Bone Mineral Density in Patients With Alopecia Areata Treated With Long-Term Intralesional Corticosteroids

February 2013 | Volume 12 | Issue 2 | Original Article | 36 | Copyright © February 2013

Aman Samrao MD,a Jennifer M. Fu MD,a,b Steven T. Harris MD,b and Vera H. Price MDa

aDepartment of Dermatology, University of California, San Francisco, CA bPrivate practice, El Cerrito, CA cDepartment of Medicine, University of California, San Francisco, CA

Background: Intralesional corticosteroid injections are a common treatment for patchy alopecia areata, the most prevalent subtype of this autoimmune hair disorder. To date, no studies have examined the potential adverse effects of this therapy on bone mineral density (BMD).
Methods: In this retrospective, cross-sectional case series, 18 patients with patchy alopecia areata treated at 4- to 8-week intervals with intralesional triamcinolone acetonide for at least 20 months were evaluated for BMD using dual-energy x-ray absorptiometry (DXA). Follow-up DXA measurements were obtained in those with abnormal findings.
Results: Nine out of 18 patients (50%) had abnormal DXA results. Patients with the following risk factors were more likely to have abnormal BMD: age older than 50 years, body mass index less than 18.5 kg/m2, lack of weight-bearing exercise, smoking history, postmenopausal status, past stress fracture, family history of osteopenia or osteoporosis, and a cumulative intralesional triamcinolone acetonide dose of greater than 500 mg.
Conclusion: Patients with patchy alopecia areata who receive chronic intralesional triamcinolone acetonide therapy should be counseled on preventive measures for osteoporosis and monitored for effects on BMD.

J Drugs Dermatol. 2013;12(2):e36-e40.


Alopecia areata is a T-cell–mediated autoimmune disease that causes hair loss in all ages and ethnic groups, and in both sexes.1,2 Average lifetime risk for developing alopecia areata has been estimated at 1.7% among the general population.2 The autoimmune attack is directed at melanocyte-derived autoantigens as well as other autoantigens. Environmental and genetic factors play a role in disease pathogenesis, with 1 in 5 patients reporting a family member with the disease and a concordance rate of 55% described in identical twin studies. Recently, a genome-wide association study identified several loci that contribute to disease susceptibility. This study upheld the previously reported robust association of human leukocyte antigen (HLA) genes in alopecia areata and implicated the natural killercell gene family for the first time.3 Prognosis remains difficult to predict, with spontaneous remissions and recurrences commonly occurring, and with a subset of patients displaying a tendency toward more extensive patterns of hair loss.4 In alopecia areata, there is not a permanent destruction of the hair follicle, and full hair regrowth is always possible with or without treatment.
A wide range of treatments are currently available for alopecia areata. For patchy disease, the most common of these include intralesional corticosteroids, topical minoxidil, topical anthralin, and topical immunotherapy with agents such as squaric acid dibutylester and diphenylcyclopropenone.5 More extensive disease may require treatment with systemic prednisone, pulse dexamethasone, or cyclosporine as well as topical immunotherapy.5
Existing therapies may induce temporary hair regrowth, but they do not change the course of the disease and must be chosen thoughtfully, following a full discussion of treatment benefits and risks. Such considerations are crucial in any patient care setting, but may be particularly important in the management of alopecia areata. Patients with alopecia areata are generally healthy and as a group have an increased incidence only of atopy and autoimmune thyroid disease. Family members have increased incidence of atopy, type 1 diabetes, rheumatoid arthritis, autoimmune thyroiditis, vitiligo, and inflammatory bowel disease. Therapy may be ongoing for long periods and therefore should be designed to minimize potential long-term side effects.
Although the risk of osteoporosis with the use of long-term oral steroids has been well-documented, there are currently no evidence-based studies regarding the risk of developing osteoporosis with intralesional corticosteroid therapy.6-10 This study was designed to evaluate changes in bone mineral density (BMD) in alopecia areata patients treated at regular intervals (every 4 to 8 weeks) with intralesional corticosteroid therapy for at least 20 months.