The positive effects of habit reversal treatment of scratching in children with atopic dermatitis: a randomized controlled study.

BACKGROUND: Scratching and itch are common clinical signs of atopic dermatitis (AD). Studies of adult patients have shown that a decrease in scratching behaviour results in regression of inflammation and improved healing of the skin. OBJECTIVES: To investigate whether a modified habit reversal (HR) treatment protocol could be used for the treatment of scratching in children to improve skin status. METHODS: The study is a single-blind, randomized controlled trial of 39 patients who started with registration a week before randomization into one of two groups (intervention or control). The participants in the intervention group received a habit-breaking therapy of their scratching behaviour (i.e. HR) in addition to a potent steroid (mometasone furoate), whereas the patients in the control group received the steroid alone. The patients were assessed by an independent dermatologist after the first week of registration (baseline assessment) and then after 3 and 8 weeks of treatment. The primary efficacy variable was a change in objective Scoring Atopic Dermatitis (SCORAD). RESULTS: At the end of the 3-week treatment period, the change in mean objective SCORAD was significantly (P = 0·027) higher in the intervention group (-31·9 ± 9·5) than in the control group (-23·8 ± 10·1). After the 8-week follow-up, the change in mean objective SCORAD was significantly (P = 0·0038) higher in the intervention group (-31·7 ± 10·4) than in the control group (-19·7 ± 9·4). CONCLUSIONS: The treatment of scratching with the HR method in combination with a potent steroid was found to improve skin status significantly after 3 and 11 weeks.

Analysis of the expression of NB1 antigen using two monoclonal antibodies.

BACKGROUND: Neutrophil-specific antigen NB1 is expressed on neutrophil subpopulations in 97 percent of healthy individuals and is located on 56- to 64-kDa glycoprotein. While the molecule carrying NB1 has been identified, the nature of the NB1 epitope has not been well characterized. STUDY DESIGN AND METHODS: Two monoclonal antibodies (MoAbs), 1B5 and the recently produced 7D8, and four alloantibodies, all specific for NB1, were used to investigate the expression of NB1 on neutrophils from several donors. RESULTS: MoAb 7D8 was shown to be specific for NB1. It reacted with NB1-positive neutrophils from 52 donors in the granulocyte immunofluorescence assay and did not react with NB1-negative neutrophils from 8 donors. MoAb 7D8 immunoblotted a 56- to 64-kDa molecule on neutrophils from eight NB1-positive donors and did not react with this molecule on NB1-negative neutrophils from two donors. When 7D8 was tested in the monoclonal antibody immobilization of granulocyte antigens assay, it reacted with two NB1 alloantibodies, but not with NA1 or NA2 alloantibodies. To determine if MoAbs 7D8 and 1B5 recognized the same epitope, both were tested against the same NB1-positive neutrophils and the cells were analyzed by two-color flow cytometry. Both antibodies bound independently to neutrophils, which indicated that the antibodies recognized different epitopes. When similar studies were performed with MoAb 7D8 and three NB1 alloantibodies, 7D8 partially inhibited the binding of two of the alloantibodies. The size of the NB1-positive subpopulation was analyzed in 25 people using flow cytometry with both MoAbs and three alloantibodies. The subpopulation of antigen-positive cells was similar in all donors when 7D8 and the three NB1 alloantibodies were tested; however, the subpopulation recognized by MoAb 1B5 was smaller in two of the donors. Neutrophils from one of these people were analyzed by immunoblotting, and no differences were detected in the molecule carrying NB1 in those neutrophils and that molecule in control neutrophils. CONCLUSION: NB1 specificity is made up of at least two separate epitopes. The expression of NB1 varied among antigen-positive individuals. While NB1 is expressed by a 56- to 64-kDa glycoprotein, the structure of this protein on antigen-negative cells has not been determined.

The effect of combined topical steroids and habit-reversal treatment in patients with atopic dermatitis.

A modified behavioural method called habit-reversal, in combination with potent and weak corticosteroid cream, was compared with the use of the creams alone in the treatment of 45 patients with atopic dermatitis. The patients were randomly assigned to four groups, which received two different cream regimes in combination with the habit-reversal treatment. The patients' skin was assessed before, during and after treatment, and they recorded the amount of scratching during the study. The skin condition improved in all groups, but to a significantly greater degree in the habit-reversal groups. A strong correlation was found between the reduction in scratching and the improvement in skin status.

Behavioural treatment of scratching in patients with atopic dermatitis.

A behavioural method of habit reversal, in combination with a hydrocortisone cream, was compared with the use of cream alone in the treatment of 17 patients with atopic dermatitis. The patients were assigned randomly to two groups, one of which received the combination treatment and the other regular ointment treatment. The patients' skin status was assessed before and after treatment, and the patients recorded their scratching during the study. Both groups improved, but the group which received habit-reversal therapy improved significantly more. A strong correlation was found between reduction in scratching and improvement in skin status.

Two different pathogenetic pathways in lichen amyloidosus and macular amyloidosis.

In lichen amyloidosus (LA) and macular amyloidosis (MA), small amyloid deposits occur in the upper papillary dermis. Previous electron-microscopic studies have indicated an epidermal origin of the amyloid, where degenerating keratinocytes drop into the dermis and undergo transformation to amyloid. While this mechanism seems possible at least in MA, we suggest an alternative pathogenetic pathway in LA, in which amyloid fibrils seem to form on the dermal surface of living basal keratinocytes. It is possible that the different morphology of the amyloid in LA and MA is explained by partially different pathogenetic mechanisms although the amyloid in both conditions may be chemically closely related.

Long-term safety of trioxsalen bath PUVA treatment: an 8-year follow-up of 149 psoriasis patients.

A thorough clinical follow-up study with regard to the occurrence of degenerative skin changes and cutaneous carcinomas was undertaken in 1982 in 149 patients with moderate to severe psoriasis treated with PUVA baths (trioxsalen + UVA). The PUVA treatment had been commenced between 1974 and 1978. With trioxsalen baths a high sensitivity to UVA is obtained. The initial UVA dosage is therefore as low as 0.04-0.08 J/cm2 and in the majority of the patients the maximum daily dose was about 1.0 J/cm2. The accumulated UVA dosage was low. Thus 89% of the patients had received less than 50 J/cm2 in 5-8 years of bath PUVA treatment. No degenerative skin changes were found on PUVA-exposed skin that were not also seen on the facial skin not exposed to PUVA. Two patients showed mild mottling of exposed skin. Otherwise no PUVA-related degenerative changes were observed. No carcinomas were found on bath PUVA-treated skin.

Immunofluorescence and histochemical studies of localized cutaneous amyloidosis.

Lichen amyloidosus (LA) and macular amyloidosis (MA) are two forms of localized cutaneous amyloidosis in which the amyloid occurs as larger and smaller deposits respectively in the papillary dermis. The histogenesis of the amyloid of these conditions is unknown. By using an indirect immunofluorescence technique we showed that LA and MA do not react with antibodies against different previously characterized amyloid fibril proteins. These results indicate that the amyloid of LA and MA is different from other known types of amyloid. Protein AP, which was demonstrated in amyloid of MA and LA, is known to be present in all forms of amyloid and is of unknown significance. Antiserum against keratin did not react with the larger homogeneous amyloid bodies, but showed a weak reaction with some small deposits. Histochemical staining failed to show keratin in any of the tissues containing LA or MA.