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Effectiveness of various barrier preparations in preventing and/or ameliorating experimentally produced Toxicodendron dermatitis.

BACKGROUND: Despite extensive research on hyposensitization and prior application of topical barrier preparations, efforts to prevent Toxicodendron dermatitis have been only minimally successful. OBJECTIVE: Seven different barrier creams were evaluated for topical protection against experimentally produced Toxicodendron dermatitis in a randomized, double-blind study. METHODS: Twenty patients had the seven barrier creams randomly applied to eight test sites (one untreated area as control) on each forearm before application of the Toxicodendron extract. Development of Toxicodendron dermatitis was followed for 8 days, with measurements of erythema, induration, vesiculation, and global severity taken at each site on days 1, 2, 3, 4, and 7 after Toxicodendron application. RESULTS: The barrier creams Stokogard, Hollister Moisture Barrier, and Hydropel significantly reduced the erythema, induration, and global severity of Toxicodendron dermatitis and did not differ from each other. The percent reductions in global dermatitis severity per day of assessment for the seven barriers in order of effectiveness were as follows: Stokogard, 59%; Hollister Moisture Barrier, 52%; Hydropel, 48%; Ivy Shield, 22%; Shield Skin, 13%; Dermofilm, 13%; and Uniderm, -9%. During the 8-day period, a significantly greater number of test sites pretreated with Stokogard, Hollister Moisture Barrier, and Hydropel were free of dermatitis compared with control sites and sites treated with the other four barriers. CONCLUSION: The results indicate that Stokogard, Hollister Moisture Barrier, and Hydropel are effective in the prevention of Toxicodendron dermatitis.

Administration, Cutaneous↗

Allergic contact dermatitis from color film developers: clinical and histologic features.

We evaluated two patients with allergic contact dermatitis that resulted from exposure to color film developers. A lichenoid eruption developed in one patient, whereas an eruption more characteristic of an acute spongiotic dermatitis developed in the second patient. Histologic findings in the first case were those of a "lichenoid dermatitis" but with features distinct from classic lichen planus. The biopsy specimens from the second patient showed a subacute spongiotic process with a bandlike infiltrate suggestive of an evolving lichenoid process. Contact allergy to color developers may result in eruptions similar to lichen planus. This process appears to evolve from an acute spongiotic dermatitis in its early phase to a lichenoid dermatitis in fully developed and more chronic forms. Although the histologic features are those of a "lichenoid" dermatitis, some features, such as the presence of spongiosis, eosinophils, and a less intense inflammatory infiltrate, may enable distinction between lichenoid allergic contact dermatitis and true lichen planus. In addition, clinicopathologic correlation with patch test results should permit accurate diagnosis in most cases.

Adult↗

Enhancement of IgE production by anti-CD40 antibody in atopic dermatitis.

It has been recently recognized that the obligate requirement for T cells in the development of IgE responses can be substituted for by anti-CD40 antibody. In this study of patients with atopic dermatitis and high IgE levels, we have analyzed the role of the CD40 molecule in IgE production. Costimulation of peripheral blood mononuclear cells (PBMCs) from normal donors with interleukin-4 (IL-4) and anti-CD40 monoclonal antibody resulted in a selective increase in IgE production; either reagent alone, however, was ineffective. In contrast, addition of anti-CD40 monoclonal antibody alone to PBMCs or B cells from patients with atopic dermatitis markedly increased IgE production, even in the absence of exogenous IL-4. With the use of an ELISA spot assay, this increase in IgE production was attributed to an expansion of IgE-secreting B cells. In anti-IgM-stimulated lymphocyte cultures from patients with atopic dermatitis the costimulation with anti-CD40 induced strong lymphocyte proliferation. Similar results were observed with anti-IgM plus IL-4. The augmentation induced by anti-CD40 was inhibited by addition of anti-IL4 to anti-CD40-treated atopic dermatitis cells. In normal subjects the effects of anti-CD40 alone on IgE production could be observed after pretreatment of normal PBMCs with IL-4 for 3 days. The effects of anti-CD40 in atopic dermatitis may be explained in part by differences in CD40 expression. In freshly isolated PBMCs from patients with atopic dermatitis, the mean fluorescence intensity of CD40 expression on B cells was increased when compared with PBMCs from nonatopic donors, ans stimulation of normal or atopic dermatitis PBMCs with IL-4 increased the intensity of CD40 staining of cells.

Adolescent↗

Antigen presenting cell-independent cytokine and spontaneous in vitro IgE production in patients with atopic dermatitis: increased interferon-gamma production and lack of effects of in vivo low-dose interferon-gamma treatment.

Atopic dermatitis is characterized by elevated serum IgE concentrations and dysregulation of T-lymphocyte function. To examine the pattern of cytokine production associated with elevated IgE levels, phorbol ester plus ionomycin-stimulated production of interleukin (IL)-4, IL-5, and interferon-gamma (IFN-gamma) by blood mononuclear cells from 16 patients with atopic dermatitis was compared with that of 18 healthy subjects. Spontaneous in vitro IgE production was also studied longitudinally in patients receiving placebo or daily treatment with 0.05 mg/m2 IFN-gamma. Spontaneous in vitro IgE production and mitogen-driven IL-4 and IFN-gamma synthesis did not differ when patients were receiving interferon treatment compared with no treatment. Furthermore, ionomycin plus phorbol ester-stimulated mononuclear cells from patients with atopic dermatitis produced less IL-4 and more IFN-gamma than did cells from healthy subjects. IL-5 production by cells from patients with atopic dermatitis did not differ from that of cells from healthy subjects. The ratio of IL-4 to IFN-gamma produced in vitro was significantly lower (p = 0.04) in the cells of patients with atopic dermatitis (0.9) as compared with those of healthy subjects (2.7). The findings suggest that when circulating T cells are stimulated under antigen presenting cell-independent conditions, atopic dermatitis is not characterized by the shift in the reciprocal relationship between IL-4 and IFN-gamma production, which has been postulated to explain the pathogenesis of IgE elevation and the therapeutic action of IFN-gamma in patients with atopic dermatitis.

Adult↗

[Atopic dermatitis: which are the diagnostic criteria used in medical literature?].

INTRODUCTION: Diagnosis of atopic dermatitis currently relies on diagnostic criteria scales developed by Hanifin and Rafka in 1980 and by the "United Kingdom Working party" in 1994. Some authors have proposed: "AEDS" [sM1] and "Atopiform Dermatitis", which has led to the distinction between different sub-populations and the exclusion of certain diseases from the diagnosis of atopic dermatitis. The aim of our study was to collect the criteria retained in the scientific medical literature during the year 2002 for the definition of atopic dermatitis and to try to understand not only the interest but also the questions that the various definitions lead to. METHOD: A PubMed research was launched with the key word "atopic dermatitis" from January to September of 2002. All the scientific articles either in French or in English were studied. RESULTS: Hanifin and Rafka's criteria were selected in 44 p. 100 of the scientific articles, and the "United Kingdom Working Party" criteria in 12 p. 100. Personal definitions were used in 21 p. 100 of the articles; these were based on the level of total and specific IgE or on personal clinical criteria. For twenty-three p. 100 of the authors, the definition of atopic dermatitis was not specified. DISCUSSION: There was not just one definition of atopic dermatitis. This may affect the interpretation of diagnostic or therapeutic papers concerning the disease, because there has been no proof that these definitions cover the same population of patients.

Dermatitis, Atopic↗

Retinal detachment with atopic dermatitis similar to traumatic retinal detachment.

PURPOSE: The cause of retinal detachment (RD) with atopic dermatitis remains uncertain. The purpose of this study is to show that the probable cause of RD with atopic dermatitis is ocular contusion. METHODS: The authors retrospectively compared the fundus findings of 24 eyes (16 patients) that had RD and atopic dermatitis with 36 eyes (36 patients) that had traumatic RD. RESULTS: The authors found similar characteristics. Retinal breaks at vitreous base borders characterized by ocular contusion occurred in 79.2% of eyes with RD and atopic dermatitis and in 75.0% of eyes with traumatic RD. Irregular retinal traumatic breaks in the equatorial zone occurred in 20.8% of eyes with RD and atopic dermatitis and in 47.2% of eyes with traumatic RD. Objective signs of ocular contusion outside the retina appeared in 54.2% of eyes with RD and atopic dermatitis. CONCLUSIONS: The authors' data support the conclusion that self-inflected ocular contusion by tapping the eyes can cause RD with atopic dermatitis.

Adolescent↗

[Etiologic implication of foods in atopic dermatitis: evidence in favor].

Some of the immunopathologic mechanisms involved in IgE responses are currently being identified; Th2 lymphocytes are known to be activated in patients with atopic dermatitis with subsequent production of the cytokines interleukin (IL)-4 and IL-5, which are responsible for IgE production and eosinophil recruitment. Nevertheless, T cell activation in this disease takes place in two phases. In the first phase, Th2 cells are activated and IL-4, IL-5 and IL-13 are produced; this first stage is produced with the initial activation induced by the antigen. In the second phase there are chronic lesions, Th1 lymphocytes are activated and IFg is produced. This chronic phase is associated with the presence of eosinophils and macrophages that produce IL-12.Numerous articles have demonstrated food sensitization to be an etiopathogenic factor in atopic dermatitis. The prevalence of sensitization varies, depending on the patient's age and the severity of the disease. Children with moderate-to-severe atopic dermatitis have been observed to have a positive skin test and high IgE concentrations to various foods. Nevertheless, a positive skin test to foods in such children does not always implicate these foods as the cause of the clinical manifestations; moreover, in children showing subsequent tolerance to these foods, skin tests can sometimes remain positive and high levels of specific IgE can persist. It is now known that IgE not only participate in the degranulation of mastocyte cells but also in reactions mediated by T cells and other antigen-presenting cells (dendritic cells) which have high-affinity receptors for IgE.The immediate IgE response is well known but it is also known that in addition to the immediate response, a delayed response is also involved, evidenced by the presence of antigen-specific T cells to foods or other allergens such as inhalant allergens. After a strict exclusion diet, children with atopic dermatitis and sensitivity to foods such as milk, egg, flour and soya can develop tolerance; for this reason provocation tests with the food in question should be repeated every 2-3 years. In children with sensitivity to other foods such as dried fruits, fish, and shellfish, sensitivity can sometimes persist into adulthood without tolerance being achieved. In conclusion, there are two groups of children with atopic dermatitis. One group consists of those with atopic dermatitis (allergic disease), which is characterized by early development, high IgE titers, the presence of antigen-specific IgE to allergens and a family history of atopy and which is clinically moderate or severe. Early diagnosis and treatment are important in these children, as is the prevention of progression of the disease to bronchial asthma. The other group consists of children whose dermatitis is clinically atopic in terms of its localization and morphology, who have no demonstrable allergic disease and whose management differs from that in children presenting allergic disease.

Child↗

Topical application of natural honey, beeswax and olive oil mixture for atopic dermatitis or psoriasis: partially controlled, single-blinded study.

OBJECTIVES: To investigate the effects of honey, olive oil and beeswax mixture on patients with atopic dermatitis (AD) or psoriasis vulgaris (PV). MATERIALS AND METHODS: Twenty-one patients with dermatitis and 18 patients with psoriasis were entered for patient-blinded, partially controlled study; 11 patients with dermatitis used topical betamethasone esters and 10 patients with psoriasis used clobetasol propionate. Honey mixture contained honey, beeswax and olive oil (1:1:1). Mixtures A, B, and C contained honey mixture with the corticosteroids ointment in a ratio of 1:1, 2:1, and 3:1 respectively. Patients with dermatitis were subjected to controlled bilateral half-body comparison to evaluate the efficacy of honey mixture against Vaseline, or mixture A against Vaseline-betamethasone esters mixture (1:1) in patients using topical corticosteroid treatment. In patients with psoriasis, the effect of honey mixture was compared with paraffin in an individual right/left-sites comparison, or mixture A against paraffin-clobetasol propionate mixture (1:1) in patients using corticosteroid topical therapy. In dermatitis, body lesions on right or left half-body were assessed for erythema, scaling, lichenification, excoriation, indurations, oozing and itching on a 0-4 points scale. In psoriasis, lesions of selected site were assessed for redness, scaling, thickening and itching, on a 0-4 points scale. RESULTS: In honey mixture group, 8/10 patients with dermatitis showed significant improvement after 2 weeks, and 5/11 patients pretreated with betamethasone esters showed no deterioration upon 75% reduction of corticosteroid doses with use of mixture C. In psoriasis, 5/8 patients showed a significant response to honey mixture. In patients using clobetasol propionate, 5/10 patients showed no deterioration upon 75% reduction of corticosteroid doses with use of mixture C. CONCLUSION: Honey mixture appears useful in the management of dermatitis and psoriasis vulgaris.

Administration, Topical↗

Textile dermatitis in Israel: a retrospective study.

BACKGROUND: The diagnosis of contact dermatitis caused by clothing may be difficult because of its clinical polymorphism. Data in the literature suggest that textile dermatitis is more common than previously thought. OBJECTIVE: Our purpose was to study our patients suspected of having textile contact dermatitis from 1991 to 1997. METHODS: The records of the patients with positive reactions to allergens from the Textile Colors and Finish series in 3 contact dermatitis clinics were reviewed. All the patients were clinically evaluated and patch tested with the European Standard series and the Textile Colors and Finish series (Chemotechnique Diagnostics, Malmö, Sweden). RESULTS: Twenty-two of the 55 patients (40%) had positive patch tests to the textile dye allergens. Four of them had occupationally related textile dermatitis. The most frequent allergens were Disperse Blue 124, Disperse Blue 85, Disperse Red 17, and Disperse Blue 106. Erythematosquamous lesions were the most common forms of textile dermatitis (56%), followed by pustular lesion (16%) and hyperpigmented patches (8%). CONCLUSIONS: The relatively high percentage of positive results (40%) was attributable to the selected cohort of patients. In our series, positive reactions to the allergens Disperse Blue 124, 85, and 106 were common findings. Clinically, pustular allergic contact dermatitis, triggered by textile dyes was observed along with the more frequent erythematosquamous clinical form.

Adolescent↗

Disperse blue dyes 106 and 124 are common causes of textile dermatitis and should serve as screening allergens for this condition.

BACKGROUND: Textile dye dermatitis is frequently undiagnosed because clinical awareness is low and because of the absence of good screening allergens in standard patch test series for this type of contact dermatitis. OBJECTIVES: To determine the incidence of textile dye allergy in patients with problematic eczemas evaluated at a contact dermatitis clinic, and to determine the incidence of allergic contact dermatitis to diperse blue dyes in these patients. METHODS: We conducted a retrospective study of 788 patients who were patch tested to either the North American Contact Dermatitis Group (NACDG) Standard Series or the European Standard Series, in addition to other relevant series. The Chemotechnique textile series was utilized in 271 patients (28%). RESULTS: Forty patients reacted positively to 1 or more textile dyes, the majority reacting positively to Disperse Blue 106 (33 of 40; 82.5%) and to Disperse Blue 124 (32 of 40; 80%). Ten of 11 tested patients reacted to their own clothing, 9 of whom reacted to the blue/black 100% acetate or 100% polyester liners in their garments. CONCLUSIONS: Textile dye allergy is more common than previously reported. It can cause marked dermatitis and widespread autoeczematization reactions. The most frequent allergens are Disperse Blue 106 and 124, which are frequently found in the 100% acetate and 100% polyester liners of women's clothing. We recommend that Disperse Blue 106 or 124 serve as the screening allergen for textile dye dermatitis.

Adult↗

IgG and IgE immune response against the surface glycoprotein gp200 of Saccharomyces cerevisiae in patients with atopic dermatitis.

The heat-stable and soluble glycoprotein gp200 (molecular weight 200 kDa) is part of the cell wall of S. cerevisiae. Recently, an association was shown between IgA and IgG against gp200 and inflammation in Crohn's disease. Gp200 is able to induce a proliferation of human lymphocytes in vitro, together with a natural killer cell associated cytotoxicity. Specific IgE against Saccharomyces cerevisiae (baker's or brewer's yeast) may be detected in approximately 73%, against Candida albicans in 68% of those patients suffering from severe atopic dermatitis. The aim of this study was to elucidate the possible role of an anti-gp200 immune response for the pathogenesis of atopic dermatitis by immunoblot analysis. Anti-gp200 IgE was found in 55% of healthy individuals, in 67% of individuals with atopic predisposition without eczema, in 63% of the patients with mild atopic dermatitis, and in 86% of patients with severe atopic dermatitis, respectively. On the contrary, anti-gp200 IgG could be shown in 55% of healthy individuals, in 89% of individuals with atopic predisposition but without eczema, in 100% of patients with mild atopic dermatitis, and in 79% with severe atopic dermatitis, respectively. No immunoreactivity was found when an extract of Arxula adeninivorans was used as antigen. These results underline the specificity of the immunoblot results with gp200 from Saccharomyces cerevisiae. It can be concluded that occurrence of specific IgE against Saccharomyces cerevisiae cannot be explained by a cross reactivity, e.g., against Candida albicans allergens. Further investigations with the recombinant gp200 will give information on the role of this glycoprotein both in atopic dermatitis and Morbus Crohn.

Antigens, Fungal↗

Serum antibodies to Malassezia yeasts in canine atopic dermatitis.

Significant numbers of humans with atopic dermatitis develop Malassezia-specific IgE. Immediate skin-test reactivity to Malassezia has been demonstrated in atopic dogs. The aim of this study was to compare the serum IgG and IgE response to Malassezia in atopic dogs with and without clinical evidence of Malassezia dermatitis and/or otitis, nonatopic dogs with clinical evidence of Malassezia dermatitis and/or otitis and healthy dogs. Cytology was used to diagnose clinically significant Malassezia dermatitis and otitis. Contact plate cultures confirmed the validity of this technique. Reproducible enzyme-linked immunosorbent assays for Malassezia-specific IgG and IgE in canine serum were established. Atopic dogs had significantly higher serum IgG and IgE levels than either healthy dogs or nonatopic dogs with clinical evidence of Malassezia dermatitis and/or otitis. There was no significant difference in IgG and IgE levels between atopic dogs with and without clinical evidence of Malassezia dermatitis and/or otitis. The implications of these findings in the pathogenesis and management of canine atopic dermatitis are discussed.

Animals↗

Association of atopic dermatitis to the beta subunit of the high affinity immunoglobulin E receptor.

IgE dysregulation is a major pathogenic feature of atopic dermatitis and other IgE-mediated allergic diseases such as asthma and rhinitis. Allergen complexed to IgE binds to the high affinity receptor for IgE (Fc epsilon RI) on the surface of epidermal Langerhans cells, mast cells and basophils, triggering the release of inflammatory mediators. The beta subunit of Fc epsilon RI has been localized to human chromosome 11q12-13, and variants within this gene have been shown to associate with asthma and measures of atopy. We have tested several polymorphisms within Fc epsilon RI-beta for association to atopic dermatitis in a panel of 60 families (panel A), recruited through a proband with atopic dermatitis. The findings were tested in a second panel of families (panel B). Significant sharing of maternal alleles was seen for atopic dermatitis and allele 2 of RsaI intron 2 (RsaIvin2*2) (P = 0.0022) and allele 1 of RsaI exon 7 (RsaIvex7*1) (P = 0.0036) Fc epsilon RI-beta gene polymorphisms. These findings were replicated in Panel B, confirming the association of Fc epsilon RI-beta RsaI polymorphisms with atopic dermatitis. The combined significance of the association of atopic dermatitis to RsaI polymorphisms was P = 0.0002 (RsaIvin2*2) and P = 0.00034 (RsaIvex7*1). The polymorphisms also showed association with asthma: P = 0.0068 (RsaIvin2*2) and P = 0.018 (RsaIvex7*1). Polymorphisms within the Fc epsilon RI-beta gene are strongly associated with atopic dermatitis.

Adolescent↗

Circulating CLA+ lymphocytes from children with atopic dermatitis contain an increased percentage of cells bearing staphylococcal-related T-cell receptor variable segments.

BACKGROUND: Atopic dermatitis is an allergic T-cell mediated skin inflammation. Staphylococcus aureus colonization is very common in cutaneous atopic dermatitis lesions. The cutaneous lymphocyte-associated antigen (CLA) is a T cell skin homing receptor that defines T lymphocytes associated with the cutaneous immune response. OBJECTIVE: To study whether CLA+ T cells from atopic dermatitis children present a selective expression for Staphylococcus aureus-related TCR Vbeta segments. METHODS: Peripheral blood T cells were stained with HECA-452 (anti-CLA) and a panel of TCR Vbeta specific monoclonal antibodies and analysed by flow cytometry. RESULTS: Atopic dermatitis patients have a higher percentage of circulating CLA+ CD3+ lymphocytes compared with healthy controls. Patients with active atopic dermatitis during the study expressed a higher percentage of cells positive for the TCR Vbeta2 and Vbeta5.1 segments in the CLA+ but not in the CLA- subset. These TCR Vbetas are recognized by staphylococcal superantigens. Moreover, there was an increased percentage of HLA-DR+ expression by CLA+ Vbeta5.1+ T cells in patients with active atopic dermatitis, but those patients whose eczema was inactive had very similar values to healthy controls regarding TCR Vbeta and HLA-DR phenotype in circulating CLA+ T lymphocytes. CONCLUSION: Our data indicate that circulating skin-homing T cells of patients with active atopic dermatitis contain an increased percentage of cells bearing TCR Vbeta segments related with Staphylococcus aureus. Staphylococcus superantigens may therefore trigger expansion or at least circulation of appropriate CLA+ T cells.

Antibodies, Monoclonal↗

Intravenous immune globulin effects on serum-soluble CD5 levels in atopic dermatitis.

BACKGROUND: Intravenous immune globulin (IVIG) therapy has been tried in the treatment of atopic dermatitis. Recently, the presence of serum-soluble CD5 (ssCD5) in atopic dermatitis was reported. OBJECTIVE: IVIG effects on ssCD5 levels in atopic dermatitis were examined and the correlation of ssCD5 level changes with clinical and laboratory parameters were investigated. METHODS: IVIG therapy was tried on 40 atopic dermatitis and 17 recurrent spontaneous abortion patients. Five atopic dermatitis patients received normal saline as a placebo control group. The clinical and laboratory parameters were evaluated on day 0, 1, 7 and 21 after administering the IVIG therapy. RESULTS: With IVIG therapy, in atopic dermatitis, the ssCD5 level was 5.5 +/- 6.2 ng/mL before infusion (day 0), 15.2 +/- 12.1 ng/mL on day 1, 13.8 +/- 14.1 ng/mL on day 7, and 3.9 +/- 4.1 ng/mL on day 21. The clinical severity score was 350.5 +/- 120.3 on day 0, 420.4 +/- 174.8 on day 1, 250.0 +/- 121.2 on day 7, and 115.5 +/- 53.9 on day 21. White blood cell (WBC) counts and serum IgE levels showed a gradual decrease with IVIG infusions. Blood eosinophil fractions were 5.3 +/- 2.8% on day 0, 8.6 +/- 5.2% on day 1, 7.3 +/- 3.7% on day 7, and 6.8 +/- 4.0% on day 21. Changes in the total eosinophil count were insignificantly parallel with those of blood eosinophil fractions CONCLUSION: In atopic dermatitis, IVIG therapy increased the ssCD5 levels. Further studies concerning the exact role of ssCD5 are needed.

CD5 Antigens↗

Prevalence and severity of allergic rhinitis in house dust mite-allergic patients with bronchial asthma or atopic dermatitis.

BACKGROUND: Allergic rhinitis, asthma and atopic dermatitis are closely associated. Although population-based studies report a high prevalence of rhinitis among asthma patients, less is known of the association between rhinitis and atopic dermatitis and the severity of concomitant rhinitis. OBJECTIVES: We aimed to determine the prevalence and severity of allergic rhinitis among asthmatics and patients with atopic dermatitis and assessed whether age and comorbidity influence the severity of rhinitis signs and symptoms. METHODS: Three hundred and twenty-five patients recruited for a multicentre trial to study the effect of encasings of mattresses, pillows and duvets on signs and symptoms of allergic rhinitis and/or asthma and/or atopic dermatitis recorded visual analogue scores (VAS) and daily symptom scores and underwent nasal challenge tests with house dust mite (HDM). RESULTS: Based on history and clinical symptoms 92% of the 164 asthmatic patients and 85% of the 86 patients with atopic dermatitis could be diagnosed as having rhinitis. Inclusion of a positive provocation to HDM did not result in a substantial lower prevalence of rhinitis. Subjects reported moderate symptoms, with mean rhinitis VAS scores ranging from 40.0 to 55.0. Presence of atopic dermatitis was associated with lower rhinitis VAS and symptoms scores, whereas in multivariate analysis the presence of asthma was positively associated with nasal responsiveness to HDM. CONCLUSION: The prevalence of nasal symptoms in patients with bronchial asthma or atopic dermatitis and sensitized to house dust mites is high. Although the majority of patients experience mild to moderate symptoms, the presence of nasal disease needs to be examined in all patients with atopic disorders.

Adolescent↗

Purpuric contact dermatitis in patients with allergic reaction to textile dyes and resins.

BACKGROUND: Purpuric lesions have been described as an uncommon manifestation of allergic contact dermatitis in individual case reports. OBJECTIVE: We describe a series of patients who developed purpuric allergic contact dermatitis to textile dyes and resins in their personal clothing. Our purpose was to study the patients clinically and histopathologically and to define the most frequent allergens, which cause purpuric allergic contact dermatitis. METHODS: One hundred and three patients were clinically evaluated and tested with the Textile Color & Finish Series (TCFS) (Chemotechnique Diagnostics) and Standard Series (TRUE Tests) because of suspected allergic contact dermatitis (ACD) to clothing. The patients with clinical features of purpura as presenting sign of ACD were studied. Biopsies from the purpuric lesions were performed in three patients. RESULTS: Thirty of the 103 patients (29.1%) had positive reaction to an allergen from the TCFS. Clinically purpuric ACD was observed in 8.7% of all the cases studied (n = 9 of 103). Nine of the 30 patch-positive patients to the TCFS (30%) demonstrated purpuric macules, papules and patches. Patch testing of the nine patients with purpuric contact dermatitis, with the TCFS, resulted in 26 positive patch test results. The major causative allergens were the following: Disperse Blue 106 and Disperse Blue 124 in 26.9% each, Disperse Blue 85 in 11.5%, and ethyleneurea melamine formaldehyde in 7.7%. Positive patch tests were observed to dimethylol dihydroxyethyleneurea, dimethylol propyleneurea, tetramethylol acetylenediurea, urea formaldehyde, melamine formaldehyde, Disperse Red 17, and Basic Red 46 3.8% in each. Purpuric patch test reaction was observed in five cases. The patch test results had present relevance in all the cases. Lesional biopsies demonstrated acanthosis, spongiosis and parakeratosis. The blood vessels were dilated, without signs of vasculitis. The inflammatory infiltrate was composed of lymphocytes and erythrocytes. The extravasated erythrocytes had a perivascular and interstitial distribution in the superficial and deep plexus and were observed at the dermo-epidermal junction as well as in the epidermis. CONCLUSION: Purpuric contact dermatitis is not an uncommon clinical form of ACD to textile dyes and resins. New allergens, which can evoke the development of purpuric allergic contact dermatitis and have not been described in the literature until now include: ethyleneurea melamineformaldehyde, dimethylol dihydroxyethyleneurea, tetramethylol acetylenediurea, urea formaldehyde, melamine formaldehyde and Disperse Red 17.

Allergens↗

Antibodies to tissue transglutaminase as serologic markers in patients with dermatitis herpetiformis.

Dermatitis herpetiformis is a gluten-sensitive disease with a symmetrically distributed blistering over extensor surfaces. The association with celiac disease is further supported by the high rate of immunoglobulin A autoantibodies to endomysium in patients with dermatitis herpetiformis, which are highly specific and sensitive indicators of celiac disease. Therefore, we determined immunoglobulin A antibodies to tissue transglutaminase, the recently discovered endomysial autoantigen in celiac disease, in patients with dermatitis herpetiformis and controls. Sera of 61 patients with dermatitis herpetiformis, as characterized by granular immunoglobulin A deposits in the subepidermal basement membrane and known endomysial antibody titers (determined by indirect immunofluorescence) as well as 84 control sera of patients with dermal or intestinal diseases unrelated to dermatitis herpetiformis, were analyzed for circulating immunoglobulin A antibodies to tissue transglutaminase by enzyme-linked immunosorbent assay. Immunoglobulin A anti-tissue transglutaminase titers in patients with dermatitis herpetiformis were significantly elevated above the controls. Furthermore, the immunoglobulin A anti-tTG titers showed a positive correlation with semiquantitative endomysial antibody data. Compared with endomysial antibodies, determination of immunoglobulin A anti-tissue transglutaminase reached a specificity and sensitivity of 97.6% and 89.1%. Patients with dermatitis herpetiformis have elevated immunoglobulin A autoantibodies to tissue transglutaminase, confirming its pathogenic relation with celiac disease and further supporting the usefulness of this novel assay for screening and therapy control.

Adolescent↗