The use of chemical peelings in the treatment of different cutaneous hyperpigmentations.

BACKGROUND: Several chemical agents including hydroquinone, retinoic acid, and azelaic acid are currently used in the treatment of cutaneous hyperpigmentations. Recently chemical peelings with kojic acid, glycolic acid, and trichloroacetic acid, either alone or in combination, have been introduced for treatment of hyperpigmentations. OBJECTIVE: The purpose of our study was to evaluate the efficacy of trichloroacetic acid as well as glycolic acid associated with kojic acid in the treatment of cutaneous hyperpigmentations. METHODS: Twenty patients with diffuse melasma were treated with a solution composed of 50% glycolic acid and 10% kojic acid whereas 20 patients with localized hyperpigmentations (lentigo) were treated with 15%-25% trichloroacetic acid. RESULTS: Complete regression of diffuse melasma was observed in 6 of 20 patients (30%), a partial regression in 12 of 20 patients (60%), and no regression in 2 of 20 patients (10%) treated with 50% glycolic acid and 10% kojic acid. Complete regression of localized hyperpigmentations was observed in 8 of 20 patients (40%), a partial regression in 10 of 20 patients (50%), and no regression in 2 of 20 patients (10%) treated with 15-25% trichloroacetic acid. CONCLUSIONS: Based on our findings, both peelings can be considered effective in the treatment of cutaneous hyperpigmentations.

Analysis of microsatellite instability and loss of heterozygosity in keratoacanthoma.

We analyzed microsatellite instability (MSI) and loss of heterozygosity (LOH) at 17 microsatellite markers located on chromosomes 2p, 3p, 5q, 6q, 9p, 9q, 17p and 18q in 19 randomly selected keratoacantomas (KAS), in one cutaneous lesion that histologically could not unequivocally be differentiated from squamous cell carcinoma, and in one patient with multiple KAs of longstanding duration. The goals of our study were to determine whether, in a similar manner to some visceral carcinomas, genomic instability could be detected in KAs and to clarify whether molecular analysis might be useful to further characterize KA. MSI was observed in 2 of 21 cases (9.5%) at 5 of 17 loci examined. In one patient with a solitary KA, the presence of MSI and a family history of visceral malignant tumours suggested that the patient might have belonged to a family with Muir-Torre syndrome. In one other MSI+ KA, a definite differential diagnosis in relation to squamous cell carcinoma could not be established. In addition, one sample displayed LOH at 2 of 17 loci analysed whereas in the patient with multiple KAs, LOH at one locus was the only alteration found. In conclusion, the low frequency of MSI and LOH detected in our study suggests that these genetic events are uncommon in KA unless it is associated with a familial disease (e.g. Muir-Torre syndrome) or it has more aggressive histological features.

Widespread microsatellite instability in sebaceous tumours of patients with the Muir-Torre syndrome.

Muir-Torre syndrome (MTS) is an autosomal dominant disorder characterized by the presence of at least one sebaceous gland tumour and a minimum of one visceral malignant tumour. Recently, microsatellite instability (MSI) has been detected in the tumours of patients with MTS and germline mutations of the hMSH2 and hMLH1 mismatch repair genes have been detected in some patients with this syndrome. To determine if the tumours of patients with MTS have widespread genomic instability and whether loss of heterozygosity (LOH) in the chromosomal regions containing hMSH2 and hMLH1 is detectable, MSI and LOH were examined at 10 dinucleotide repeats on chromosomes 2p, 3p, 5q, 9p, 17p and 18q. Data were obtained from six sebaceous gland tumours and two adenocarcinomas of the colon from three patients of two Muir-Torre families. MSI was detected at more than half of the loci tested in all sebaceous tumours examined. In addition, there was LOH at D2S119 in one sebaceoma and one sebaceous carcinoma from one patient. The colon carcinomas from two patients showed MSI at five of the 10 loci analysed. These results show that widespread MSI is a feature of tumours in patients with MTS. In addition, the finding of LOH at D2S119, a marker located in the vicinity of hMSH2, in sebaceous tumours of one patient indicates that this gene may have a pathogenetic role in this patient.

Correlation of lesional skin corneometry values with serum E-selectin levels and disease severity in patients affected by plaque-type psoriasis: recovery after effective therapy.

Ten subjects with plaque-type psoriasis (5 females, 5 males, median age 47, range 20-71 years, median psoriasis area and severity index [PASI] score = 15.5, range 8.1-23.0) were observed before (week 0) and at the second and sixth week after starting treatment (PASI = 10.5, range 7.8-14.6; PASI = 8.5, range 1.6-11.6, respectively). At each of these times, the patients were evaluated for both lesional and unlesional skin corneometry and serum E-selectin values, previously shown to be increased in psoriatic subjects. At time 0, both the corneometry and the E-selectin values were significantly correlated with the PASI, infiltration and desquamation scores. As expected, the corneometry was statistically higher in the unlesional than in the lesional areas (p < 0.001). After therapy, the lesion improvement was related both to the PASI scores and E-selectin level decreases (from median levels of 15.5 to 8.5 and from 18 to 13.2 ng/ml, respectively, p < 0.05) as well as to the corneometric level increases (from a median value of 34.5 to 42, p < 0.05). Considering the data obtained at all of these times, significant correlations were found between the PASI scores, lesional skin corneometry and serum E-selectin levels. In conclusion, lesional corneometry seems to represent an objective alternative method for reliably monitoring psoriatic patients.