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Treatment of severe atopic dermatitis with ‘wet-to-dry’ dressings: A case report
J ALLERGY CLIN IMMUNOL VOLUME 109, NUMBER 1
1 ~ ' ~ g ~ EpicutaneousExposure of High IgE ResponderBeagle PupIUllJl~]l pies to Dfarinae Induces Dermatitis and Anti-Mite IgE and T Cell Responses Catherine McCall, Katie Clarke, Kim Stedman, Steve Dreitz, Karen Sellins Heska Corporation, Fort Collins, CO Atopic dermatitis in dogs has many similarities to the human disease, including genetic predisposition, age of onset and distribution of symptoms. Exposure to house dust mites - particularly D. farinae, induces perennial atopic dermatitis in susceptible animals. We have developed a model of atopic dermatitis in a strain of laboratory beagle dogs selected for persistent high IgE responses to perinatal allergen exposure. Puppies were sensitized epicutaneously by painting a small area (maximum 1.0 x 1.0 cm) of intact untreated skin in the inguinal or axillary regions, with a paste made by sonicating D. farinae mites in saline. The D. farinae paste was applied at least once per week until the puppies were 4 months old. 8/10 puppies had measurable D. farinae specific serum IgE at 3 months of age, and all puppies developed dermatitis at the site of allergen exposure within 16 weeks. Patch testing of seven 6 - 12 month old sensitized dogs elicited reactions ranging from mild induration and erythema to pruritic, erythematous papular rashes at the site of allergen application. In positive patch test dogs, histology of 24 and 48 hour biopsies of the reactive skin revealed a cellular infiltrate of eosinophils and mononuclear cells. In 4/6 dogs with serum IgE to D. farinae, patch testing boosted IgE, measured 7 days after allergen application. In addition, in 5/7 dogs, peripheral blood mononuclear cells obtained at 7 days showed enhanced proliferation to D.farinae extract, compared to cells obtained prior to patch testing. In a separate experiment, treatment of patch test skin with FK-506 ointment (a recently approved treatment for human atopic dermatitis) prior to allergen application in 3 dogs abolished the macroscopically visible response to allergen. High IgE responder beagles may therefore be a useful system for preclinical evaluation of new treatments for human atopic dermatitis.
t j r ~ * l ~ l g E Autoantihodies Monitored in an Atopic Dermatitis I U U U Patient Under CyclosporinA Treatment Reflect "tissue Damage Tamar Kinaciyan*, Susanne Natter§, Dietrich Kraft§, Georg Stingl~,, R Valenta~ *Dermatology, University of Vienna, Vienna, Austria §Division of Immunopathology, Department of Pathophysiology, University of Vienna Medical School, Vienna, Austria ¥Division of Immunology, Allergy and Infectious Diseases, Department of Dermatology, University of Vienna Medical School, Vienna, Austria ~University of Vienna, Vienna, Austria Sera from patients with atopic dermatitis, a chronic pruritic skin disease, often exhibit IgE antibody reactivities not only against various exogenous allergens, but also frequently contain IgE autoantibodies. Whether IgE autoantibodies play a pathogenetic role in atopic dermatitis or merely reflect chronic tissue damage is an open question. We have monitored IgE autoantibody reactivities to nitrocellulose-blotted human epithelial cell extracts as well as IgE antibodies to environmental allergens (natural mite-, recombinant pollen allergens) in a patient suffering from severe atopic dermatitis during systemic Cyclosporin A treatment. In parallel, the SCORAD index was used to document extent, severity and subjective symptoms of skin manifestations. We observed a marked reduction oflgE autoantibodies during Cyclosporin A-induced improvement of skin symptoms and an increase in IgE autoantibody reactivities during worsening of skin manifestations caused by exposure to exogenous allergens. IgE antibodies to mite allergens and pollen allergens appeared to be boosted mainly by exogenous allergen contact. Our results support the concept that lgE autoantibody reactivity reflects T cell-mediated tissue damage in atopic dermatitis and, thus, could be useful for monitoring the extent of cellular injury occurring in this disease.
1 0 8 7 withdrawn
Abstracts
$349
1 ~ ' ~ g g Treatment of Severe Atopic Dermatitis With 'Wet-to-Dry' V I , JlIJI Dressings:A Case Report Wei Zhao*, Pamela Daffern§, Anne-Marie Irani* *Medical College of Virginia, Virginia Commonwealth University, Richmond, VA §Virginia Commonwealth University, Richmond, VA Atopic dermatitis (AD) is a chronic relapsing form of eczema. Despite advances in the understanding of its pathogenesis, severe AD still presents a management challenge to clinicians. Hydration and moisturizing plays an important role in the management of AD. Here we report a severe case of AD successfully treated with 'Wet-to-Dry' dressing in conjunction with topical steroids. This two-year-old white male patient had a long standing history of AD since infancy with multiple flares. His typical presentation included severe pruritus that led to erythematous, excoriated plaques with lichenification. Lesions occupied most of the body surface sparing only the upper back and diaper area. He had undergone multiple courses of topical steroids, antifungals, and antibiotic preparations with minimal improvement. He also developed several episodes of secondary cellulitis that required systemic antibiotic treatment. His symptoms were temporarily controlled with systemic steroids; however, severe flares recurred with attempted tapering. At 2 years of age, the patient developed severe secondary infection with fever and erythematous swelling of extremities. He was hospitalized for systemic antibiotic treatment. After control of infection, 'Wet-to-dry' dressing treatment regimens were initiated. He was first bathed in tepid water and patted dry. While the skin was still damp, a layer of mometasone furoate 0.1% cream was applied to eczematous areas. A layer of petroleum jelly followed the cream and was applied to the entire extremity, which was then dressed with a double-layered wet gauze dressing. Finally, a double-layered dry gauze dressing was applied on top of the wet gauze. Dressings were changed at least once a day. Improvement was apparent by the following day and by the 4th day, the patient's eczema had diminished significantly. He was discharged with instructions to continue nighttime bathing followed by application of mometasone cream and petroleum jelly at home. However, wet long-john pajamas were substituted for the dressings and continued until his skin was completely cleared. Thereafter, the patient's regimen was further simplified to application of petroleum jelly following the nighttime bath. Only 3-4 small local flares over the next 18 months were reported during return visits. These flares responded well to reinstitution of topical steroids in conjunction with 'wet-to-dry' dressings. Wet-dry dressing technique is very well tolerated due to the cooling effect and rapid improvement of skin inflammation. It has proved to be an extremely effective treatment for severe chronic AD in our clinical practice.
~ ' ~ g Q Response to Cyclosporin in Tacrolimus Resistant Patient 1 l~ll, ll~Jl With Atopic Dermatitis Roger Nguyen, Francis C Yu, William B Klaustermeyer Veterans Administration Greater Los Angeles Healthcare System, Los Angeles, CA Tacrolimus (FK506) ointment is a macrolide used in patients with severe atopic dermatitis recalcitrant to steroids, emollients, and phototherapy. Tacrolimus inhibits the expression of interleukin-2 in T-cells. Initially, oral tacrolimus was used to prevent graft rejection after organ transplantation. General adverse reactions to topical tacrolimus range from skin discomfort (burning) to flu-like symptoms and headache. We report a patient who responded favorably to cyclosporin after initial resistance to tacrolimus. For 30 years, a 56 year old male patient suffered from severe atopic dermatitis with intractable itching and xerosis. The patient had previously been treated with high dose topical, intramuscular, and oral steroids, as well as phototherapy with limited success. Topical tacrolimus was administered and discontinued after one month secondary to a severe skin burning sensation and unresponsiveness. A trial of oral cyclosporin at 1.5mg/kg/day over a three week period resulted in a satisfactory improvement in his dermatitis and pruritis. The decrease in pruritis lengthened the patient's sleep duration by an average of 4 hours per night. Cyclosporin appears to be an efficacious and well-tolerated therapy for this patient. In selected atopic dermatitis patients who manifest intolerance or refractoriness to tacrolimus, cyclosporin may be considered.
1 ~ ' ~ g ~ EpicutaneousExposure of High IgE ResponderBeagle PupIUllJl~]l pies to Dfarinae Induces Dermatitis and Anti-Mite IgE and T Cell Responses Catherine McCall, Katie Clarke, Kim Stedman, Steve Dreitz, Karen Sellins Heska Corporation, Fort Collins, CO Atopic dermatitis in dogs has many similarities to the human disease, including genetic predisposition, age of onset and distribution of symptoms. Exposure to house dust mites - particularly D. farinae, induces perennial atopic dermatitis in susceptible animals. We have developed a model of atopic dermatitis in a strain of laboratory beagle dogs selected for persistent high IgE responses to perinatal allergen exposure. Puppies were sensitized epicutaneously by painting a small area (maximum 1.0 x 1.0 cm) of intact untreated skin in the inguinal or axillary regions, with a paste made by sonicating D. farinae mites in saline. The D. farinae paste was applied at least once per week until the puppies were 4 months old. 8/10 puppies had measurable D. farinae specific serum IgE at 3 months of age, and all puppies developed dermatitis at the site of allergen exposure within 16 weeks. Patch testing of seven 6 - 12 month old sensitized dogs elicited reactions ranging from mild induration and erythema to pruritic, erythematous papular rashes at the site of allergen application. In positive patch test dogs, histology of 24 and 48 hour biopsies of the reactive skin revealed a cellular infiltrate of eosinophils and mononuclear cells. In 4/6 dogs with serum IgE to D. farinae, patch testing boosted IgE, measured 7 days after allergen application. In addition, in 5/7 dogs, peripheral blood mononuclear cells obtained at 7 days showed enhanced proliferation to D.farinae extract, compared to cells obtained prior to patch testing. In a separate experiment, treatment of patch test skin with FK-506 ointment (a recently approved treatment for human atopic dermatitis) prior to allergen application in 3 dogs abolished the macroscopically visible response to allergen. High IgE responder beagles may therefore be a useful system for preclinical evaluation of new treatments for human atopic dermatitis.
t j r ~ * l ~ l g E Autoantihodies Monitored in an Atopic Dermatitis I U U U Patient Under CyclosporinA Treatment Reflect "tissue Damage Tamar Kinaciyan*, Susanne Natter§, Dietrich Kraft§, Georg Stingl~,, R Valenta~ *Dermatology, University of Vienna, Vienna, Austria §Division of Immunopathology, Department of Pathophysiology, University of Vienna Medical School, Vienna, Austria ¥Division of Immunology, Allergy and Infectious Diseases, Department of Dermatology, University of Vienna Medical School, Vienna, Austria ~University of Vienna, Vienna, Austria Sera from patients with atopic dermatitis, a chronic pruritic skin disease, often exhibit IgE antibody reactivities not only against various exogenous allergens, but also frequently contain IgE autoantibodies. Whether IgE autoantibodies play a pathogenetic role in atopic dermatitis or merely reflect chronic tissue damage is an open question. We have monitored IgE autoantibody reactivities to nitrocellulose-blotted human epithelial cell extracts as well as IgE antibodies to environmental allergens (natural mite-, recombinant pollen allergens) in a patient suffering from severe atopic dermatitis during systemic Cyclosporin A treatment. In parallel, the SCORAD index was used to document extent, severity and subjective symptoms of skin manifestations. We observed a marked reduction oflgE autoantibodies during Cyclosporin A-induced improvement of skin symptoms and an increase in IgE autoantibody reactivities during worsening of skin manifestations caused by exposure to exogenous allergens. IgE antibodies to mite allergens and pollen allergens appeared to be boosted mainly by exogenous allergen contact. Our results support the concept that lgE autoantibody reactivity reflects T cell-mediated tissue damage in atopic dermatitis and, thus, could be useful for monitoring the extent of cellular injury occurring in this disease.
1 0 8 7 withdrawn
Abstracts
$349
1 ~ ' ~ g g Treatment of Severe Atopic Dermatitis With 'Wet-to-Dry' V I , JlIJI Dressings:A Case Report Wei Zhao*, Pamela Daffern§, Anne-Marie Irani* *Medical College of Virginia, Virginia Commonwealth University, Richmond, VA §Virginia Commonwealth University, Richmond, VA Atopic dermatitis (AD) is a chronic relapsing form of eczema. Despite advances in the understanding of its pathogenesis, severe AD still presents a management challenge to clinicians. Hydration and moisturizing plays an important role in the management of AD. Here we report a severe case of AD successfully treated with 'Wet-to-Dry' dressing in conjunction with topical steroids. This two-year-old white male patient had a long standing history of AD since infancy with multiple flares. His typical presentation included severe pruritus that led to erythematous, excoriated plaques with lichenification. Lesions occupied most of the body surface sparing only the upper back and diaper area. He had undergone multiple courses of topical steroids, antifungals, and antibiotic preparations with minimal improvement. He also developed several episodes of secondary cellulitis that required systemic antibiotic treatment. His symptoms were temporarily controlled with systemic steroids; however, severe flares recurred with attempted tapering. At 2 years of age, the patient developed severe secondary infection with fever and erythematous swelling of extremities. He was hospitalized for systemic antibiotic treatment. After control of infection, 'Wet-to-dry' dressing treatment regimens were initiated. He was first bathed in tepid water and patted dry. While the skin was still damp, a layer of mometasone furoate 0.1% cream was applied to eczematous areas. A layer of petroleum jelly followed the cream and was applied to the entire extremity, which was then dressed with a double-layered wet gauze dressing. Finally, a double-layered dry gauze dressing was applied on top of the wet gauze. Dressings were changed at least once a day. Improvement was apparent by the following day and by the 4th day, the patient's eczema had diminished significantly. He was discharged with instructions to continue nighttime bathing followed by application of mometasone cream and petroleum jelly at home. However, wet long-john pajamas were substituted for the dressings and continued until his skin was completely cleared. Thereafter, the patient's regimen was further simplified to application of petroleum jelly following the nighttime bath. Only 3-4 small local flares over the next 18 months were reported during return visits. These flares responded well to reinstitution of topical steroids in conjunction with 'wet-to-dry' dressings. Wet-dry dressing technique is very well tolerated due to the cooling effect and rapid improvement of skin inflammation. It has proved to be an extremely effective treatment for severe chronic AD in our clinical practice.
~ ' ~ g Q Response to Cyclosporin in Tacrolimus Resistant Patient 1 l~ll, ll~Jl With Atopic Dermatitis Roger Nguyen, Francis C Yu, William B Klaustermeyer Veterans Administration Greater Los Angeles Healthcare System, Los Angeles, CA Tacrolimus (FK506) ointment is a macrolide used in patients with severe atopic dermatitis recalcitrant to steroids, emollients, and phototherapy. Tacrolimus inhibits the expression of interleukin-2 in T-cells. Initially, oral tacrolimus was used to prevent graft rejection after organ transplantation. General adverse reactions to topical tacrolimus range from skin discomfort (burning) to flu-like symptoms and headache. We report a patient who responded favorably to cyclosporin after initial resistance to tacrolimus. For 30 years, a 56 year old male patient suffered from severe atopic dermatitis with intractable itching and xerosis. The patient had previously been treated with high dose topical, intramuscular, and oral steroids, as well as phototherapy with limited success. Topical tacrolimus was administered and discontinued after one month secondary to a severe skin burning sensation and unresponsiveness. A trial of oral cyclosporin at 1.5mg/kg/day over a three week period resulted in a satisfactory improvement in his dermatitis and pruritis. The decrease in pruritis lengthened the patient's sleep duration by an average of 4 hours per night. Cyclosporin appears to be an efficacious and well-tolerated therapy for this patient. In selected atopic dermatitis patients who manifest intolerance or refractoriness to tacrolimus, cyclosporin may be considered.