Published on 18/03/2015 by admin
Filed under Dermatology
Last modified 22/04/2025
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Sally H. Ibbotson and Robert S. Dawe
Evidence Levels: A Double-blind study B Clinical trial ≥ 20 subjects C Clinical trial < 20 subjects D Series ≥ 5 subjects E Anecdotal case reports
Chronic actinic dermatitis (CAD), previously photosensitivity dermatitis/actinic reticuloid (PD/AR) syndrome, is a chronic dermatitis (sometimes with pseudoreticuloid features) predominantly of photo-exposed sites. Objective abnormal photosensitivity (to ultraviolet B [UVB] and often UVA and visible light) is an essential component of the syndrome. It usually arises on a background of a preceding dermatitis, whether endogenous or exogenous. It always involves photoexposed sites, but half the cases also report covered site involvement. More than three-quarters have contact allergens, often multiple. It typically presents in men over the age of 50 years, but it can occur in younger patients and women. All skin phototypes can be affected.
Phototesting investigations are essential. Without investigation, definitive distinction between photoaggravated eczemas, drug-induced photosensitivity, and CAD is not possible.
Photoprotection advice should include environmental measures (use of window film to prevent UVA transmission and avoidance of single envelope compact fluorescent lamps for those with extreme UVA and visible light sensitivity), behavioral measures (including avoidance of sunlight in the middle of the day), clothing measures (tightly woven clothing, dark colors for those with visible wavelength sensitivity), and topical sunscreens. Patient education to reduce exposure to their contact allergens is necessary. Contact allergy tends to persist indefinitely, whereas photosensitivity can eventually resolve.
For active disease, use of emollients and potent/very potent topical corticosteroids is also required. Inpatient admission, with nursing behind photoprotective screens, may be necessary for acute flares, especially if causing erythroderma. Systemic corticosteroids can be used for acute flares and reduced over weeks, with continued use of topical steroids for maintenance control. If these measures do not suffice and if the patient is not too UVA sensitive, controlled use of PUVA may be appropriate. UVB phototherapy is an alternative, although in our experience patients are usually too UVB-sensitive to tolerate this. For others a variety of systemic immunosuppressants can be tried.
Phototesting (with UVB, UVA, and visible light from monochromator or broadband sources)
Provocation testing (with solar simulator or other broadband source)
Patch and photopatch tests
Consider concomitant disease
MacKenzie LA, Frain-Bell W. Br J Dermatol 1973; 89: 251–64.
Phototesting using an irradiation monochromator if available should be performed.
Kerr AC, Dawe RS, Lowe G, Ferguson J. Br J Dermatol 2010; 162: 1406–8.
Ferguson J, Ibbotson SH. Br J Dermatol 2012; 167: 214–15.
If testing shows severe photosensitivity despite topical corticosteroid therapy this can make the diagnosis, but topical corticosteroid therapy or even low-dose oral prednisolone (10 mg/day) can lead to misleading negative testing.
Dawe RS. Drugs Aging 2005; 22: 201–7.
Phototesting is required to diagnose CAD. This review gives guidance on testing where specialized facilities are not available.
Eadie E, Ferguson J, Moseley H. Br J Dermatol 2009; 160: 659–64.
Be aware that patients with CAD may be at risk from exposure to UV radiation from compact fluorescent (’energy saving’) lamps.
Frain-Bell W, Johnson BE. Br J Dermatol 1979; 101: 503–12.
Menagé H du P, Ross JS, Norris PG, Hawk JLM, White IR. Br J Dermatol 1995; 132: 543–7.
Contact allergy is common in CAD. Patch testing, repeated at intervals as indicated by history, is an essential investigation in order not to ‘miss’ new allergens. As many CAD patients are abnormally sensitive to the UVA sources used for photopatch testing, this technique may be difficult to undertake and interpret. Photopatch testing with sub-erythemal UVA doses should be undertaken.
Chew AL, Bashir SJ, Hawk JLM, Palmer R, White I, McFadden JP. Contact Dermatitis 2010; 62: 42–6.
Be aware of changing allergen patterns with alteration in exposure over time. Para-phenylenediamine reactions in CAD may have increased.
Tan AW, Lim KS, Chong WS. Photoderm Photoimmunol Photomed 2011; 27: 172–5.
Three of 26 Singaporean patients with CAD were positive for HIV.
Other case series have found even greater proportions of CAD patients to have HIV. This does not prove a cause and effect relationship, but the possible association should be considered.
Reid SM, Robinson M, Kerr AC, Ibbotson SH. Photoderm Photoimmunol Photomed 2012; 28: 91–6.
We need to be vigilant about vitamin D status of patients with photosensitivity diseases, such as CAD.
Jong CT, Finlay AY, Pearse AD, Kerr AC, Ferguson J, Benton EC, et al. Br J Dermatol 2008; 159: 192–7.
Photosensitivity can have a major adverse effect on quality of life. In this study more than one-third of patients with CAD had a DLQI (Dermatology Life Quality Index) score of >10.
Yap LM, Foley P, Crouch R, Baker C. Australas J Dermatol 2003; 44: 256–62.
Restriction of sunshine and allergen exposure, along with sunscreens and topical steroids, gave relief in 36% of CAD patients. The remainder also required oral immunosuppressants or phototherapy.
Healy E, Rogers S. Acta Derm Venereol 1995; 75: 72–4.
Of nine CAD patients treated with sunscreens, emollients, topical steroids and antigen avoidance, six responded well, two achieved complete remission, and four were controlled on topical steroids alone, although five also required oral steroids initially.
Gambichler T, Rotterdam S, Altmeyer P, Hoffmann K. BMC Dermatol 2001; 1: 6.
Summer clothing textiles (n = 236) were investigated spectrophotometrically for their ultraviolet protection factors (UPF). Over 70% of wool and polyester, but less than 30% of cotton, linen and viscose fabrics, had UPFs over 30.
Murphy GM, Maurice PD, Norris PG, Morris RW, Hawk JL. Br J Dermatol 1989; 121: 639–46.
Five of eight patients with CAD treated in this randomized trial had complete clinical disease remission within 6 months of azathioprine (150 mg/day) commencement. No useful clinical response was seen in 10 patients treated with placebo. It is not known whether azathioprine causes objective improvement in photosensitivity.
Tan BB, Gawkrodger DJ, English JSC. Br J Dermatol 1997; 136: 351–5.
A questionnaire survey of 253 UK dermatologists demonstrated that 68% use azathioprine in CAD, 66% alone, and the others as a steroid-sparing agent. Most used 100 mg daily, only 13% prescribing it by body weight. CAD had the highest proportion of perceived efficacy (62%) of all disorders treated with azathioprine.
Paquet P, Piérard GE. Ann Dermatol Venereol 2001; 128: 42–5.
Two patients with CAD unresponsive to high-dose oral steroids responded well to oral cyclosporine without significant adverse effects. One was in remission for 3 years after stopping cyclosporine.
Thomson MA, Stewart DG, Lewis HM. Br J Dermatol 2005; 152: 784–6.
Two patients with CAD who had failed to respond to topical steroids, prednisolone, PUVA, azathioprine, and cyclosporine were treated with mycophenolate mofetil, resulting in clearance over weeks, without adverse effects.
Gramvussakis S, George SA. Br J Dermatol 2000; 143: 1340.
Hydroxycarbamide (previously called hydroxyurea) at 500–1000 mg/day induced remission of CAD in one patient.
Hindson C, Spiro J, Downey A. Br J Dermatol 1985; 113: 157–60.
Four patients with severe CAD were treated twice weekly with PUVA, with starting UVA doses of 0.25 J/cm2 and increases of 0.25–1 J/cm2 up to a maximum 10 J/cm2. Topical steroids were applied immediately after each of the first six exposures. All patients responded well and remained controlled on twice-monthly treatments of 10 J/cm2.
Khaled A, Kerkeni N, Baccouche D, Zeglaoui F, Kamoun M, Mohamed R. EDP Sciences 2011; 66: 453–7.
Two patients were successfully treated with narrowband UVB under cover of systemic corticosteroid therapy.
Toonstra J, Henquet CJ, van Weelden H, van der Putte SC, van Vloten WA. J Am Acad Dermatol 1989; 21: 205–14.
Fifteen CAD patients were treated with broadband UVB phototherapy five times a week, starting at a 10% minimal erythemal dose, with gradual increments as tolerated. Thirteen improved well clinically, with increased sunlight tolerance. Discontinuation of therapy was followed by gradual relapse.
Ma Y, Lu Z. J Dermatolog Treat 2010; 21: 171–7.
Forty patients with CAD were treated with topical tacrolimus 0.1% and skin biopsies were performed pre- and post-treatment in 15 patients. Clinical efficacy was seen in 25 (63%), with significant downregulation of Langerhans/dendritic cell function.
Evans AV, Palmer RA, Hawk JLM. Photodermatol Photoimmunol Photomed 2004; 20: 59–61.
An erythrodermic patient with CAD resistant to oral immunosuppressants and phototherapy responded well to topical tacrolimus.
Larangeira de Almeida H. Int J Dermatol 2005; 44: 343–4.
Pimecrolimus can be considered as an alternative therapy.
No comparative studies have been reported. Potent topical corticosteroids should generally be favored over topical calcineurin inhibitors, but these newer topical immunomodulators are appropriate to consider for those with inadequate responses to topical corticosteroids.
Lim HW, Morison WL, Kamide R, Buchness MR, Harris R, Soter NA. Arch Dermatol 1994; 130: 1284–9.
Photoprotection and topical steroids were useful in 51 patients with CAD. Azathioprine (50–200 mg/day) was also commonly helpful. PUVA and oral steroids were beneficial in seven patients, cyclosporine in four, and etretinate in two. Hydroxychloroquine (200 mg once or twice daily) achieved partial/good responses in nine patients.
Humbert P, Drobacheff C, Vigan M, Quencez E, Laurent R, Agache P. Br J Dermatol 1991; 124: 195–7.
A patient with CAD, with low α1-antitrypsin levels responded dramatically to danazol (600 mg/day for 3 weeks), relapsed on stopping, improved on restarting and remained controlled 18 months later whilst still on drug. Danazol raises low serum α1-antitrypsin and protease inhibitor levels, and a protease–antiprotease imbalance has been said to cause abnormal inflammatory responses in several dermatoses.
Safa G, Pieto-Le Corvaisier C, Hervagault B. J Am Acad Dermatol 2005; 52: E6.
A patient with CAD resistant to PUVA, azathioprine, cyclosporine, and hydroxychloroquine responded dramatically to thalidomide (100 mg/day reduced to 50 mg twice weekly) over 5 months without adverse effect.
Parodi A, Gallo R, Guarrera M, Rebora A. Acta Derm Venereol 1995; 75: 80.
In one patient with CAD in whom cyclosporine had to be discontinued because of hypertension, natural α-interferon (3 MU three times per week) was effective.
Schopf RE, Poblete-Gutiérrez P. Exp Dermatol 2009; 18: 302 (abstract at 36th Annual Meeting of Arbeitsgemeinschaft Dermatologische Forschung, Heidelberg, 2009).
Infliximab infusions were associated with marked improvement in one patient who had not shown useful response to previous therapies including topical corticosteroids, PUVA and cyclosporine.
Treatment of Skin Disease Comprehensive Therapeutic Strategies 4e
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Photoprotective measures
Avoidance of relevant contact allergens
Topical corticosteroids
Topical emollients
Azathioprine
Cyclosporine
Mycophenolate
Hydroxycarbamide
PUVA
UVB
Topical calcineurin inhibitors
Hydroxychloroquine
Etretinate
Danazol
Thalidomide
Interferon
Infliximab
