Pemphigus: trigger and predisposing factors.

Pemphigus is a life-threatening autoimmune blistering disease affecting skin and mucous membranes. Despite its etiopathogenesis remains largely unknown, several trigger and predisposing factors have been reported. Pemphigus is caused by autoantibodies that target desmoglein 1 and desmoglein 3, impacting desmosome function. However, circulating autoantibodies are often the consequence of a precipitating factor that occurs in predisposed individuals. This review aims to describe and discuss almost all trigger and predisposing factors reported as possible or probable cause of the disease. Among the reported trigger factors that may induce or exacerbate pemphigus, we have found of particular interest: drug intake (especially thiol- and phenol-containing compounds), vaccines, infections, as well as some reports about pregnancy, radiations, emotional stress, pesticides and physical trauma. Moreover, we discuss the possible role of food intake in pemphigus onset and particular attention is given to dietary factors containing thiol, phenol and tannin compounds. A trigger factor is "the straw that breaks the camel's back," and often acts together with predisposing factors. Here we discuss how pemphigus onset may be influenced by genetic susceptibility and comorbidities like thyroid diseases, malignancies and other autoimmune disorders. To identify other hitherto unknown trigger and predisposing factors, well designed prospective studies are needed. In this context, future research should explore their connection with the aim to advance our understanding of pemphigus pathogenesis.

Bullous Pemphigoid: Trigger and Predisposing Factors.

Bullous pemphigoid (BP) is the most frequent autoimmune subepidermal blistering disease provoked by autoantibodies directed against two hemidesmosomal proteins: BP180 and BP230. Its pathogenesis depends on the interaction between predisposing factors, such as human leukocyte antigen (HLA) genes, comorbidities, aging, and trigger factors. Several trigger factors, such as drugs, thermal or electrical burns, surgical procedures, trauma, ultraviolet irradiation, radiotherapy, chemical preparations, transplants, and infections may induce or exacerbate BP disease. Identification of predisposing and trigger factors can increase the understanding of BP pathogenesis. Furthermore, an accurate anamnesis focused on the recognition of a possible trigger factor can improve prognosis by promptly removing it.

Underestimated clinical features of postadolescent acne.

BACKGROUND: Postadolescent acne is usually described as an inflammatory, mild-to-moderate dermatosis, frequently involving the lower third of the face, the jawline, and the neck. However, we have also frequently observed a clinical form predominantly characterized by retention lesions (microcomedones and macrocomedones), with few inflammatory lesions (comedonal postadolescent acne [CPAA]), which appears significantly correlated with cigarette smoking. OBJECTIVE: We sought to investigate the clinical features of postadolescent acne in a group of female patients affected by acne and its relationship with cigarette smoking. METHODS: A total of 226 women with acne (25-50 years) attending our department were examined by a team of 3 dermatologists, to assess the age of onset of the disease, and the number, type, and distribution of acne lesions. RESULTS: In all, 192 of 226 patients (85.0%) were classified as having CPAA and 34 as having papulopustular postadolescent acne. A smoking habit was confirmed in 150 of 226 (66.3%). Remarkably, 72.9% of patients with CPAA were smokers as compared with only 29.4% of those with papulopustular postadolescent acne (P < .0001). LIMITATIONS: Possible limitations are related to geographic area or to the prevalence of darker skin types (III and IV) (data about skin types have not been collected). Other possible aggravating factors (ie, stress and diet) have not been investigated. CONCLUSIONS: According to our results, CPAA appears as the most frequent clinical form of postadolescent acne and seems to be strictly correlated with cigarette smoking.

Acne and smoking.

BACKGROUND.: Post-adolescent acne is an inflammatory disorder, whose cause is unknown. Contrasting data are available on correlation between acne and smoking habit. OBJECTIVES.: To verify the frequency of clinically non-inflammatory (atypical) post-adolescent acne (APAA) among women, a possible correlation with cigarette smoking, possible differences in sebum composition in a group of female smokers with acne compared to healthy smokers and non-smokers. METHOD AND RESULTS.: 1046 randomly selected women (25-50-years-old) participated at the study. In 60 selected female subjects we analyzed sebum composition for alpha-tocopherol, squalene and squalene monohydroperoxide. We found a high prevalence of APAA among women (74.6%), a strong correlation with smoking habit (p < 0.0001), as well as an increase in the grade of sebum peroxidation (p < 0.05) with a reduction in vitamin E (p = 0.02), in the subjects with acne compared to the controls. CONCLUSIONS.: Clinical evidence and experimental data showed a straight correlation between smoking habit and post-pubertal acne in which the clinically non-inflammatory type-APAA-is the most frequent. In the more severe cases we could consider APAA as a new entity (smoker's acne).

Antigen specific cytokine response in pediatric patients with atopic dermatitis.

The physiopathology of atopic dermatitis (AD) has still to be elucidated. T effector cells with cutaneous homing receptors or T-cell derived cytokines have been assumed to be implicated in the pathogenetic mechanisms in AD and to be responsible for the different immunologic responses of patients. In fact, the large majority of AD patients display high IgE levels while others do not develop an abnormal IgE response. Although, there are not significant clinical features characterizing the two different groups, patients with normal IgE belong to a younger age range, raising the possibility that the hypothesized dichotomy of AD might be due to age. In the present study we included 172 outpatient children attending the Pediatric Department of our institution. Serum IgE levels and percentages of peripheral T lymphocytes expressing the cutaneous homing antigen (CLA) were evaluated and results were analyzed in relation to the activity of the disease (SCORAD index) or age. In the overall patients, the IgE levels increased significantly with age (0-1 yr: 19.50 IU/ml; 1-3 yr: 62.0 IU/ml; 3-8 yr: 96.0 IU/ml; >8 yr: 148.5 IU/ml; p<0.001) and with the severity of the disease (SCORAD low: 46.80 IU/ml; medium: 42.90 IU/ml; high: 148.5 IU/ml; p=0.01). Percentages of CLA+ peripheral T lymphocytes also increased with age (0-1 yr: 3.3; 1-3 yr: 4.85; 3-8 yr: 10.6; >8 yr: 12.5; p<0.001), although they were not significantly different in patients with different SCORAD (p=0.89). We further investigated the cellular immune response to a specific antigen in 25 subjects, matched for age, SCORAD, and CLA+ T-cell percentages. Among them, 13 patients had casein serum specific IgE and 12 had no evidence of casein sensitization. Peripheral blood mononuclear cells were kept in short-term culture with endotoxin-free casein fractions and IFN-gamma, TNF-alpha, IL-5, IL-10 cytokine-producing cells were detected by ELISpot. Statistical analysis showed significant higher numbers of TNF-alpha- or IL-10-producing cultures (stimulation index >3) in the 'allergic' patients than in the milk tolerant subjects (p=0.01 and 0.05). The analysis of individual responses confirmed this finding but also provide evidence of a significant increase in IFN-gamma-producing cells (p=0.05) induced by casein stimulation in the group of 'non-allergic' children. Our data showed that immunologic parameters as IgE levels or CLA+ T cells in AD pediatric patients are influenced by the age, confirming that age could represent a bias in the analysis of immune response in those patients. Although, we demonstrated in children with AD the existence of different cytokine patterns of the lymphocyte response that could account for the different immunologic features between the two hypothesized forms of AD, which are not dependent on age.