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Several factors, such as amount of allergen, vehicle, anatomic site, immunologic status and previous eczema, may influence delayed hypersensitivity reactions. In an extended model, we have studied the significance of previous allergic contact dermatitis for elicitation of delayed hypersensitivity to nickel in 25 nickel-allergic females. On 3 occasions, 8, 4 and 1 months before the final challenge patch testing, an experimental allergic contact dermatitis from nickel was induced on the lower back. At the challenge patch testing, 4 identical dilution series of nickel were tested on 4 areas on the lower back 3 with previous but healed dermatitis and 1 control area. The tests were read in a blind way. A significantly higher test reactivity was found at the areas with a previous allergic contact dermatitis, the shorter the time interval between the previous provocation and the challenge, the stronger the reaction. These results may be of importance for the understanding of factors contributing to chronicity of allergic contact dermatitis.

The efficacy of UV-B irradiation, administered by a new unit, Handylux, in patients with chronic hand eczema was investigated. 15 patients were treated in the clinic and 11 patients at home. Treatments were performed 4-5 x weekly for approximately 10 weeks. According to the strict criteria used for clearing, none of the patients cleared during the study, but 18 of the 26 patients were defined as much improved by the investigator, while 17 of the patients considered themselves as > 80% improved. The compliance in both groups was very good and side-effects limited and dose-related. According to our experience, the effect of high dose UV-B in chronic hand eczema is almost comparable to PUVA, and offers an opportunity for patients to treat themselves at home.

22 DNCB sensitized guinea pigs were challenged with varying amounts dissolved in alcohol, acetone and olive oil. DNCB applied in alcohol resulted in almost 100% positive reactions; the test scores correlated to dose. When similar amounts were applied in alcohol and acetone, the former produced a significantly higher degree of positivity. The importance of defining allergen concentration, volume or weight of test substance applied and test area size, when comparing test results in guinea pigs and humans, is emphasized.

Serum from guinea pigs exposed to a single high dose of UVB and from controls was injected into the spleen of normal animals 5 days prior to sensitization. When 1.0 ml was transferred 4.5 h after irradiation, immunosuppression was obtained. Transfer of 1.5 ml of serum 2.5 h after irradiation failed to induce immunosuppression. This experimental model in guinea pigs might be valuable in further studies investigating the effect of other modalities of ultraviolet exposure (e.g., PUVA or high-dose UVA) on the release of soluble serum factor(s) inducing immunosuppression in allergic contact dermatitis.

63 female patients with nickel allergy and hand eczema were reinvestigated 6 years after the primary investigation. 30% of the patients were healed. Patients with the pompholyx-type eczema had the worst prognosis. The start of hand eczema was not correlated to any particular occupation. There was a strong correlation between a history of metal sensitivity and a positive patch test reaction. High frequencies of personal and family atopy were found, and atopy made the prognosis worse. Determination of serum IgE was not found to be of any use in predicting the prognosis in patients with nickel allergy and hand eczema.

Chinese cabbage plants were watered with different concentrations of NiCl2 solutions and the effect on growth and uptake of nickel in the plants were studied. No toxic effect on plant growth was observed. A higher content of nickel was found in the plants exposed to more concentrated nickel solutions. Nickel contamination and its clinical consequences are discussed.

Open, closed and intradermal testing with NiCl2 was performed in 15 subjects with patch-test-proven allergy to 5% NiSO4 in pet. Intradermal testing proved to be a reliable method in confirming nickel sensitivity within 24 h. Open testing with non-toxic concentrations of NiCl2 in alcohol resulted in 73% and 93% positive reactions at 24 h and 48 h readings, respectively. This test method can be used as a reliable screening method in nickel allergy. Open testing often resulted in positive reactions within a few hours. This makes it possible to investigate pathogenetic events of acquired allergic contact dermatitis at a much earlier stage than with the usual 48-h occlusion. 24-h occlusion with Finn Chambers is not sufficient if one is to avoid false negative reactions in nickel allergy. Occlusion with Finn Chambers seems to delay the reaction.

Previous studies in humans and guinea pigs indicate that Langerhans cells (LC) participate in elicitation of allergic contact dermatitis. The number and morphology of LC was determined in acute and healed allergic patch test sites, control (petrolatum) sites and normal skin in nickel-sensitive individuals using OKT6 monoclonal antibody and avidin-biotin/peroxidase labeling. Compared to normal skin, the staining intensity and number of epidermal LC was significantly increased in allergic (p less than 0.02) and petrolatum control (p less than 0.02) sites, and in 6- to 8-week old allergic patch test sites (p less than 0.006). The in situ changes in LC induced by petrolatum alone may be a result of the occlusive patch test, or may suggest that petrolatum is not as neutral as previously believed. The nickel-induced increase in LC may indicate changes in the LC present in the epithelium at the time of testing, or migration of additional LC into the epithelium, which can then remain in situ for weeks after the antigenic challenge. The specificity of the LC increase in allergic contact dermatitis is questioned on the basis of the increase noted with petrolatum.

Sodium cromoglycate was applied to the forearm of 9 subjects with known delayed hypersensitivity, and to the back of 14 dinitrochlorobenzene-sensitized guinea pigs before challenge with the allergen and sodium lauryl sulphate. Sodium cromoglycate did not decrease the intensity of allergic of toxic-irritant reactions in either humans or guinea pigs.

The release of nickel to boiling water from new and used saucepans of different material was measured. No nickel was released from aluminium, teflon and enamel. Certain amounts of nickel were released from stainless steel, but only at acid pH.

A provocation study was performed in twelve female patients with contact allergy to nickel and hand eczema of the pompholyx type. Intense handling of nickle-contaminated metal objects did not induce any visible eczematous activity. Oral administration of nickle in a double-blind test provoked an aggravation of the hand eczema in nine of the twelve patients, and in seven of the patients this was accompanied by secondary eruptions including outbreaks of earlier, healed eczema. The nickle dose given is probably in the upper limit of the presently known daily intake of the metal, but should be considered to be within the physiologic range. It is concluded that ingestion of small amounts of nickel may be of greater importance in maintaining the hand eczema than external contacts with the metal.

Healthy volunteers without nickel hypersensitivity were given 5.6 mg nickel orally. The nickel concentration was assayed in urine, serum and sauna-provocated sweat from hands and trunk before and after nickel ingestion. The nickel concentration in serum increased in all subjects, and in most cases in urine, but not decisively in sweat.

Flare-up reactions were induced in potassium dichromate hypersensitive guinea pigs by a single oral dose of 55 mg/kg. This dose is systemically toxic and higher than the dose required to induce the same reactions in humans. A total oral dose of potassium dichromate of 90-115 mg/kg induced immunological unresponsiveness for at least 6 weeks. With limitations, the guinea pig model may be helpful in screening the hyposensitization capacity of different haptens dosed orally.

A clinical study was performed in 66 female patients with hand eczema and contact allergy to nickel. They were drawn from a basic material of 165 patients with nickel allergy in which hand eczema occurred in 86 cases (52%). The hand eczema started at an average age of 32 years and it had been preceded by a metal hypersensitivity for an average of 6 years. The eczema was found to be chronic with a mean duration up to the time of examination of 8 years. It was associated with secondary eruptions in half of the cases. The hand eczema showed a low degree of relevance with regard to dependance of occupation or vacation, as well as to exacerbation of the dermatitis after a direct contact with nickel-coated objects. The clinical examination disclosed in 77% a pompholyx, i.e. a symmetric vesicular eruption mainly located on the palms and volar aspects of fingers, and sides of fingers. The eczema often showed a periodic activity, with about 15 annual eruptions in the pompholyx cases. It is concluded that simple external contact with the metal can hardly explain the most common clinical pattern of the hand eczema in nickel allergy.