By Gary M. White, MD
Alopecia areata [AA] is a common cause in children and young adults of the loss of circular patches of hair. It represent an attack on the hair roots by the body's own immune system. See also gallery, alopecia universalis and AA of the eyelashes.
Alopecia areata typically presents with round, bald spots on the scalp. The beard, eyebrows, or eyelashes may be affected but it is unusual for isolated lesions elsewhere on the body. One or more may be present at any one time. The exclamation point hair is characteristic and appears as a short terminal hair, tapered at the proximal end. There is no scarring, scale, or other alteration of the scalp skin.
The follicular openings are not lost in contrast to a scarring alopecia.
Patients may rarely go on to lose extensive amounts of hair of the scalp and body, but again, this is unusual. Most patients regrow their hair. The term alopecia totalis refers to patients who have lost all of their scalp hair. The term alopecia universalis (AU) refers to patients who have lost all hair on the scalp and body.
A new subtype of AA called "acute diffuse and total alopecia of the female scalp" has been described where the woman suffers complete hair loss within one month of presentation. The histology is that of AA except for a significant eosinophilic tissue infiltrate. Fortunately, the vast majority of these women do well with cosmetically acceptable hair regrowth at six months with or without steroid administration.
Deficient serum 25(OH)D levels are present in patients with alopecia areata and inversely correlate with disease severity. Thus, screening patients and supplementing, if indicated, seems prudent [BJD 2014;170;1299–304]. It would also be reasonable to screen patients for iron and zinc deficiency and supplement as appropriate[J Drugs Dermatol 2016;15;1235].
|Age of Onset||Associated Disease|
|< 10 years||atopic dermatitis, lupus|
|11-20 years||psoriasis, rheumatoid arthritis|
|21-60 years||atopic and autoimmune diseases|
|> 60 years||thyroid disease|
|All ages||anxiety, depression, and obsessive compulsive disorders|
Sporadic cases of alopecia areata developing during anti-TNF-α therapy have been reported [J Am Acad Dermatol. 2014;70:1146]. One third of the cases had a positive (personal or family) history of AA. Most of them presented with rapid extensive AA, usually involving the ophiasis area. Prognosis was usually poor, with slight response to treatments. In the cases where anti-TNF-α therapy was maintained, the course did not seem to change.
Alopecia areata need not be treated as it is a benign condition and regrowth is typical. In fact, spontaneous remission occurs in up to 80% of patients with limited disease within a year. However, it often causes great embarrassment and thus therapy is often desired to speed regrowth.
Individual lesions may be injected with Kenalog every month. This usually induces hair regrowth for isolated areas although atrophy of the skin may occur. The injection should be done into the deep dermal/upper subcutaneous plane using a 30 gauge needle. One may cover several square centimeters of skin with one injection point by fanning out in various directions with the needle and injecting while with drawing. This helps distribute the medication more evenly than multiple small injection points. The maximum dose often cited is 20 mg per month, e.g., 8 cc of 2.5 mg/cc. In a DBPCT comparing injection with 2.5, 5, and 10 mg/cc in AA of < 50% of the scalp, the 2.5 mg/cc concentration was just as effective as the 5 and 10 [JAAD 2015;73;338].
Any AA patient may benefit from a class I topical steroid for several months, although the area should be monitored for the development of atrophy. For example, topical clobetasol (given as a foam) grew modestly more hair than placebo in a DBPC trial.
Some use fexofenadine 120-180 mg/day for adults either as monotherapy or as an adjunct for other therapies. In a retrospecive study of extensive alopecia treated with contact immunotherapy, the mean regrowth score of the fexofenadine group was 1.33 and that of the control 0.47 [J Dermatol. 2009 Jun;36(6):323-7].
Minoxidil 5% is recommended by many, but its use is off-label in the US. In one study, topical minoxidil applied BID and nightly occluded with petrolatum for 1 year outperformed placebo modestly.
A study in which 30 patients applied mometasone cream QD or bimatoprost 0.03% solution (Lumigan, Allergan, 3 ml) BID to two separate patches of AA found that bimatoprost grew hair sooner and better than mometasone [Dermatology 2015;230:308-313].
Systemic steroids are usually only considered for extensive disease because of potential side effects. In one study, pulse oral prednisone 300 mg every 4 weeks was used. Otherwise, one may give the steroid daily orally and taper to the lowest effective dose. Alternatively, Kenalog 60 mg IM monthly x 3 may be tried but no more should be given and the patient risks the hair falling out once treatment is stopped.
In a small study, 14 patients with alopecia universalis were treated with azathioprine 2.5 mg/kg/day. Forty-three percent achieved complete regrowth at a mean of 4.7 months [JAAD 2016;74;1007].
Methotrexate has been used with benefit for AA in several small series of patients. It is usually combined with IL or oral steroids--often the steroids are given early and then the patient treated with methotrexate alone or in combination with topical minoxidil. Hammerschmidt and Brenner reviewed treatment of 31 patients and found regrowth greater than 50% was observed in 67.7% of patients, with the best responses observed in those with <5 years of disease progression (79%), age over 40 years (73.3%), male patients (72.8%), cumulative dose of methotrexate 1000-1500 mg, and multifocal alopecia areata (93%) [An. Bras. Dermatol 89;5;Sept./Oct. 201].
Topical immunotherapy with diphenylcyclopropenone (DPCP) and anthralin of 25 patients with severe AA resulted in complete regrowth of hair in 72% [JAAD 2015;72;640].
The topical application of squaric acid dibutylester (SAD) induces an allergic contact dermatitis and can grow hair both in adults and children. Various protocols exist, but one common approach is to first do an application on the arm to induce sensitivity and then one month later, start topical application of 5% SAD on the affected areas of the scalp. Patients return monthly to monitor progress and for reapplication of the 5% if the hair is regrowing. If there is too much reaction (e.g., burning, blistering), the concentration is reduced to 2.5%. If no hair is growing, then the concentration can be increased to 10%.
Inducing an irritant contact dermatitis can sometimes cause regrowth. Typically, one has the patient apply 1% anthralin for 1 hour and then wash off. The main side effect is irritation, but that is the goal. Rarely, there can be facial edema, vesicles, blisters, etc., if the reaction is too severe.
Ninety patients with severe AA were treated with tofacitinib 5 mg BID for 2-3 months initially. Then, non-responders were eligible for pulse prednisone or higher doses of tofacitinib [JAAD 2017;76;22]. Seventy-seven percent achieved a clinical response, with 58% achieving a greater than 50% improvement in SALT score over 4-18 months. There were no serious adverse events.
68% (9/13) pediatric patients with severe AA experienced clinically significant regrowth of hair in a study using tofacitinib (5 mg BID x 5 months) [JAAD 2017;76;29]. Most of the patients studied had either alopecia universalis or totalis. No serious side effects were reported.
Oral ruxolitinib (a JAK1 and JAK2 blocker) led to almost complete hair regrowth in 3 AA patients in 5 months [Nature Med 2014;20;1043-9]. In another study, 9/12 patients achieved at least 50% regrowth most by 6 months [JCI Insight 2016;1(15);e89790]. Also see Ruxolitinib-induced reversal of alopecia universalis in a patient with essential thrombocythemia [Am J Hematol. 2015 Jan;90(1):82-3].
A wig or hair piece may be needed for more extensive disease. Patients with more diffuse hair loss, e.g., alopecia totalis or universalis, may desire more aggressive therapy. IM triamcinolone 40-60 mg or a tapering course of systemic steroids may be tried although controlled studies are lacking. Cyclosporin has been tried. Topical immunotherapy, with e.g., phenol, has been reported.
Adalimumab did not help AA in one report but did in another [JAMA Derm 2014;150;1341]. Apremilast did not help 9 patients with severe AA [JAAD 2017;77;773].
Treatment with Platelet-rich plasma (PRP) was studied in 45 patients with AA [BJD 2013;169;690]. IL PRP grew more hair than IL triamcinolone 2.5 mg/cc or placebo without significant side effects. The PRP was prepared by drawing the patient's blood, centrifuging it for 8 minutes at 70 "g"s, and separating the PRP fraction.
One may use IL triamcinolone 2.5 mg/cc Q month, but the patient must accept the rare risk of ocular complications. For example, IL Kenalog 40 mg for vitiligo of the forehead (a much higher dose than would be used for AA) caused immediate stroke and blindness in a 15-year-old boy [Indian J Dermatol Venereol Leprol 2014;80:177]. One patient of mine who had not had eyebrows for 20 years developed reasonable regrowth after several injections.
IL triamcinolone 2.5 mg/cc may be injected every cm--about 0.1 cc per injection. When the patient returns often there is regrowth in tufts. One can then inject in between the tufts.
Exclamation point hairs may be seen.
Hair growing in white.
Alopecia areata of the eyebrows and eyelashes.
Rarely, AA may affect the legs in isolated spots.
This author has seen several circular lesions of AA centered about a benign nevus. The mole shown here proved to be a benign congenital nevus on biopsy. The same patient presented two years later with another area of AA centered about another nevus on the scalp. Is the association a coincidence or halo phenomenon?
For more pictures of alopecia areata, see gallery.
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