Of 60 patients with atopic dermatitis (30 males and 30 females, 15-30 years old) 30 were treated with gamma-linolenic acid of (C18:3 n-6) at a dosage of 274 mg twice a day; the other 30 patients were given placebo. The patients were treated for 12 weeks, during which their symptoms were assessed on a linear scale both by a dermatologist and by themselves every 4 weeks. The patients who received gamma-linolenic acid, showed gradual improvements in pruritus, erythema, vesiculation and oozing, which were statistically significant compared with the control group (P < 0.001). Only one patient had presented with scaling at the beginning of the study and this symptom appeared to be less influenced by the effects of gamma-linolenic acid. The assessments of symptoms made by the dermatologist were generally consistent with those made by the patients themselves. gamma-linolenic acid was found to be effective and without side-effects for the treatment of atopic dermatitis.

A reduced amount of total ceramides could be responsible for functional abnormalities of the skin of atopic dermatitis (AD) patients. The ability of an experimental cream containing sonicated Streptococcus thermophilus to increase skin ceramide levels in healthy subjects has been previously reported. The aim of the present work was to investigate the effects of the topical administration of a S. thermophilus-containing cream on ceramide levels of stratum corneum from AD patients. A 2-week application of the cream, containing a sonicated preparation of the lactic acid bacterium S. thermophilus, in the forearm skin of 11 patients led to a significant and relevant increase of skin ceramide amounts, which could have resulted from the sphingomyelin hydrolysis through the bacterial sphingomyelinase. Moreover, in all patients the topical application of our experimental cream also resulted in the improvement of the signs and symptoms characteristic of AD skin (i.e. erythema, scaling, pruritus).

This study investigates lymphocyte subsets in both the gastrointestinal mucosa and blood, in patients with nickel allergic contact dermatitis, after 10 mg oral nickel challenge (double-blind, placebo-controlled). 6 such patients with cutaneous symptoms induced only by skin contact with nickel (group A), 6 with a flare-up of cutaneous symptoms after food nickel ingestion (group B) and 6 healthy controls (group C) were enrolled. Blood lymphocyte subsets (CD4, CD45RO, CD8) were analyzed before and after 4 and 24 h from the challenge (test 1, 2, and 3), and intestinal biopsies were performed 2 days later. Challenges were positive in group B and negative in group A and controls. Serum and urine nickel levels significantly increased after nickel ingestion, with no differences between the 3 groups. At test 3, a significant decrease of the all CDs studied was found in group B. Biopsies of this group showed higher levels of CD45RO+ cells in the lamina propria and in the epithelium and lower levels of epithelial CD8+ lymphocytes. This study confirms that ingested nickel may induce flare-up of cutaneous reactions in some nickel-allergic patients, independently of the degree of sensitization and the intake of metal. In these patients, oral nickel stimulates the immune system, inducing maturation of T lymphocytes from virgin into memory cells; these latter cells seem to accumulate in the intestinal mucosa. The immunoreaction also involves CD8+ cells, whose role is not yet clear.

Two patients suffering from eosinophilic gastroenteritis (EG) were treated with sodium cromoglycate (SCG). Before treatment they showed enteric and cutaneous symptoms, such as abdominal pain, nausea, vomiting, diarrhoea and recurrent urticaria and angioedema. The histological findings were a notable amount of eosinophilic infiltration in the lamina propria and gastric glands, a villous shortening and thickening and weak eosinophilic inflammation in the duodenum. The patients were treated with 300 mg SCG, 4 times daily, for 4/5 months. During treatment, the clinical symptoms disappeared and at the end of treatment a reduced inflammation with an almost complete decrease of eosinophilic infiltration was observed. The results provide evidence of SCG efficacy in the treatment of EG and suggest its employment as an alternative to the steroids commonly used in EG.

15 women with a positive patch test only to nickel (Ni) and without atopy and 10 control women were selected for the study. Blood and urine specimens were collected with a standard procedure either before (at 8 a.m.) or 4 and 24 h after the ingestion of 10 mg of Ni (as Ni sulfate). 7 of the Ni-sensitized patients showed a flare-up of eczema and/or urticaria during the test, while the other women were non-symptomatic. Serum and urine Ni of controls and Ni-sensitized women did not significantly differ. Serum and urine Ni levels determined before the oral Ni challenge were in the range of reference values recently reported by other authors (0.2-2.0 micrograms/l of serum or urine). Ni was greatly augmented in urine and serum 4 h after the challenge (25th-75th percentiles: 43-264 micrograms/l urine Ni and 15-52 micrograms/l serum Ni). 24 h after Ni ingestion, urine Ni was 41-153 micrograms/l and serum Ni 4-17 micrograms/l. Our study confirms a previous investigation showing similar levels of serum and urine Ni following ingestion of the metal in control and Ni-sensitized women without atopy.