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PubMed1998

Sensitization and development of allergic contact dermatitis caused by a single contact with an electrosurgical grounding plate containing acrylates.

Acrylates are known as potent sensitizers which can cause sensitization even during patch testing. A single exposure to concentrated acrylates can induce primary sensitization and contact dermatitis. Here we describe a 50-year-old man who developed contact dermatitis at the site of an electrosurgical grounding plate 2 weeks after orthopedic surgery. Patch testing revealed positive reactions to the electrosurgical plate and its components hydroxyethyl acrylate and hydroxyethyl methacrylate. As the patient has never had contact with acrylate-containing materials before, there is a high probability of primary sensitization by a single contact with the grounding plate during surgery.

Acrylates↗

PubMed2001

Contact dermatitis: clinics and pathology.

Contact dermatitis or eczema is a polymorphic inflammation of the skin. It occurs at the site of contact with irritating or antigenic substances. In the acute phase there is occurrence of itching erythema, papules, and vesicles, whereas in the chronic phase there is dryness, hyperkeratosis, and sometimes fissures. Contact dermatitis can be divided into irritant and allergic types. Allergic contact dermatitis is a type-IV T-cell-mediated reaction occurring in a sensitized individual after contact with the antigen/allergen. Such antigens are usually low molecular weight substances (MW approximately 500), called haptens; 3000 contact allergens are known. The diagnosis of contact allergy is made on the basis of the history, clinical findings, and a positive epicutancous test result. Allergic, but not irritative, contact dermatitis can spread beyond the area of contact to other body parts. Eczematous lesions are characterized by a mononuclear infiltrate consisting mainly of T cells in the dermis and epidermis, together with an intercellular epidermal edema that is. spongiosis. In allergic contact dermatitis, skin-applied antigen is taken up by epidermal Langerhans cells and transported with the afferent lymph to the regional lymph nodes. Here, naive T lymphocytes are sensitized to become antigen-specific effector T cells, which then leave the lymph node, enter the circulation, and are recruited to the skin by means of specific cell surface molecules, to form the infiltrates. Cytokines released by infiltrating T cells eventually cause keratinocyte apoptosis.

Allergens↗

PubMed1985

Contact dermatitis to Biobrane.

Contact dermatitis to Biobrane has not been reported previously. We report a patient who developed a bullous skin reaction directly related to a second exposure to Biobrane. The second exposure occurred 18 days after initial use of Biobrane, and the bullous reaction developed within 48 hours of repeat exposure. Sensitivity was confirmed by patch testing. Clinicians should be aware of the possibility of contact dermatitis to Biobrane.

Adult↗

PubMed1980

Measurement and differentiation of the cellular infiltrate in experimental toxic contact dermatitis.

Toxic (irritant) contact dermatitis was elicited by epicutaneous application of dinitrochlorobenzene (DNCB) and croton oil in unsensitized guinea pigs. The course of the skin reaction was studied with the naked eye, low-power microscopy, and a method based on counting of infiltrating cells in the upper corium. A weakly toxic dose of DNCB (100 microgram/cm2) gave marked erythema and moderate swelling, more pronounced 6 h after application of the DNCB than at 24 h or 48 h. A significant increase in mononuclear cells in particular but also in neutrophil and eosinophil granulocytes was noted in the upper corium. A more strongly toxic dose (500 microgram/cm2) gave a similar visible reaction, this too most marked at 6 h, but here there was an increase in neutrophil granulocytes in particular. Over and above predominant mononuclear-cell infiltration, croton oil (10 microgram/cm2) caused a slight increase in basophil cells. The reaction thus resembled a contact allergic reaction. In the light of earlier findings in allergic contact reactions the results suggest that weak stimuli, toxic or allergenic, elicit a non-specific skin response. With stronger stimulation the histological picture is modified and the cellular response acquires a pattern characteristic of toxic or allergic contact dermatitis.

Animals↗

PubMed1990

Contact dermatitis in hospital patients.

Contact dermatitis in hospital patients resulting from diagnostic and therapeutic procedures presents various causes and clinical aspects. Antiseptics are the most frequent cause of contact dermatitis in patients undergoing surgery. Thimerosal may cause allergic sensitization mainly in patients previously exposed to contact with different sources of these mercurials, such as tinctures and preservatives in other products. Iodine-containing solutions and quaternary ammonium compounds rarely sensitize. They may cause irritation under certain circumstances, however. Adhesive tapes formulated on a rubber and colophony base are rarely found nowadays in medical adhesives; however, some tapes and skin closures have still been found to contain them. Acrylate-based adhesives sensitize less frequently. Cardiology patients may present contact dermatitis from several different sources. Electrode gels and pastes may cause allergic contact dermatitis mainly from preservatives. Modern electrocardiographic equipment does not require the use of these products, so many of these problems are now easy to avoid. Adhesive-coated pregelled foam disks for holding long-term chest contacts may cause irritant dermatitis. Transdermal drug delivery systems such as nitroglycerin disks may cause irritation attributable to the acrylic adhesives. Silicone-based adhesive disks are a good alternative in this case. Sensitization to nitroglycerin itself is rare. Dermatitis originated from implantation of pacemakers is attributable either to epoxy resin or to the metal used for the casing of the pacemaker. Changing to a different material solves the problem. In other instances, the etiology remains unclear. Dermatoses in patients with stomas constitute an important problem not only because of their frequency but also because of the multiplicity of pictures involved. Irritant dermatitis from intestinal efflux in ileostomy patients is the most frequent problem. Allergic dermatitis may originate from the ostomy device, cementing materials, or topical medicaments. Individuals receiving hemodialysis have been reported to develop widespread dermatitis, probably secondary to rubber or metal components leached out from the hemodialysis apparatus. Systemic exposure to these compounds, although not certainly proved, seems to be the explanation. Allergic dermatitis at the puncture site on arteriovenous shunts has been demonstrated to be produced by epoxy resin adhesives present in catheters. Identification of the allergen allows one to find a safe alternative for these patients who depend on this procedure to survive. Contact dermatitis in hospital patients requires a precise diagnosis. Extensive patch testing is sometimes needed for establishing the cause, which in turn provides a more accurate prognosis and a rational treatment.

Adhesives↗

PubMed2003

Afferent and efferent phases of allergic contact dermatitis (ACD) can be induced after a single skin contact with haptens: evidence using a mouse model of primary ACD.

Allergic contact dermatitis is a T cell-mediated delayed type hypersensitivity reaction that occurs upon hapten challenge in sensitized individuals. The inflammatory response in classical allergic contact dermatitis requires both a sensitization phase and an elicitation phase responsible for the recruitment and activation of specific T cells at the site of hapten skin challenge. Conversely, previously unsensitized patients may develop a "primary allergic contact dermatitis" after the first skin contact with potent contact sensitizers leading to a skin inflammation with all the features of classical allergic contact dermatitis. In this study we used an experimental murine model, referred to as contact hypersensitivity, to study the pathophysiology of primary allergic contact dermatitis and its relationship to classical allergic contact dermatitis. We show that one epicutaneous application of a nonirritant dose of hapten (2,4-dini-trofluorobenzene, fluorescein isothiocyanate) was sufficient to induce an optimal allergic contact dermatitis reaction at the site of primary contact with the hapten without subsequent challenge. As in classical allergic contact dermatitis, the skin inflammation in primary allergic contact dermatitis was mediated by interferon-gamma producing, CD8+ effector T cells that were induced in the draining lymph nodes at day 5 postsensitization and downregulated by CD4+ T cells. Reverse transcription-polymerase chain reaction analysis revealed that the primary allergic contact dermatitis reaction was mediated by a recruitment of CD8+ T cells at the sensitization skin site at day 6 postsensitization. Analysis of the fate of the hapten fluorescein isothiocyanate applied once on the skin revealed its persistence in the epidermis for up to 14 d after skin painting. These results suggest that the development of primary allergic contact dermatitis (i.e., without secondary challenge) is associated with persistence of the hapten in the skin, which allows the recruitment and activation of CD8+ T cells at the site of the single hapten application.

Acute Disease↗

PubMed2002

Early inflammatory markers in elicitation of allergic contact dermatitis.

BACKGROUND: Allergic Contact Dermatitis (ACD) is regarded as a T-cell-mediated delayed-type hypersensitivity reaction. We studied the kinetics of the expression of CS-1 fibronectin, thymus and activation-regulated chemokine (CCL17/ TARC) and different chemokine receptors (CR) in skin biopsies from individuals suffering from back problems, with the antigen responsible of their contact dermatitis and an irrelevant antigen. METHODS: Samples were taken at 2, 10, and 48 hours for histological and immunohistochemical studies using monoclonal antibodies against human CS-1 fibronectin, CCL17, CD3, CD68, CD49d, CXCR3, CCR5, and CCR3. RESULTS: At positive antigen stimulated sites there was an early expression of CS-1 fibronectin (2 hours), followed by CCL17 and a later accumulation of alplha4/beta1+ (CD49d), CD3+, CD68+, CXCR3+ and CCR5+ mononuclear cells. At 48 hours, approximately 59 % of infiltrating cells were CXCR3+, 42% CCR5+, and only 14 % CCR3+. CONCLUSIONS: These results showed for the first time a very early expression of CS-1 fibronectin which preceded production of CCL17 in blood endothelial cells (BCEs) from patients' skin with ACD. The role of these molecules in recruitment of monocytes and effector T cells in ACD is discussed.

Adult↗

PubMed1987

Occupational dermatitis in bakers: a clue for atopic contact dermatitis.

6 patients are described who developed contact dermatitis after cereal contact on atopic skin for periods of 2 to 20 years. 2 patients were wheat flour patch-test-positive. They had punch biopsies taken for standard histological and immunohistochemical investigation by labeling with monoclonal antibodies, anti-DR and anti-IgE. Sections showed features of contact dermatitis. There were many dendritic cells located perivascularly in the papilla and in the epidermidis, intensely positive for monoclonal anti-IgE antibody. In control atopic subjects, there were a few perivascular IgE positive cells, probably mastocytes. This study shows that there may be a relationship between some allergens and atopic eczema in patients exposed to them in the course of their work. In some cases, there was a true allergic contact dermatitis, seen through the clinical and histological characteristics, and the results of immunohistochemical study.

Adult↗

PubMed1977

Allergic contact dermatitis from ultraviolet cured inks. Allergic contact sensitization to acrylates.

Eight men employed in the manufacture of ultraviolet cured inks developed allergic contact dermatitis predominantly on the exposed areas. Patch testing revealed sensitization to trimethylol propane triacrylate in seven employees, to 1,6-hexanediol diacrylate in six employees, to pentaerythritol triacrylatylate in four employees and to epoxy acrylate oligomers in three employees. Either cross-sensitization or concomitant sensitization may have accounted for the multiple reactions in several employees. One sensitized employee was patch tested with four different commercially available epoxy acrylate oligomers and reacted only to two, suggesting that variations possibly in chain length between these oligomers are important variables in the allergic reactions. The polyfunctional acrylic monomers and certain epoxy acrylate oligomers should be handled carefully to avoid the development of allergic contact dermatitis.

Acrylates↗

PubMed1990

Review of contact dermatitis for non-dermatologists.

Contact dermatitis is common. Occupational contact dermatitis is one of the commonest occupational diseases. Allergic contact dermatitis to topical medications is frequent. This article provides an update on the two main types of contact dermatitis: irritant and allergic. The role of patch testing in evaluating patients is discussed and guidelines for treatment are given. Clinical features, prognosis, risk factors, and prevention are discussed.

Dermatitis, Contact↗

PubMed2004

TARC and RANTES, but not CTACK, are induced in two models of allergic contact dermatitis. Effects of cilomilast and diflorasone diacetate on T-cell-attracting chemokines.

BACKGROUND: Skin-infiltrating T cells play a predominant role in allergic and inflammatory skin diseases such as atopic dermatitis and allergic contact dermatitis. These T cells are attracted by chemotactic factors, e.g. RANTES (regulation on activation, normal T cell expressed and secreted; CCL5), TARC (thymus and activation regulated chemokine; CCL17) and CTACK (cutaneous T-cell attracting chemokine; CCL27). OBJECTIVES: To investigate which T-cell-attracting chemokines are involved in allergic contact dermatitis in mice. METHODS: Allergic contact dermatitis was induced by application of dinitrochlorobenzene (DNCB) or toluene-2,4-diisocyanate (TDI), and chemokine concentrations were determined by enzyme-linked immunosorbent assay. The effects on chemokine concentrations of the highly selective phosphodiesterase 4 inhibitor cilomilast and the glucocorticoid diflorasone diacetate were studied in mouse ears. RESULTS: RANTES and TARC were elevated in both models of allergic contact dermatitis 24 h after challenge, whereas CTACK remained unchanged. The increase in RANTES was diminished in mouse ears pretreated with cilomilast or diflorasone diacetate. TARC was reduced by diflorasone diacetate in the DNCB model but was highly induced in the TDI model; in contrast, TARC was not influenced by cilomilast. CONCLUSIONS: TARC and RANTES, but not CTACK, are involved in these two models of allergic contact dermatitis.

Animals↗

PubMed1990

The prognosis of contact dermatitis.

This article reviews the prognosis of contact dermatitis, particularly of occupational contact dermatitis. Most studies document a poor prognosis for occupational and nonoccupational contact dermatitis. The prognoses of occupational and nonoccupational contact dermatitis, irritant contact dermatitis, and allergic contact dermatitis are similar. Only a minority of studies on the prognosis of occupational contact dermatitis have found that a job change by the affected worker leads to clearing of the dermatitis. Dermatologic and nondermatologic factors associated with a poor prognosis are discussed.

Chronic Disease↗

PubMed1997

Systemic contact dermatitis to hydroxyzine.

Systemic contact dermatitis is an underreported type of delayed hypersensitivity caused by a systemically administered substance. When interpreting patch test reactions, it is important to obtain a history of all current related oral medications. Many oral medications can cross-react with structurally similar topical antigens and induce systemic contact dermatitis. Identification and elimination of the inciting agent can lead to resolution of otherwise chronic, unresponsive eczema. We report a case of systemic contact dermatitis to hydroxyzine in a patient who was patch tested positive to ethylenediamine. Repeated oral provocation with hydroxyzine reproduced her eczema on several occasions. We conclude that systemic contact dermatitis to hydroxyzine, a common medication used to treat pruritus, must be considered as a potential cause for unresponsive eczema.

Antipruritics↗

PubMed2001

Do cool water or physiologic saline compresses enhance resolution of experimentally-induced irritant contact dermatitis?

Acute irritant contact dermatitis (ICD) is frequently treated with cool water or saline compresses. While presumed effective, little quantitative evaluation documents the treatment's benefit. This study sought to determine the efficacy of both distilled water and physiologic saline compresses on experimentally-induced ICD. 24-h application of both the lipophilic nonanoic acid (NAA) and the hydrophilic sodium lauryl sulfate (SLS) were used to induce irritant contact dermatitis in 9 healthy volunteers. Following irritation, compresses were applied 0.5 h 2x daily for 4 consecutive days. Transepidermal water loss (TEWL), laser Doppler flowmetry (LDF), chromametry and visual scoring were used to quantify results. Cool compresses of both water and saline significantly reduced TEWL and LDF, with no statistically significant difference between the efficacy of the saline or water compresses. Chromametry and visual scoring did not detect a significant effect with either the water or saline compresses. The results suggest an improvement with 2x-daily application of either water or physiologic saline compresses in the treatment of acute ICD, though true clinical benefit will be elucidated through further experimentation. Certainly, the current recommendation regarding the use of cool compresses for treating ICD should not be discarded.

Adult↗

PubMed1987

Epidermal class II human lymphocyte antigen expression in atopic dermatitis: a comparison with experimental allergic contact dermatitis.

Epidermal patterns of class II human lymphocyte antigen (HLA) expression in atopic and allergic contact dermatitis have been compared, using monoclonal antibodies recognizing each subregion. Expression of class II human lymphocyte antigens on keratinocytes has been confirmed in allergic contact dermatitis, while we have found them to be absent in atopic dermatitis. This finding argues that cell-mediated immune responses, possibly to epicutaneous contact with allergen, are not implicated in the pathogenesis of atopic dermatitis.

Adult↗

PubMed1996

Mechanisms of resolution of allergic contact dermatitis.

Photoallergic and allergic contact dermatitis are examples of type IV hypersensitivity reactions that involve T cell-mediated immune responses against haptens that come into contact with the skin. These two types of allergies differ in that for routine contact allergens, the hapten is usually a chemically reactive species that readily couples to host proteins; for photoallergic reactions, UV light (320 - 400 nm) is necessary to generate ("photoactivate") the chemically reactive hapten. From this point on, both photoallergic and allergic contact dermatitis are likely to proceed along the same pathways. For both types of cutaneous delayed-type hypersensitivity, there are naturally occurring mechanisms that terminate this type of T cell-mediated inflammation (tolerance induction). An important tolerance mechanism in the skin involves the induction of T-cell clonal anergy by "amateur" antigen-presenting cells such as keratinocytes. Advances in the understanding of the molecular pathways of T-cell activation and inactivation by antigen-presenting cells have identified critical signaling molecules such as B7/BB-1 antigen. The overexpression of these signaling molecules by the keratinocytes of transgenic mice disrupts the normal kinetics of resolution of murine contact hypersensitivity. These animals have prolonged contact hypersensitivity reactions that resemble some chronic dermatologic conditions in humans. This animal model may be a useful tool to better understand chronic allergic and photoallergic contact dermatitis.

Animals↗

PubMed1980

Allergic contact dermatitis in the hamster.

Allergic contact dermatitis to strong, low molecular weight contact allergens can regularly be induced in the hamster. By its clinical course, histopathology and susceptibility to intensification with complete Freund's adjuvant, this hypersensitivity appears congruent with the allergic contact dermatitis observed in other experimental animals and the allergic contact dermatitis seen in humans. Further, in the hamster, we find that pretreatment with cyclophosphamide intensifies the acquisition of allergic contact dermatitis to dinitrochlorobenzene and to oxazolone; the target of cyclophosphamide immunopotentiation has been shown in the mouse and guinea pig to be a regulator suppressor cell. In addition, we have induced in the hamster specific immune tolerance to dinitrochlorobenzene with dinitrobenzene sulfonate; in the mouse and guinea pig it has been demonstrated that the induction of specific immune tolerance to contact allergens by parenteral hapten involves the elaboration of specific suppressor cells. These findings, then, imply the existence of regulatory suppressor cells for T-cell phenomena in the hamster. This contrasts with reports that suppressor cell function in hamsters, as against other rodents, is defective as it relates to the regulation of, for instance, allogeneic reactions, antibody formation and tolerance to contact allergens.

Animals↗

PubMed1989

[Comparative histology and immunohistochemistry of tests of immediate allergic reaction and type I contact dermatitis].

Contrary to type IV contact dermatitis, histochemical studies of immunological mechanisms in type I contact dermatitis are rare. To analyse the immunohistochemical kinetics of immediate type I reactions we followed up prick-test reactions to individual specific allergens in 5 atopics with respiratory allergy (group I) and in 4 patients with proven type I contact dermatitis (group II). Punch biopsies (diameter 6 mm) were taken 20 minutes, 6, 24 and 72 h after prick testing. Histological investigations were performed on paraffin-embedded tissue; immunohistochemical studies were done one frozen tissue with a panel of monoclonal antibodies applying the alkaline-phosphatase-anti-alkaline-phosphatase-complex method. In type I contact dermatitis a moderate lympho-monocytic dermal infiltrate appeared, which increased until 72 hrs after testing. In contrast, the immediate allergic reactions of group I revealed only mild lympho-monocytic infiltration in all proven sequential biopsies. No quantitative differences concerning the immunohistochemical pattern of OKM-1, OKM-5, Leu-2a and Leu-3a were observed between the two groups. Group II showed an increase in HLA DR, OKT6, anti-IgE- and anti-IL-2-receptor immunoreactivity whereas group I exhibited only moderate or no immunoreactivity. A dendritic anti-IgE-staining pattern, most probably on Langerhans cells, was only observed in the epidermis of group II patients. A pathogenetic concept of IgE-mediated type I contact dermatitis is presented and possible relationships with atopic dermatitis are discussed.

Adolescent↗