14: Focal hair loss

Abstract:

Hair loss is divided into focal hair loss and diffuse hair loss. This chapter reviews common causes of focal hair loss, including alopecia areata, trichotillomania, discoid lupus, traction alopecia, and central centrifugal cicatricial alopecia.

Key terms:

alopecia areata

trichotillomania

discoid lupus

traction alopecia

central centrifugal cicatricial alopecia

folliculitis decalvans

Chapter outline

Alopecia Areata
Trichotillomania
Central Centrifugal Cicatricial Alopecia
Discoid Lupus (See Chapter 1, scalp dermatitis, DLE)
Traction Alopecia
Tinea Capitis (See Chapter 1 Scalp Dermatitis)

Alopecia areata

Rana Abdat

Clinical features

Alopecia areata (AA) is a common cause of hair loss that affects men and women equally and can affect patients of all ages.

• AA is the second most common cause of nonscarring hair loss after androgenetic alopecia (AGA; also known as “male/female pattern hair loss”).

• It is of unclear etiology but is thought to be immune mediated via loss of tolerance and has a link to other autoimmune diseases.
• This disease happens in all age groups but is more common in younger individuals.
• AA can affect any hair-bearing area, but the scalp is most commonly affected (Fig. 14.1).
- • Other affected areas include the eyebrows, facial hair (Fig. 14.2), and body hair.
• There are multiple different clinical subtypes. These include patchy, pattern, totalis, and universalis.

• Patchy is the most common subtype and involves one or more (typically annular) patches, which can present on any hair-bearing area.

• Pattern is less common but comes in many patterns, ranging from diffuse to ophiasis, sisiapho, and reticular.

• In totalis AA, all of the hair on the scalp is affected.

• In universalis AA, all of the hair on the body is affected.

• There may also be nail findings of AA, typically involving pitting.
• AA involves one or more painless patchy areas of hair loss, although white hairs may be spared and when new hair growth (short hair) is visible, it may also be white.
• The area of hair loss does not appear to be red or inflamed on a physical examination.
• AA typically presents as a sudden patch of hair loss on the scalp. The process is painless and noninflammatory.

• Patients often state, “I lost this patch of hair overnight.” The patient does not report clumps of hair coming out as is reported in telogen effluvium (TE).
• AA is an autoimmune disease, which is associated with other autoimmune diseases, including rheumatoid arthritis, vitiligo, and autoimmune thyroid disease.

• AA is also strongly associated with atopic dermatitis (AD).
• Because AA has a strong genetic component, it is important to ask about family history.
• As with all conditions, AA may exist within the context of other hair pathologies (i.e., a patient with AGA may have coexisting AA).
• Prognosis depends on age of first presentation (younger is worse) and extent of disease (more extensive is worse).
• About 50% of patients have hair regrowth without treatment within 1 year.

Differential diagnosis

The differential for AA includes tinea capitis, AGA, trichotillomania, TE, anagen effluvium, and psychogenic pseudoeffluvium.

• Tinea capitis, especially in children, can present as one or more patches of hair loss. It is distinguished from AA because tinea capitis has inflammation and scale. If the diagnosis is unclear, a fungal culture can differentiate between the two. Tinea capitis also resolves with antifungal treatment and has classic potassium hydroxide (KOH) of hair scraping, showing a hyphae (long) and yeast (round) with spaghetti (long) and meatball (round) appearance.
• AGA can coexists in middle-aged to older patients with AA where the patient will present with a new patch of hair loss in the background setting of AGA. Other subtypes of AA, including the diffuse subtype, can present with diffuse hair thinning and can be easily mistaken for AGA. Timing is very important here. AGA is a much slower process (years) compared with AA (days or weeks) and thus completing a patient history is critical before providing additional work-up. The pattern of hair loss (location on the head) is also important because AGA favors the frontotemporal and occipital areas.
• Trichotillomania, which commonly presents in children, is caused by obsessive hair pulling/twisting and can cause patchy hair loss, which resembles AA. Patients can be observed for hair-pulling behavior and there are various physical examination findings, including hairs of various different lengths and an abundance of split ends, which should raise suspicion. Trichotillomania often coexists with other psychiatric conditions, including obsessive-compulsive disorder (OCD).
• TE patients typically present with complaints of hair shedding in clumps. This type of hair loss is diffuse; therefore it should be easily distinguished from the classic patchy AA. Distinguishing between diffuse AA and TE can be very difficult and relies on biopsy findings or results of a modified hair wash test.
• Anagen effluvium is a form of diffuse hair loss that is triggered by chemotherapeutic-based destruction of hair follicles, leading to rapid, diffuse hair loss. Patient history is critical for establishing this diagnosis.
• Psychogenic pseudoeffluvium is another psychiatric-associated hair condition, and it occurs when patients are intentionally causing hair loss for secondary gain. This is usually discovered when work-up, including biopsy, is not revealing.

Work-up

Work-up for AA is divided into history taking, clinical examination, and laboratory work-up.

History taking

• Patients should specifically be queried about the duration of hair loss. When did it start? How long has it been happening?
• AA is a recurrent disease that can involve any area of hair, so asking about prior episodes or other affected areas is important. AA is an autoimmune disease, so asking if the patient has a history of another autoimmune disease, such as thyroid disease, systemic lupus erythematosus, or vitiligo, is important.
• Ask about any treatments and their effects and inquire about a family history of AA.