ABSTRACT
The significance of allergen-specific IgE as marker for severity of atopic dermatitis is controversial. The aim of this study was to determine the frequency of IgE-mediated sensitisation to food and environmental allergens in 132 children and 67 adults with atopic dermatitis, and its correlation to severity of atopic dermatitis (SCORAD). Total IgE was elevated (> 100 kU/l) in 79.7% of adults and 46.8% of children. Sensitisation frequencies to allergens, particularly microbial allergens, were up to 10-fold higher in adults compared to children. Severity of atopic dermatitis correlated with elevated total IgE in adults (r = 0.549, p < 0.001) and children (r = 0.344, p = 0.005) and with Malassezia spp.-specific IgE in adults (r = 0.429, p = 0.007). Total IgE is a marker for severe atopic dermatitis in both age groups. Malassezia spp.-specific IgE is an important allergen-specific marker for severity of atopic dermatitis in adults.
Subject(s)
Allergens/immunology , Antibodies, Fungal/blood , Dermatitis, Atopic/diagnosis , Immunoglobulin E/blood , Malassezia/immunology , Adult , Biomarkers/blood , Child , Child, Preschool , Dermatitis, Atopic/blood , Dermatitis, Atopic/immunology , Dermatitis, Atopic/microbiology , Female , Food Hypersensitivity/blood , Food Hypersensitivity/diagnosis , Food Hypersensitivity/immunology , Humans , Infant , Male , Middle Aged , Predictive Value of Tests , Risk Factors , Serologic Tests , Severity of Illness Index , Young AdultABSTRACT
Merkel cell carcinoma (MCC) is an aggressive, rare tumour of the skin. For advanced cases with distant organ metastases several different regimens of chemotherapeutics have been described. Disease specific 5-year survival rates for these patients are approximately 11%. In this case series we report our experience with orally administered etoposide (100 mg at days 1 to 10 in a 31 day cycle) in 4 patients. We treated two male and two female patients with a median age of 68.5 years. In our four treated patients the disease control rate (complete remission, partial remission, stable disease) was 100%. Three out of four patients reached complete remission. Promisingly, two of our patients had long lasting, durable responses which, until now, have lasted for 16 and 36 months, respectively. The mean follow up time after start of therapy was 14.25 months (range 1-36 months). Etoposide treatment was generally well tolerated, the most common side effect was neutropenia, in one case CTC grade 3. In conclusion, orally administered etoposide in metastatic Merkel cell carcinoma was highly effective and well tolerated.
Subject(s)
Antineoplastic Agents, Phytogenic/therapeutic use , Carcinoma, Merkel Cell/drug therapy , Etoposide/therapeutic use , Skin Neoplasms/drug therapy , Administration, Oral , Adult , Aged , Aged, 80 and over , Antineoplastic Agents, Phytogenic/administration & dosage , Antineoplastic Agents, Phytogenic/adverse effects , Carcinoma, Merkel Cell/pathology , Carcinoma, Merkel Cell/surgery , Combined Modality Therapy , Etoposide/administration & dosage , Etoposide/adverse effects , Female , Humans , Male , Middle Aged , Neoplasm Metastasis , Neutropenia/etiology , Remission Induction , Skin Neoplasms/pathology , Skin Neoplasms/surgery , Treatment OutcomeSubject(s)
Dermatitis, Atopic/therapy , Dermatologic Agents/adverse effects , Skin Diseases/chemically induced , Skin Pigmentation/drug effects , Skin/drug effects , alpha-MSH/analogs & derivatives , Adult , Dermatologic Agents/administration & dosage , Humans , Injections, Subcutaneous , Male , Self Administration , Skin/pathology , Skin Diseases/pathology , alpha-MSH/administration & dosage , alpha-MSH/adverse effectsABSTRACT
Dystrophic epidermolysis bullosa is a group of inherited skin blistering disorders caused by mutations in the COL7A1 gene coding for type VII collagen. More than 500 different COL7A1 mutations have been detected in dystrophic epidermolysis bullosa to date. Clarification of genotype-phenotype correlations is of particular importance for the development of novel therapeutic approaches. Here we report a female patient with mild dystrophic epidermolysis bullosa harbouring two compound heterozygous COL7A1 mutations, namely the intronic splice site mutation c.3832-2Aâ>âG and the glycine substitution p.G1347W. Our data extend the current knowledge on genotype-phenotype correlations in dystrophic epidermolysis bullosa.
