Case Reports

Unique Treatment for Alopecia Areata Combining Epinephrine With an Intralesional Steroid

Author and Disclosure Information

Alopecia areata (AA) is an autoimmune disorder characterized by well-demarcated patches of hair loss with preservation of the hair follicle (HF). It generally is a nonscarring alopecia that can be extensive and refractory to treatment. We propose modification to an already widely used first-line treatment by diluting intralesional triamcinolone acetonide (ILTA) to 2.5 mg/mL in 1% lidocaine and epinephrine 1:100,000 in place of normal saline (NS). Our 2 cases of severe AA are among many in our practice that responded with seemingly permanent hair regrowth using this novel combination regimen. We hypothesize that local vasoconstriction due to epinephrine potentiates the ILTA and that epinephrine also may play an independent role.

Practice Points

  • Patients with alopecia areata that is refractory to first-line treatments may benefit from intralesional triamcinolone acetonide (ILTA) diluted to 2.5 mg/mL in 1% lidocaine and epinephrine 1:100,000 in place of normal saline.
  • Local vasoconstriction due to epinephrine may potentiate ILTA effects and play an independent role.


 

References

Alopecia areata (AA) is an autoimmune disorder characterized by transient hair loss with preservation of the hair follicle (HF). The lifetime incidence risk of AA is approximately 2%,1 with a mean age of onset of 25 to 36 years and with no clinically relevant significant differences between sex or ethnicity.2 Most commonly, it presents as round, well-demarcated patches of alopecia on the scalp and spontaneously resolves in nearly 30% of patients. However, severe disease is associated with younger age of presentation and can progress to a total loss of scalp or body hair—referred to as alopecia totalis and alopecia universalis, respectively—thus severely impacting quality of life.3,4

First-line treatment options for AA include potent topical steroids5,6 and intralesional (IL) steroids, most commonly IL triamcinolone acetonide (ILTA). Intralesional steroids have been found to be more effective than topicals in stimulating hair growth at the injection site.7,8 A recent systemic therapy—the Janus kinase inhibitor baricitinib—was approved by the US Food and Drug Administration for AA.9 Other systemic therapies such as oral corticosteroids have been studied in small trials with promising results.10 However, the risks of systemic therapies may outweigh the benefits.9,10

Another less common topical therapy is contact immunotherapy, which involves topical application of an unlicensed non–pharmaceutical-grade agent to areas affected with AA. It is reported to have a wide range of response rates (29%–87%).11

We report 2 cases of extensive AA that were treated with a novel combination regimen— 2.5 mg/mL of ILTA diluted with lidocaine 1% and epinephrine 1:100,000 in place of normal saline (NS)— which is a modification to an already widely used first-line treatment.

Case Reports

Patient 1—An 11-year-old girl presented with nonscarring alopecia of the vertex and occipital scalp. Three years prior she was treated with topical and IL corticosteroids by a different provider. Physical examination revealed almost complete alopecia involving the bottom two-thirds of the occipital scalp as well as the medial eyebrows (Figures 1A and 1B). Over the span of 1 year she was treated with betamethasone dipropionate cream 0.05% and several rounds of ILTA 2.5 mg/mL buffered with NS, with minimal improvement. A year after the initial presentation, the decision was made to initiate monthly injections of ILTA 2.5 mg/mL buffered with 1% lidocaine and epinephrine 1:100,000. Some hair regrowth of the occipital scalp was noted by 3 months, with near-complete regrowth of the scalp hair and eyebrows by 7 months and 5 months, respectively (Figures 1C and 1D). During this period, the patient continued to develop new areas of alopecia of the scalp and eyebrows, which also were injected with this combination. In total, the patient received 8 rounds of IL injections 4 to 6 weeks apart in the scalp and 6 rounds in the eyebrows. The treated areas showed resolution over a follow-up period of 14 months, though there was recurrence at the right medial eyebrow at 5 months. No localized skin atrophy or other adverse effects were noted.

An 11-year-old girl with alopecia areata

FIGURE 1. A, An 11-year-old girl with alopecia areata of the occipital scalp before treatment. B, Alopecia of the eyebrows before treatment. C, Near-complete regrowth of hair on the occipital scalp was seen after 7 months of treatment with intralesional triamcinolone acetonide 2.5 mg/mL plus 1% lidocaine and epinephrine 1:100,000 at monthly intervals. D, Near-complete regrowth of the medial eyebrows was seen after 5 months of this combination regimen.

Patient 2—A 34-year-old woman who was otherwise healthy presented with previously untreated AA involving the scalp of 2 months’ duration. Physical examination revealed the following areas of nonscarring alopecia: a 10×10-cm area of the right occipital scalp with some regrowth; a 10×14-cm area of the left parieto-occipital scalp; and a 1-cm area posterior to the vertex (Figure 2A). Given the extensive involvement, the decision was made to initiate ILTA 2.5 mg/mL buffered with 1% lidocaine and epinephrine 1:100,000 once monthly. Appreciable hair regrowth was noted within 1 month, mostly on the parietal scalp. Substantial improvement was noted after 3 months in all affected areas of the hair-bearing scalp, with near-complete regrowth on the left occipital scalp and greater than 50% regrowth on the right occipital scalp (Figure 2B). No adverse effects were noted. She currently has no alopecia.

A 34-year-old woman with alopecia

FIGURE 2. A, A 34-year-old woman with alopecia of the right occipital scalp before treatment. B, Partial regrowth (>50%) of hair on the right occipital scalp was seen after 3 months of treatment with intralesional triamcinolone acetonide 2.5 mg/mL plus 1% lidocaine and epinephrine 1:100,000 at monthly intervals.

Comment

Alopecia Pathogenesis—The most widely adopted theory of AA etiology implicates an aberrant immune response. The HF, which is a dynamic “mini-organ” with its own immune and hormonal microenvironment, is considered an “immune-privileged site”—meaning it is less exposed to immune responses than most other body areas. It is hypothesized that AA results from a breakdown in this immune privilege, with the subsequent attack on the peribulbar part of the follicle by CD8+ T lymphocytes. This lymphocytic infiltrate induces apoptosis in the HF keratinocytes, resulting in inhibition of hair shaft production.12 Other theories suggest a link to the sympathetic-adrenal-medullary system and hypothalamic-pituitary-adrenal axis.13

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