to Derm. If the ANA is high (≥1:320), or I suspect SLE from history, I also send to Rheum.
** Numerous Conditions Requiring Dermatologic Evaluation — Lots of obscure conditions cause scarring (aka cicatricial) alopecia. When I see hair loss with skin involvement of the scalp, & don’t really think it fits with any of the few above conditions described, I refer to Derm. That’s especially so because most of those conditions don’t have effective treatment; in my opinion, anyone with a disfiguring or disabling condition that can’t be treated, even if I can identify it, should usually see a specialist.
SUMMARY APPROACH TO “HAIR LOSS”
1. Determine if there’s Skin Disease of the scalp
Normal Scalp: Determine if hair Loss is Diffuse or FocalIf Diffuse Hair Thinning:
- “Inciting Event” 1-6 months prior → Telogen Effluvium
- Abrupt onset w/o “inciting event” → Telogen Effluvium
- Post-menopausal woman, insidious onset → Female-pattern Hair Loss
- History of hair pulling/twisting → Tricotillomania
- Seek history compatible w/ Vitamin A toxicity
- Obtain CBC, TSH, serum ferritin
- If debilitated, alcoholic, cirrhotic → empiric trial of Multivitamins
- If diffuse complete hair loss → refer to Derm
Patches of near-complete baldness → Alopecia AreataHair Style suggests traction → Traction Alopecia
- Obtain RPR (→ Syphilis) and ANA (→ consider SLE)
- History of hair pulling/twisting → Tricotillomania
- Man with insidious onset hair loss → Male-pattern Baldness
Skin Involvement of Scalp (scarring alopecia)Consider some Common Diagnoses
- Child w/ round scaly plaque → Tinea Capitus
- Scales along hairline → Seborrheic Dermatitis / Psoriasis
- Discrete erythema/pustules of follicles → Folliculitis
- Patch of diffuse erythema → Cellulitis
- Red, scaly patches → Discoid Lupus
- None of Above → Refer to Derm
- Treatment of above not helpful → Refer to Derm
If you haven’t clicked the link for Pictures yet, try it now. And that’s it for the various causes of Alopecia; hope the topic wasn’t too hairy.