Summary Eighty‐nine patients with chronic actinic dermatitis (CAD) were retrospectively studied: 69 (78%) male and 20 (22%) female, with mean ages of 66 and 64 years, respectively; nine (10%) were dark skinned. Eight (9%) were abnormally sensitive to UVB wavelengths alone, 74 (83%) to UVB and UVA, and seven (8%) to UVB, UVA and visible radiation. Eighty‐six patients were patch tested to an extended standard European series of contact allergens, including in 80 cases a 0.1% mix of three sesquiterpene lactones, and photopatch tested to a standard photopatch series. Sixty‐four of these 86 patients (74%) had positive patch or photopatch tests; 36% (29 of 80) were sensitive to the sesquiterpene lactone mix, 21% (18 of 86) to fragrance compounds, 20% (17 of 86) to colophony, and 14% (12 of 86) to rubber chemicals. Ten (12%) had positive photopatch tests; five (6%) to musk ambrette, six (7%) to sunscreens and one to both. Fourteen of the eighty‐nine patients with CAD (16%) had preceding endogenous eczema. In 18 of 86 patients (21%), CAD occurred alone, with neither detectable contact nor photocontact allergy, nor a preceding history of endogenous eczema. This study confirms the association between Compositae (sesquiterpene lactone) dermatitis and CAD.

We have examined the effects of low-dose monochromatic UVB irradiation (295 +/- 5 nm), biologically equivalent to that generally incident on the skin during a 12-session sun-bed course, on the expression of the CD1a epidermal Langerhans cell surface marker in human skin in vivo. In five subjects, 1.5 minimal erythema doses (MEDs) at 295 nm depleted its expression by 50%. In five further subjects, a single 1.5 MED dose, 1.5 MEDs in 10 equal fractions on alternate days, and a single 1.5 MED dose at one-tenth the previously used irradiance, delivered to separate sites, also led to variable but significant depletion of CD1a expression of around 30-50%. Thus, low-dose UVB irradiation, whether received rapidly or slowly, appears significantly and approximately equally to deplete human epidermal Langerhans cell numbers as measured by CD1a expression.

Fourteen patients suffering from actinic prurigo were treated with thalidomide. Eleven patients showed lasting improvement on the drug and three of these remained symptom-free after discontinuing therapy. No major side-effects were observed. Thalidomide is an effective drug in the treatment of actinic prurigo but it must be used with adequate contraception in women of child-bearing age.

A double-blind controlled trial of low-dose prophylactic oral psoralen photochemotherapy (PUVA) and ultraviolet-B (UVB) irradiation therapy was undertaken from April to September 1983 in 42 patients with polymorphic light eruption (PLE). Patients were randomly allocated to three groups, PUVA with oral 8-methoxypsoralen (8-MOP), UVB with oral placebo, and control low-dose UVA with oral placebo. The initial dose given to each active treatment group was a third of the predetermined minimal phototoxic or erythema dose, followed three times weekly for 6 weeks by doses incremented by an eighth on each occasion in the PUVA group and by a seventh in the UVB group. Ultraviolet radiation exposure was monitored throughout with polysulphone film lapel badges. Patients recorded their symptoms on a visual analogue scale. Symptoms of rash and itch in patients treated with PUVA and UVB were significantly less affected by increasing exposure to ultraviolet radiation than were these symptoms in control patients.

Fifteen adolescent children with severe, persistent atopic eczema were treated with oral psoralen photochemotherapy (PUVA). This resulted in initial clearance of eczema in 14 of the 15 children, nine of whom achieved a remission. Apart from its effectiveness, a major benefit of this therapeutic approach was that it was associated with resumption of normal growth in children who were previously growing poorly, either as a direct result of severe eczema or its treatment. Nevertheless, against the considerable advantages of PUVA for this group of patients have to be balanced the possible hazards, because relatively high exposures are required in some individuals, both initially to induce clearance and subsequently to maintain it.

Seven patients with porphyria cutanea tarda received a total of ten courses of low-dose oral chloroquine therapy (125 mg chloroquine phosphate twice weekly). Patients were treated for a mean 14.9 months during which time all went into clinical and biochemical remission. Relapse occurred in four patients on a total of six occasions after a mean 17 months. In four patients there was no relapse after a mean 47.3 months. There were no adverse side-effects from the treatment. Low-dose oral chloroquine therapy appears to be a safe, effective and convenient treatment for porphyria cutanea tarda, although relapses may occur requiring further therapy.

Oral azathioprine was compared with placebo in a double-blind controlled trial of therapy in chronic actinic dermatitis (CAD), a rare eczematous photodermatosis. Eighteen severely affected patients were randomly allocated to azathioprine 50 mg t.d.s. or placebo over a 2-year period. Severity of itch and rash were assessed weekly by each patient on a visual analogue scale and overall clinical status monthly by a medical observer. Monitoring of patient ultraviolet radiation (UVR) exposure was undertaken throughout treatment by polysulphone film lapel-badge dosimetry. Five of 8 patients treated with azathioprine but none of 10 placebo patients achieved remission within 6 months. One patient could not tolerate treatment because of gastrointestinal effects. No haematological or hepatic abnormality was noted. The marked improvement in clinical status of actively treated patients (P less than 0.02, Fisher's exact test), led to early termination of the trial. Oral azathioprine therapy is an effective and usually well tolerated treatment in chronic actinic dermatitis.

Summary The incidence and nature of cutaneous photosensitivity were studied in 10 patients suffering from dermatomyositis. Five reported an abnormality, which consisted of photoaggravation of preexisting cutaneous lesions in three, and abnormal transient erythemal responses in two. Monochromatic irradiation testing of all 10 patients demonstrated reduced minimal erythemal doses in two, at 307.5nm, and at 340 and 360nm, respectively; only the latter individual had clinical light sensitivity. Exposure to low‐dose, solar‐simulated radiation of the unaffected skin of the former patient, and five others who agreed to the procedure, three of whom complained of light sensitivity, induced a lesion with the clinical and immunofluorescence characteristics of dermatomyositis in only the first one. Four other patients replied to a mailed questionnaire, and three of these reported aggravation of their rash and provocation of new lesions by sunlight. Photosensitivity may thus be an important cutaneous feature of dermatomyositis.