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Pratique clinique Clinical Practice

CAN YOU IDENTIFY THIS CONDITION?

A

n 11-year-old boy presented with patches of hair loss on his scalp. The hair loss had begun as a solitary lesion 6 months before and had progressed until he came to the clinic. The hair loss was asymptomatic, and all other hair-bearing areas were spared. He was taking no medications, and his medical history was unremarkable.

The most likely diagnosis is:

1. Telogen effluvium 2. Trichotillomania 3. Alopecia areata 4. Androgenic alopecia 5. Anagen effluvium

Answer on page 960

DermaCase

Patricia T. Ting,

md

,

msc

Benjamin Barankin,

md

Dr Ting is a recent graduate of the University of Calgary Medical School in Alberta. Dr Barankin is a dermatology resident at the University of Alberta in Edmonton.

Vol 52:  august • août 2006 Canadian Family PhysicianLe Médecin de famille canadien

957

FOR PRESCRIBING INFORMATION SEE PAGE 998

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Pratique clinique Clinical Practice

Answer to Dermacase

continued from page 957

3. Alopecia areata

Alopecia areata manifests as nonscarring hair loss and is estimated to have a lifetime prevalence of 1% to 2%

in the general population.1 It affects men and women equally and can happen at any age; peak incidence occurs in the third to fifth decades.2 Alopecia areata is one of the most common hair disorders of childhood.3

Alopecia areata is characterized by single or multiple well demarcated patches of hair loss, typically on the scalp and occasionally in the beard, eyebrows, eyelashes, or other hair-bearing areas of the body. Patterns of hair loss due to alopecia areata include the following1,4:

• patchy (most common): circular patches of hair loss;

• reticular: network patterns of hair loss;

• ophiasis: bandlike hair loss on the parietal temporo- occipital scalp; and

• ophiasis inversus (rare): bandlike hair loss on the fron- tal parietotemporal scalp.

Less common forms of alopecia areata include alopecia totalis (complete loss of hair on the scalp) and alopecia universalis (a generalized pattern of total body hair loss).

Patients with alopecia areata usually present with massive shedding of hair within a short period. The lesions are typically round or oval well demarcated smooth patches on hair-bearing areas.4 The hair cycle has three sequential stages: anagen, catagen, and telo- gen. In early alopecia areata, the hair follicles enter the late catagen and telogen phases prematurely, resulting in malformation of the hair shaft and subsequent distal fracturing.2 As a result, short “exclamation point” hairs that taper proximally form and are visible at the mar- gins of the hairless lesions; these hairs are considered pathognomonic of alopecia areata. Positive results of a hair-pull test at the margins of the lesion indicate an active disease process. Most patients are asymptom- atic; a few describe mild-to-moderate pruritus, pain, or a burning sensation before a patch of alopecia appears.2,4

Nail dystrophy can be seen in 10% to 66% of patients on careful inspection.2,4 The most common nail change appears as an irregular pattern of pitting, sometimes described as “hammered silver” or “sandpaper.” Other presentations include opacification; longitudinal ridging;

superficial splitting, thinning or thickening of the nail matrix; and onycholysis with nail loss. A few patients also have associated autoimmune disorders, such as atopic dermatitis, vitiligo, autoimmune diseases (eg, pernicious anemia, lupus erythematosus, rheumatoid arthritis, ulcerative colitis), and endocrine abnormalities (eg, thyroid disease, diabetes).1,2,4,5

Although the etiology and pathophysiology of alo- pecia areata are unknown, genetic predisposition and environmental factors are thought to be responsible.

About 40% of patients with early-onset alopecia areata have an affected family member.5 The current hypothesis

f r o m a n i m a l m o d - els attributes alopecia areata to a T lympho- cyte autoimmune reac- tion to hair follicles. A detailed medical history can rule out hair loss from recent stressful life events or severe illness (ie, telogen effluvium) or self-inflicted hair loss secondary to psychiatric conditions (ie, tricho- tillomania).6 Diagnosis

is most often made clinically, but a skin biopsy of the affected area can be useful in difficult cases to differenti- ate alopecia areata from androgenetic alopecia, telogen effluvium, and trichotillomania.

Treatment for alopecia areata aims to suppress the autoimmune process and promote regrowth of hair.

Wiseman and Shapiro7 have recommended a useful treatment plan. For patients older than 10 years with less than 50% scalp involvement, first-line therapy con- sists of intralesional corticosteroids every 4 to 6 weeks for up to 6 months. This can be combined with topi- cal therapies, including 5% minoxidil and potent corti- costeroids or short-contact anthralin in isolation. For patients younger than 10 years with more than 50%

scalp involvement, therapy could commence with topi- cal immunomodulatory agents that act as contact sen- sitizers, including diphenylcyclopropenone, squaric acid dibutyl ester, and dinitrochlorobenzene, followed by the aforementioned topical therapies. Other therapies rec- ommended for children younger than 10 years include topical 5% minoxidil solution with potent corticosteroids or short-contact anthralin in isolation.3,4,8

While many cases of alopecia areata resolve spontane- ously within a year without medical intervention, some patients have a chronic form of the disease and are unre- sponsive to therapy. Referral to a dermatologist is recom- mended for moderate-to-severe cases or if the condition causes patients severe psychosocial distress.

References

1. Papadopoulos AJ, Schwartz RA, Janniger CK. Alopecia areata. Pathogenesis, diagnosis, and therapy. Am J Clin Dermatol 2000;1(2):101-5.

2. Fitzpatrick TB, Eisen AZ, Wolff K, Freedberg IM, Austen KF. Dermatology in general medicine. 4th ed. New York, NY: McGraw-Hill Inc; 1999.

3. Skelsey MA, Price VH. Noninfectious hair disorders in children. Curr Opin Pediatr 1996;8(4):378-80.

4. Madani S, Shapiro J. Alopecia areata update. J Am Acad Dermatol 2000;42(4):549-66.

5. Shellow WV, Edwards JE, Koo JY. Profile of alopecia areata: a questionnaire analysis of patient and family. Int J Dermatol 1992;31(3):186-9.

6. Ruiz-Doblado S, Carrizosa A, Garcia-Hernandez MJ. Alopecia areata: psychi- atric comorbidity and adjustment to illness. Int J Dermatol 2003;42(6):434-7.

7. Wiseman MC, Shapiro J. Therapeutic approach to alopecia areata. J Cutan Med Surg 1999;3(Suppl 3):S31-5.

8. Meidan VM, Touitou E. Treatments for androgenetic alopecia and alopecia areata: current options and future prospects. Drugs 2001;61(1):53-69.

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Canadian Family PhysicianLe Médecin de famille canadien Vol 52:  august • août 2006

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