Eczema Diseases Research Articles

A genome‐screen experiment to detect quantitative trait loci affecting resistance to facial eczema disease in sheep

Facial eczema (FE) is a secondary photosensitization disease arising from liver cirrhosis caused by the mycotoxin sporidesmin. The disease affects sheep, cattle, deer and goats, and costs the New Zealand sheep industry alone an estimated NZ$63M annually. A long-term sustainable solution to this century-old FE problem is to breed for disease-resistant animals by marker-assisted selection. As a step towards finding a diagnostic DNA test for FE sensitivity, we have conducted a genome-scan experiment to screen for quantitative trait loci (QTL) affecting this trait in Romney sheep. Four F(1) sires, obtained from reciprocal matings of FE resistant and susceptible selection-line animals, were used to generate four outcross families. The resulting half-sib progeny were artificially challenged with sporidesmin to phenotype their FE traits measured in terms of their serum levels of liver-specific enzymes, namely gamma-glutamyl transferase and glutamate dehydrogenase. In a primary screen using selective genotyping on extreme progeny of each family, a total of 244 DNA markers uniformly distributed over all 26 ovine autosomes (with an autosomal genome coverage of 79-91%) were tested for linkage to the FE traits. Data were analysed using Haley-Knott regression. The primary screen detected one significant and one suggestive QTL on chromosomes 3 and 8 respectively. Both the significant and suggestive QTL were followed up in a secondary screen where all progeny were genotyped and analysed; the QTL on chromosome 3 was significant in this analysis.

Periorbital dermatitis-a recalcitrant disease: causes and differential diagnoses

Periorbital dermatitis is common and frequently recalcitrant to treatment. Due to the exposed and visible location, patients often suffer severely from periorbital dermatitis. To determine the frequency and causes of periorbital dermatitis including contact sensitizers. We investigated two cohorts of patients (Erlangen and IVDK without Erlangen) between 1999 and 2004. The differences between the two cohorts with periorbital dermatitis [Department of Dermatology at University Hospital Erlangen (n = 88) and the German Information Network of Departments of Dermatology (IVDK) collective (n = 2035)] were determined by the MOAHLFA (male, occupational dermatosis, atopic eczema, hand dermatitis, leg dermatitis, facial dermatitis, age > or = 40 years) index. Statistically significant factors for periocular eczema are female sex, atopic skin diathesis and age > or = 40 years. In both cohorts allergic contact dermatitis was the main cause of periorbital eczema (Erlangen 44.3%, IVDK 31.6%), followed by periorbital atopic dermatitis (Erlangen 25%, IVDK 14.1%), airborne dermatitis (Erlangen 10.2%, IVDK 1.9%), irritant contact dermatitis (Erlangen 9.1%, IVDK 7.6%), periorbital rosacea (Erlangen 4.5%, IVDK 2.2%), allergic conjunctivitis (Erlangen 2.3%, IVDK included in 'others') and psoriasis (Erlangen 2.3%, IVDK included in 'others'). The most relevant allergens/allergen sources inducing periorbital eczema were consumers' products (facial cream, eye shadow and ophthalmic therapeutics) (31%), fragrance mix (19%), balsam of Peru (10%), thiomersal (10%) and neomycin sulphate (8%); 12.5% of patients with allergic periocular dermatitis could be exclusively elucidated by testing patients' own products. Our data demonstrate the multiplicity of causes for periorbital eczematous disease manifestation, which requires patch testing of standard trays as well as consumers' products to elucidate the relevant contact sensitization.

Emerging Treatment of Atopic Dermatitis

Atopic dermatitis is a chronically relapsing eczematous disease of the skin. A wide range of therapeutic regimens has been used for atopic dermatitis. A better understanding of its pathogenesis will also lead to the development of novel approaches to treating this disease. This article reviews the recent advances in allergen-specific sublingual immunotherapy and therapy with antileukotriene drugs, probiotics, mycophenolate mofetil, leflunomide, and intermittent fluticasone propionate ointment, which the authors expect will be clinically useful therapies in the near future.

Cloning, mapping and association studies of the ovine ABCG2 gene with facial eczema disease in sheep

Facial eczema (FE) is a hepatogenous mycotoxicosis in sheep caused by the fungal toxin sporidesmin. Resistance to FE is a multigenic trait. To identify QTL associated with this trait, a scan of ovine chromosomes was implemented. In addition, ABCG2 was investigated as a possible positional candidate gene because of its sequence homology to the yeast PDR5 protein and its functional role as a xenobiotic transporter. The sequence of ovine ABCG2 cDNA was obtained from liver mRNA by RT-PCR and 5' and 3' RACE. The predicted protein sequence shares >80% identity with other mammalian ABCG2 proteins. SNPs were identified within exon 6, exon 9 and intron 4. The intron 4 SNP was used to map ABCG2 to ovine chromosome 6 (OAR6), about 2 cM distal to microsatellite marker OarAE101. Interestingly, this chromosomal region contains weak evidence for a FE QTL detected in a previous genome-scan experiment. To further investigate the association of ABCG2 with FE, allele frequencies for the three SNPs plus three neighbouring microsatellite markers were tested for differences in sheep selected for and against FE. Significant differences were detected in the allele frequencies of the intronic SNP marker among the resistant, susceptible and control lines. No difference in the levels of ABCG2 expression between the resistant and susceptible animals was detected by Northern hybridisation of liver RNA samples. However, significantly higher expression was observed in sporidesmin-dosed sheep compared with naïve animals. Our inference is that the ABCG2 gene may play a minor role in FE sensitivity in sheep, at least within these selection lines.

Effect ofBifidobacteriuminfantison Interferon- γ- Induced Keratinocyte Apoptosis: A Potential Therapeutic Approach to Skin Immune Abnormalities

Current management of atopic dermatitis is mainly directed to the reduction of cutaneous inflammation. Since patients with atopic dermatitis show abnormalities in immunoregulation, a therapy aimed to adjust their immune function could represent an alternative approach, particularly in the severe form of the disease. Indeed, T-lymphocytes constitute a large population of cellular infiltrate in atopic/allergic inflammation and a dysregulated T-cell induced keratinocyte apoptosis appears to be an important pathogenetic factor of the eczematous disease. In recent years, attention has been focused on the interaction between host and probiotics which may have anti-inflammatory properties and immunomodulatory activities. The aim of the present work is to investigate the effect of a selected probiotic extract, the Bifidobacterium infantis extract, on a human keratinocyte cell line (HaCaT) abnormal apoptosis induced by activated-T-lymphocyte. An in vitro model of atopic dermatitis was used to assess the ability of the probiotic extract to protect HaCaT from apoptosis induced by soluble factors (IFN-gamma and CD95 ligand) released by human T-lymphocytes in vitro activated with anti-CD3/CD28 mAbs or Phytohemoagglutinin. Evidence is given that the bacterial extract treatment was able to totally prevent T lymphocyte-induced HaCaT cell apoptosis in vitro. The mechanism underlying this inhibitory effect has been suggested to depend on the ability of the bacterial extract to significantly reduce anti-CD3/CD28 mAbs and mitogen-induced T-cell proliferation, IFN-gamma generation and CD95 ligand release. These preliminary results may represent an experimental basis for a potential therapeutic approach mainly targeting the skin disorders-associated immune abnormalities.

Fexofenadine, an H1‐receptor antagonist, partially but rapidly inhibits the itch of contact dermatitis induced by diphenylcyclopropenone in patients with alopecia areata

Antihistamines have been used for the treatment of not only allergic diseases such as allergic urticaria and rhinitis, but also of eczematous skin diseases because of their anti-pruritic effects. Moreover, the pruritus associated with eczematous diseases is considered to be induced, in part, by histamine. However, it is unclear whether antihistamines inhibit the itch of eczematous diseases in the absence of topical corticosteroids. In this study, we investigated the anti-pruritic effect of the antihistamine, fexofenadine, on the itch of contact dermatitis that was induced by topical application of diphenylcyclopropenone for the treatment for alopecia areata. Thirteen patients with alopecia areata, who had been treated weekly with topical immunotherapy with diphenylcyclopropenone for 3 months to 2 years, recorded the severity of their itching on a visual analog scale before and 3, 6, 12, 24, 48 and 72 h after application of diphenylcyclopropenone for 4 consecutive weeks. Seven patients took fexofenadine during the first and third weeks, and six patients took fexofenadine during the second and fourth weeks. The severity of itching reached a maximum 6-12 h after the induction of the contact dermatitis in most of the patients. However, fexofenadine partially but rapidly reduced the severity of itching for 72 h during the entire period of treatment in the absence of topical corticosteroids. Our results suggest that fexofenadine can be beneficial in the daily management of patients with itching due to eczematous disease.

Co-Localization of Susceptibility Loci for Psoriasis (PSORS4) and Atopic Dermatitis (ATOD2) on Human Chromosome 1q21

Psoriasis (PS) is a chronic inflammatory skin disorder characterized by keratinocyte hyperproliferation and altered differentiation. Atopic dermatitis (ATOD) is a chronic inflammatory, pruritic and eczematous disease frequently associated with respiratory atopy. These diseases are associated with distinct immunologic abnormalities and represent typical examples of complex diseases triggered by both genetic and environmental factors, as demonstrated by independent twin studies. Genome wide linkage studies have mapped susceptibility loci on several chromosomes (PSORS1–9; ATOD1–5). Four of them overlap on chromosomes 1q21, 3q21, 17q25 and 20p although ATOD is quite distinct from PS and these two diseases rarely occur together in the same patient. An association fine-mapping study has been performed to refine PSORS4 and ATOD2 susceptibility loci on chromosome 1q21 analyzing two independently collected cohorts of 128 PS and 120 ATOD trios. Genotype and haplotype analysis of PSORS4 and ATOD2 led us to detect significant p value for haplotypes defined by MIDDLE and ENDAL16 markers in both PS (p = 0.0000036) and ATOD (p = 0.0276), suggesting a strict co-localization within an interval of 42 kb. This genomic interval contains a single gene, LOR, encoding for loricrin. Polymorphic markers mapping in regulatory and coding regions did not show evidence of association in neither of the two diseases. However, expression profiles of LOR in skin biopsies have shown reduced levels in PS and increased levels in ATOD, suggesting the existence of a specific misregulation in LOR mRNA production.

Pediatric allergic rhinitis drug therapy

BACKGROUND AND EPIDEMIOLOGY Allergic rhinitis strikes up to 30% of adults and approximately 40% of children. In children, boys are more likely to be affected than girls, and symptoms typically develop before 20 years of age (Dykewicz, 1998). Children who exhibit perennial symptoms tend to grow into adulthood with the disorder, while up to 20% of children with seasonal symptoms will have resolution of the disorder by early adulthood (Sly, 1999). Risk factors for the development of allergic rhinitis include residing within a polluted area, nonwhite race, and higher socioeconomic status. Other factors that have been linked with a higher likelihood of developing the disorder include: exposure to indoor allergens in early childhood, maternal smoking, and the early introduction of foods or formula during infancy (Dykewicz, 1998). There appears to be a genetic predisposition in that 60% of patients have a family history of allergic rhinitis (Cookson, 1989). Patients with a history of atopic dermatitis, eczema, asthma, or other atopic diseases are more likely to have concomitant allergic rhinitis. Approximately 20% of patients with allergic rhinitis also have asthma (Dykewicz, 1998). A number of culprits are responsible for the triggers for allergic rhinitis. Seasonal allergic rhinitis typically occurs when levels of allergens (such as trees, pollens, grasses, weeds, and fungi) are elevated in outdoor air; seasonal allergic rhinitis also varies depending on the area of the country (AAAAI, 2005). In the United States, spring is typically when tree pollen is problematic, late spring and summer for grass pollen, and late summer or early fall for weed pollen. Mold spore levels are affected by temperature, wind, rain, and humidity (AAAAI, 2005). Outdoor molds are found on decaying vegetation and soil and are released into the atmosphere when the earth is disturbed. Perennial allergic rhinitis is present year-round and is usually noted in indoor environments. Triggers include allergens from insects, animals, molds, and house OBJECTIVES

Cutaneous T‐cell Lymphoma of 12 Years Duration Initially Presenting in a Two Year Old

A 14‐year‐old Caucasian girl presented with an eczematous patch on the left proximal inner arm of 12 years duration. She had previously been treated with emollients and topical steroids without complete resolution. The patient denied constitutional symptoms but did note eczematous patches on her buttocks of one‐year duration and new eczematous patches on her inner left thigh and right inner upper arm. Upon exam, all lesions were slightly scaly without induration. The primary lesion was a poikilodermatous 4 × 10 cm rough plaque. No lymphadenopathy was noted. A total of five lesional biopsies were obtained. All of the biopsies demonstrated a superficial infiltrate of atypical lymphocytes with cerebriform nuclei and prominent epidermotropism including the formation of Pautrier’s microabcesses. The diagnosis of mycosis fungoides was rendered. This case is significant for its onset at two years of age, the benignity of its course over a 12 year period and the long duration before definitive diagnosis was obtained. Mycosis fungoides needs to be considered in the differential diagnosis of recalcitrant eczematous disease even in young children.

FS08.5 Does childhood atopic dermatitis influence the future working life?

Aim: To investigate the risk of adult hand eczema and possible influence on later working life in persons with childhood atopic dermatitis.Method: After reviewing medical records from the school healthcare in Stockholm regarding individuals born 1960–69, 600 individuals where signs of atopic dermatitis were noted (“cases”) and 600 matched controls without eczema or allergic disease (“controls”) were identified. 405 cases and 378 controls answered a questionnaire regarding past and present skin disease, choice of job, exposure at work and possible change of job due to eczema.Results: Hand eczema was more than 3 times more common among cases, 42%, compared to controls, 13%(p < 0.001). Hand eczema during the past 12 months was reported by 24% of the cases and 9% of the controls (p < 0.001). The proportion of individuals working in jobs with high‐risk for hand eczema was equal between the groups, as well as exposure to water, detergents, chemicals and hand washing. Among the cases 9% reported change of job due to eczema compared to 2% of controls (p < 0.001) and sick leave 10% compared to 2%(p < 0.001).Conclusions: Childhood atopic dermatitis is a risk factor for hand eczema. As the proportion of individuals in jobs with high‐risk for hand eczema and the exposure was the same in cases and controls measures preventive measures are important to reduce consequences like sick leave and change of job.

Lichen simplex chronicus (atopic/neurodermatitis) of the anogenital region.

Lichen simplex chronicus (LSC) of the anogenital area is an eczematous disease characterized by unremitting itching and scratching. In most instances, it arises in individuals who are genetically atopic, and as such, LSC can be viewed as a localized variant of atopic/neurodermatitis. Common triggers for the development of the disease include psychological distress, and local environmental problems such as heat, sweating, and excess dryness. Lichen simplex chronicus may also develop as a superimposed condition in the presence of other anogenital diseases such as candidiasis, psoriasis, lichen sclerosus, tinea cruris, and neoplasia. Lichen simplex chronicus frequently persists as an itch-scratch cycle, even when environmental triggers are removed and the underlying disease is treated. For this reason, successful therapy requires attention not only to trigger factors, but also to repair of the damaged barrier layer, reduction in inflammation, and breakup of the itch-scratch cycle.

The relationship between atopic dermatitis and contact dermatitis

Atopic dermatitis (AD) and contact dermatitis are common eczematous disorders mediated through inflammatory mechanisms. As with other eczematous disorders, they are both characterized by a serous accumulation in the epidermis and a dermal inflammatory infiltrate, expressed clinically as erythema, with or without concomitant edema and/or blistering. AD is a recurrent, hereditary eczematous condition that typically begins in childhood, affecting patients with a personal or family history of hayfever, asthma, and/or chronic dermatitis. Multiple genetic abnormalities render atopics susceptible to flares of disease activity in the presence of environmental triggers including various allergens, as well as climate and temperature change. Exacerbation of AD can, however, occur in the absence of a known environmental stimulus. Contact dermatitis is an inflammatory condition caused by direct skin exposure to an offending chemical with or without a requirement for ultraviolet light. There are two distinct types of contact dermatitis: irritant contact dermatitis (ICD) and allergic contact dermatitis (ACD). ICD is an inflammatory reaction caused by a chemical insult that results in direct cellular injury upon skin contact. The majority of cases of ICD are associated with soaps, detergents, solvents, acids, and alkali. There are two categories of ICD: acute reactions that develop minutes to hours after exposure to a very strong irritant chemical, and cumulative insult reactions, which follow repeated contact with milder irritants. Since ICD is essentially an injury, all individuals will develop an eruption when certain parameters of chemical concentration and frequency of exposure are exceeded. ACD, like AD, is an eczematous disease mediated through immune mechanisms. ACD is an acquired skin disorder that occurs at sites of contact with small chemical haptens in only those individuals who have been previously exposed to, and immunologically sensitized to, a particular chemical. In contrast to ICD, only a small percentage of the population develops an eruption when exposed to chemicals causing ACD. The most common chemical allergens causing the condition in North America include nickel sulfate, found in everything from keys to buttons on clothing, as well as the pentadecylcatechols, the active moiety in plants of the Rhus family, which include poison ivy, poison oak, and poison sumac. Active skin disease, such as ICD or AD, which disturb the integrity of the body’s epidermal barrier, can be predisposing factors for ACD, allowing easier access of potential chemical allergens to the immune system. Despite differing etiologies, AD and contact dermatitis have been the focus of many studies examining the potential association of the two conditions. In the past, it was believed that patients suffering from AD were less likely to suffer from ACD. However, more recent studies indicate that ACD is equally prevalent among atopics and nonatopics. Current research also indicates that AD patients may be more prone to suffer from ICD. Understanding the potential links between AD and contact dermatitis, and the parallel aspects of their pathogenesis, diagnosis, and treatment, can be helpful to clinicians caring for patients suffering from the disorders.

Use of the Self-Administered Eczema Area and Severity Index by parent caregivers: results of a validation study.

The Eczema Area and Severity Index (EASI) is used by dermatological investigators world-wide to assess eczema disease severity. EASI measures are, however, time-consuming and require trained personnel, thereby limiting its application to large-scale epidemiological studies. Additionally, the use of self-assessed severity indices in dermatology is restricted to adult subjects and conditions, thereby not addressing the needs of paediatric patients. To develop and validate an instrument for a caregiver's self-assessment of the severity of his/her child's atopic dermatitis (AD), the Self-Administered EASI (SA-EASI). Trained investigators performed a modified EASI assessment on the same day as an SA-EASI was obtained from 47 caregivers of children with AD. The SA-EASI was found to be a valid measure of the severity of AD. Total, acute and chronic SA-EASI scores predicted total, acute and chronic modified EASI scores (P < 0.0001). SA-EASI body surface area (BSA) scores predicted EASI BSA scores (P < 0.0001). SA-EASI pruritus scores correlated with the acute, chronic and total EASI scores (P = 0.0001). The SA-EASI may provide caregivers the means to report the severity of their child's skin disease objectively. The high correlation with the EASI score observed in this sample implies that statistical inferences with the SA-EASI will be valid for large populations. In future studies, this will permit analysis of the relationship of skin disease severity to such measures as quality of life, disability, patient satisfaction and the costs of various therapies. Moreover, this SA-EASI instrument may allow older children, over 12 years old, to assess the severity of their AD.

Dental gold alloys and contact allergy.

Contact allergy to gold as demonstrated by patch testing is very common among patients with eczematous disease and seems to be even more frequent among patients with complaints from the oral cavity. There is a positive correlation between gold allergy and the presence of dental gold. Gold allergy is often found in patients with non-specific stomatitides as well as in those with lichenoid reactions or with only subjective symptoms from the oral cavity. The therapeutic effect of substituting other dental materials for gold alloys is conspicuous in casuistic reports but less impressive in larger patient materials. The amount of dental gold is correlated qualitatively and quantitatively to the blood level of gold and the effects if any of circulating blood gold are unknown. There is clearly a need for prospective studies in the field and gold sodium thiosulfate is considered an important item in the dental series for patch testing.

Gold concentration in blood in relation to the number of gold restorations and contact allergy to gold

Previous studies have demonstrated an association between gold allergy and the presence of dental gold restorations. The aim of the present study was to investigate the relationship between the concentration of gold in blood (B-Au) and the number of tooth surfaces with gold alloys in subjects with and without contact allergy to gold. In 80 patients referred for patch testing because of eczematous disease, blood samples were taken and analyzed for B-Au using inductively coupled plasma mass spectrometry. The detection limit for the Au determination was 0.04 µg/L. In addition, a dentist made a clinical and radiological examination of the patients and registered the number of dental gold surfaces. Patients with dental gold restorations had a statistically significantly higher B-Au in Mann-Whitney U test (P = 0.025), (range <0.04-1.07 µg/L) than patients without (range <0.04-0.15 µg/L). Furthermore, a positive correlation was found between B-Au and the number of dental gold surfaces (P < 0.01). There was no statistically significant difference in B-Au between persons with and without contact allergy to gold. The study thus indicates that gold is released from dental restorations and taken up into the circulation.

Catalase gene is associated with facial eczema disease resistance in sheep.

Facial eczema (FE) is a hepatogenous photosensitization disease of ruminant animals, particularly in sheep which vary widely in their susceptibility to the disease. The liver damage is caused by the mycotoxin, sporidesmin. There is evidence that the toxicity of sporidesmin is due to its ability to generate 'active oxygen' species. We evaluated the catalase gene, which encodes an enzyme with antioxidant functions, as a candidate for determining the susceptibility of sheep to the disease. Two microsatellite markers, OarSHP3 and OarSHP4, which flank the sheep catalase gene, were isolated from a Yeast Artificial Chromosome (YAC) clone. These markers mapped the catalase locus by linkage to ovine chromosome 15. Eleven informative markers spaced throughout chromosome 15, inclusive of the catalase marker OarSHP4, gave no significant linkage with the disease traits when analysed in four outcross resource pedigrees. However, OarSHP3 and OarSHP4 allele frequencies showed significant differences between FE resistant and susceptible selection-lines. Comparison of sequences of catalase cDNAs from sheep of resistant and susceptible lines showed only two silent mutations. A single nucleotide polymorphisms (KP1) in exon 6 of the catalase gene also showed significant differences in allele frequencies between the selection lines. The lack of evidence for linkage in outcross pedigrees, but the significant association in the genetic lines, implies that catalase is involved in determining the susceptibility of sheep to facial eczema, and that the candidate gene's effect is probably recessive or minor.

Delayed contact hypersensitivity to non-steroidal anti-inflammatory drugs.

Several non-steroidal anti-inflammatory drugs (NSAIDs) are available for topical treatment of acute soft tissue trauma or degenerative musculoskeletal disorders; the NSAID bufexamac is mainly used for therapy of chronic inflammatory skin diseases. In order to assess the occurrence of contact allergy to NSAIDs in 371 consecutive patients presenting for diagnosis of presumed contact allergy, patch tests were performed with a standard series and additionally with a series of NSAIDs, comprising acetylsalicylic acid, bufexamac, diclofenac, etofenamate, felbinac, flufenamic acid, ibuprofen, indomethacin, and piroxicam. 17 individuals (4.6%) exhibited delayed hypersensitivity to one of the NSAID preparations: 12 patients (3.2%) had patch test reactions to bufexamac, 2 (0.5%) to etofenamate, 2 (0.5%) to indomethacin, and 1 patient (0.3%) to flufenamic acid. These patch test results corresponded well to the individual history in 11 individuals (including 10 patients with reactions to bufexamac), and in 2 patients the clinical relevance of the reactions was probable. In view of the high frequency of allergic contact reactions to bufexamac, we propose to test this drug particularly in patients with atopic eczema or other chronic eczematous diseases.

Long-term follow-up of eczema patients treated with cyclosporine.

Cyclosporine is efficacious in short-term treatment of various eczematous disorders. In a follow-up study we have evaluated the long-term efficacy of cyclosporine in 75 patients, who in previous studies had been treated with cyclosporine for chronic actinic dermatitis (6 patients), atopic dermatitis (42 patients) and chronic hand eczema (27 patients), 4, 2 and 1 year after the initial treatment, respectively. Three out of 6 patients with chronic actinic dermatitis showed long-term efficacy. Two years after the initial treatment with cyclosporine (5 mg/kg/day for 1-2 treatment periods of 6 weeks) for atopic dermatitis the mean disease activity was significantly lower compared to baseline (58% decrease), and compared to the time of treatment stop no significant change had occurred. Of 37 evaluable patients 35 were still in remission. One year after the initial treatment with cyclosporine (3 mg/kg/day for 6 weeks) for chronic hand eczema the mean disease activity was significantly lower than at baseline (54% decrease), and compared to the time of treatment stop no significant change had occurred. Of 27 evaluable patients 21 patients were still in remission. The study suggests that long-term remissions are possible in eczematous diseases treated with cyclosporine, even for a relatively short treatment period. It must be stressed, however, that we did not have control groups for any of the studied patient groups.

Contact sensitization to 6α-methylprednisolone aceponate

Increasing attention has been focused on contact sensitization to topical corticosteroids in the past several years. In most cases, allergy to topical corticosteroids occurs in patients with long-lasting eczematous diseases. Cross-allergy between topical corticosteroid molecules is very common, and four groups of cross-reacting molecules have been recognized. In this report, we describe a girl with atopic dermatitis and sensitized to hydrocortisone-17-butyrate who became sensitized to 6α-methylprednisolone aceponate. Cross-sensitization between the two molecules is suggested.

Allergic and irritant patch test reactions and atopic disease

This study presents a profile of patients with chronic recalcitrant eczematous disease referred by dermatologists for contact allergy evaluation. Allergic contact dermatitis (ACD) and irritant responses were carefully defined, as was the presence or absence of atopy obtained by history. Of 410 patients studied, 44% had no history of atopic disease and 46% were classed as definitely atopic. Among relevant ACD patch test reactors (n = 198), 51.5% had atopy, compared with 40.9% with no atopy but this difference was not significant. Likewise, among atopics (n = 189), 54% had definite, relevant ACD patch test responses while 33.9% had negative ACD (again not significant). Significance was seen in the higher mean number of positive allergic patch tests in the atopic group (2.7 versus 2.0, p = 0.0223). Irritant patch tests were highest among patients with both ACD and atopy (p = 0.0308) and the proportion of irritant responses correlated with increasing numbers of positive ACD tests. We conclude that atopics are at least as likely to have ACD as are non-atopics. Irritancy is increased in these patients with chronic dermatitis and the frequency of irritant reactions correlates with both greater numbers of ACD responses and with presence of atopy.