Journal of the American Academy of Dermatology
Volume 52, Issue 5 , Pages E9-E10, May 2005

Recalcitrant chronic actinic dermatitis treated with low-dose thalidomide

Department of Dermatology, Centre Hospitalier de Saint-Brieuc, Saint-Brieuc, France

Accepted 31 January 2002.

Article Outline

 

To the Editor: Chronic actinic dermatitis (CAD), also known as the persistent photosensitivity dermatitis and actinic reticuloid syndrome, is a severe, often disabling, chronic photodermatitis.1, 2 Treatment is difficult and not standardized. We report a case of recalcitrant CAD successfully treated with thalidomide.

A 37-year-old healthy white man presented with a 5-year history of recalcitrant CAD. The diagnosis was made on the basis of clinical and histologic findings and phototesting data. Five years ago, the patient had extremely severe chronic eczematous dermatitis develop on sun-exposed skin involving the face, ears, forearms, and the back aspect of the hands (Fig 1). Histologic findings disclosed changes consistent with photodermatitis: dermal infiltrate of T lymphocytes CD4, CD8+, and macrophages with epidermal hyperplasia. Phototesting showed decreased minimal erythema doses to both ultraviolet A (UVA) (2 J/cm2) and UVB (<50 mJ/cm2). Photopatch tests were negative to sunscreens and personal care products. Patch tests revealed sensitization to nickel. Aside from protection from sunlight, treatment modalities that had been used included 8-methoxypsoralen and UVA, azathioprine, cyclosporine, and hydroxychloroquine sulfate, without any improvement. Therefore, the patient was placed on a regimen of oral thalidomide (100 g/day) and gradually tapered to a dose of 50 mg twice a week. At 5 months, the clinical course of the patient showed a slow but dramatic response to this therapeutic regimen (Fig 2). The patient experienced no drug-related side effects.

To our knowledge, this is the first report of severe CAD successfully treated with thalidomide. As shown in our patient, CAD is defined by 3 criteria3, 4: (1) clinical—a persistent eruption of eczematous character affecting sun-exposed skin; (2) histologic—appearances consistent with chronic eczema, with or without the presence of lymphoma-like changes; and (3) photobiologic—reduction in the minimal erythema doses to UVB, UVA, visible light, or a combination of these. The pathophysiology of CAD is not completely understood. Sensitization to carrier proteins altered by exposure to photons, defective ability to repair damages caused by oxygen-free radicals, and contact or photocontact responses to fragrance materials have been postulated to play a role in the pathogenesis of this condition. Treatment is difficult and not standardized. In addition to sun avoidance, the use of broad-spectrum sunscreens, and the use of topical steroids, treatment modalities that have been effective in some patients include psoralen plus UVA, azathioprine, cyclosporine, and hydroxychloroquine sulfate.4 In our patient, none of these systemic treatments was effective.

Thalidomide has been successfully used in several inflammatory dermatoses with photosensitivity, especially lupus erythematosus.5, 6, 7 Although thalidomide possesses immunomodulatory and anti-inflammatory properties, its precise mechanism of action is unknown. In vitro, thalidomide inhibits neutrophil chemotaxis, decreases phagocytosis by polymononuclear leucocytes, selectively inhibits production of tumor necrosis factor-α by monocytes, and inhibits proliferative T cell responses.8 The numerous immunomodulatory and anti-inflammatory properties of thalidomide may account for its efficacy in a variety of inflammatory skin diseases, such as erythema nodosum, Behçet's syndrome, prurigo nodularis, aphtous stomatitis, graft-versus-host disease, and discoid lupus erythematosus.9

The teratogenic potential of thalidomide is well known. Besides teratogenicity, the most serious side effect of thalidomide is a dose-related sensory neuropathy that may be irreversible. Sedation and constipation are the most frequently observed adverse effects.9

In our patient with CAD, we have found low-dose thalidomide to be greatly beneficial with a dramatic response. However, because of potential serious side effects with thalidomide, further study needs to be done to definitely establish its efficacy in CAD.

Back to Article Outline

References 

  1. Hawk JLM, Magnus IA. Chronic actinic dermatitis: an idiopathic photosensitivity syndrome including actinic reticuloid and photosensitive eczema. Br J Dermatol. 1979;101:24
  2. Norris PG, Hawk JLM. Chronic actinic dermatitis: a unifying concept. Arch Dermatol. 1990;126:376–378
  3. Lim HW, Morison WL, Kamide R, Buchness MR, Harris R, Soter NA. Chronic actinic dermatitis: an analysis of 51 patients evaluated in the United states and Japan. Arch Dermatol. 1994;130:1284–1289
  4. Lim HW, Epstein J. Photosensitivity diseases. J Am Acad Dermatol. 1997;36:84–90
  5. Knop J, Bonsmann G, Happle R, Ludolph A, Matz D, Mifsud E. Thalidomide in the treatment of sixty cases of chronic discoid lupus erythematosus. Br J Dermatol. 1983;108:461–466
  6. Bessis D, Guillot B, Monpoint S, Dandurand M, Guilhou JJ. Thalidomide for systemic lupus erythematosus. Lancet. 1992;339:549–550
  7. Warren KJ, Nopper AJ, Crosby DL. Thalidomide for recalcitrant discoid lesions in a patient with systemic lupus erythematosus. J Am Acad Dermatol. 1998;39:293–295
  8. Barnhill RL, Doll NJ, Millikan LE, Hastings RC. Studies on the anti-inflammatory properties of thalidomide: effects on polymorphonuclear leucocytes and monocytes. J Am Acad Dermatol. 1984;11:814–819
  9. Tseng S, Pak G, Washenik K, Pomeranz MK, Shupack JL. Rediscovering thalidomide: a review of its mechanism of action, side effects, and potential uses. J Am Acad Dermatol. 1996;35:969–979

PII: S0190-9622(03)01131-9

doi:10.1016/S0190-9622(03)01131-9

Journal of the American Academy of Dermatology
Volume 52, Issue 5 , Pages E9-E10, May 2005