Patchy hair loss on 
a bearded chin - Clinical Advisor

Patchy hair loss on 
a bearded chin

Slideshow

  • August 2014 CME/CE

    0814CA_DermClinic

    August 2014 CME/CE

By Esther Stern, NP-C

A 27-year-old man presented to the office complaining of a sudden onset of patchy hair loss in his beard. He noted that the area of hair loss appeared to be slowly enlarging. He denied any itching or pain in the area.

His medical history was unremarkable, and he did not take any medications.

There was no family history of alopecia or thyroid disease. Physical exam revealed 3 distinct patches of hair loss on the chin with “exclamation-point” hairs in the center.

There was no evidence of perifollicular erythema or scarring. Exam of the nails was also unremarkable.



This Clinical Advisor CME activity consists of 3 articles. To obtain credit, you must also read Solitary plaque on dorsal hand and Long-term scaly skin
. Then take the post-test here.


Alopecia areata (AA) is a form of nonscarring hair loss that can occur on the scalp or on any other hair-bearing area of the skin. It is believed to be a T-cell-mediated autoimmune condition, with autoantibodies attacking the anagen-phase hair...

Submit your diagnosis to see full explanation.

Alopecia areata (AA) is a form of nonscarring hair loss that can occur on the scalp or on any other hair-bearing area of the skin. It is believed to be a T-cell-mediated autoimmune condition, with autoantibodies attacking the anagen-phase hair follicle.

AA is often associated with other autoimmune conditions, such as thyroid disease, lupus, diabetes, atopy, and vitiligo. There also appears to be a genetic component to AA, as evidenced by the fact that multiple members of the same family are often affected.


AA occurs fairly commonly, striking up to 2% of the population, including an estimated 6.5 million people in the United States.1Men and women are equally affected by this form of hair loss.

The 3 subtypes of AA are AA with variable patchy hair loss; AA totalis, with loss of all scalp hair; and AA universalis, with loss of all hair on the scalp and body.

Falling under the subtype of AA with variable patchy hair loss are the two unique patterns of AA of the scalp, both of which occur infrequently:

The ophiasis type presents with alopecia localized to the temporal and occipital scalp, whereas the sisaipho type presents with alopecia that specifically spares the temporal and occipital scalp. (“Sisaipho” is nearly “ophiasis” spelled backward and is so named because this pattern of hair loss has an inverse appearance to the ophiasis pattern of hair loss.) 


Physical examination of a patient with AA reveals single or multiple oval or round well-demarcated areas of hair loss with no signs of scarring, scaling, or inflammation. The short, tapered hairs that are known as exclamation-point hairs are often seen at the periphery of the lesion and aid in the diagnosis.

A positive hair-pull test done at the periphery of the patch indicates that the disease is still active and will likely progress. In 10% to 20% of AA cases,2the person’s nails are affected with superficial pitting and, less commonly, with trachyonychia, Beau’s lines, koilonychia, or leukonychia.

Diagnosis of AA is usually straightforward and based on physical examination findings. However, if the diagnosis is doubtful, a biopsy is beneficial. Typical histopathologic exam in the acute phase of AA shows a peribulbar lymphocytic infiltrate.


AA has a variable prognosis. Spontaneous improvement may occur in all forms of AA, but recurrences are also possible. One study showed that more severe disease carried a poorer prognosis and good response to treatment was correlated with a better prognosis.3In addition, children typically had a worse outcome. Although AA is a benign condition and usually asymptomatic, clinicians need to be aware of the severe psychological impact the disease can have.

There are no FDA-approved treatment options specific to AA but several options have been shown to be beneficial, although responses are variable and unpredictable. Patients need to be informed that treatments are not curative but rather are attempts to induce hair growth during periods of disease activity.


Intralesional triamcinolone injections administered every 4 to 6 weeks may be helpful in stimulating hair regrowth in mild, patchy hair loss. Unfortunately, this therapy does not prevent new areas of hair loss. Typically, a concentration of 2.5 mg/mL to 5 mg/mL is injected intradermally for facial hairs; a concentration of 5 mg/mL to 10 mg/mL is usually necessary for the scalp. 


Such topical high-potency steroids as clobetasol propionate, applied under occlusion, also offer some, but more limited, benefit. Therefore, these agents should be reserved for specific patients who cannot tolerate injections, such as younger children.


A 5% solution of topical minoxidil applied twice daily also has been shown to be helpful in limited disease. Although its exact mechanism of action is unknown, the solution is thought to signal the follicle to resume normal cyclical activity. This treatment is usually best started in conjunction with other therapies, such as intralesional triamcinolone or topical anthralin.


Topical anthralin has been enlisted in the treatment of AA by inducing dermatitis. As Keen and Majid reported, the exact mechanism of action is unknown, but it is thought that the resulting inflammation may produce free radicals, which have immunosuppressive benefits.4

An 8-to 12-week regimen in which the person with AA applies topical anthralin every day, leaving it in place for 30 to 60 minutes before rinsing it off, may be used to promote hair regrowth. However, the use of topical anthralin is limited by associated side effects such as skin irritation, folliculitis, and skin staining.

Oral corticosteroids are often successful at promoting hair growth. However, due to the adverse effects of these drugs and because the benefit is quickly lost when the medication is stopped, this treatment should only be used in rare circumstances when an immediate short-term benefit is needed. 


In more severe cases of AA, the clinician may want to discuss with the patient the two very different options of wearing a wig to hide the effects of the disease versus seeking expert consultation to attempt experimental topical immunotherapy with squaric acid dibutylester (SADBE) and diphencyprone (DPCP). SADBE and DPCP are thought to induce hair growth by somehow circumventing the aborted hair cycle. 


Other infrequently used treatments for AA include psoralen plus ultraviolet-A light therapy, cyclosporine, and methotrexate.


The patient in this case was counseled regarding the unpredictable prognosis of AA. After extensive review of the various therapeutic options available to him, the patient ultimately underwent treatment with monthly injections of intralesional triamcinolone at a concentration of 5 mg/mL.

In addition, the patient applied topical minoxidil every day between visits. 
After three months of treatment, the condition had improved overall by 80%. 


Esther Stern,NP-C is a family nurse practitioner at Advanced Dermatology & Skin Surgery, P.C., in Lakewood, N.J.



This Clinical Advisor CME activity consists of 3 articles. To obtain credit, you must also read Solitary plaque on dorsal hand and Long-term scaly skin
. Then take the post-test here.


References


  1. About Alopecia Areata. National Alopecia Areata Foundation website. www.naaf.org/site/PageServer?pagename=about_alopecia_intro.
  2. Paller AS, Mancini AJ. Disorders of hair and nails. In: Hurwitz Clinical Pediatric Dermatology: A Textbook of Skin Disorders of Childhood and Adolescence, 4th ed. Philadelphia, Pa: Elsevier Saunders; 2011:148-151.
  3. Tosti A, Bellavista S, Iorizzo M. Alopecia areata: A long-term follow-up study of 191 patients. J Am Acad Dermatol. 2006;55(3):438-441.
  4. Majid I, Keen A. Management of alopecia areata: an update. British Journal of Medical Practitioners (BJMP) . 2012;5[3]:a530. Available at www.bjmp.org/content/management-alopecia-areata-update

All electronic documents accessed August 6, 2014.


Next hm-slideshow in Clinical Quiz