171 Papular urticaria Dana Turker and Jacob O. Levitt Evidence Levels: A Double-blind study B Clinical trial ≥ 20 subjects C Clinical trial < 20 subjects D Series ≥ 5 subjects E Anecdotal case reports Papular urticaria (PU) is a common disease characterized by chronic or recurrent eruptions of 3–10 mm pruritic papules, wheals, and/or vesicles caused by hypersensitivity to the bites of arthropods, including fleas, mosquitoes, scabies, and bedbugs. Not all individuals who are bitten by an offending arthropod develop a reaction to the bite. However, when a bite reaction resulting in a papular skin eruption does occur, this is defined as papular urticaria. Although the antigenic stimulus cannot be identified in all cases, an eosinophilic infiltrate on histology supports that etiology. Papules tend to appear on extensor surfaces of the extremities and may have a central punctum; lesions last between 2 and 10 days. Excoriations, lichenification, and secondary infection are often noted. Cases are generally seen in children between the ages of 2 and 7 and in adults, with a predilection for the spring and summer months. Bed bugs (Cimex lectularius) are an increasingly common cause of PU. They live in wallpaper, mattress seams, couches, and headboards but can also be found in luggage, vehicles, and clothing. Importantly, they can live off of the host up to 1 year after just one blood meal and can be spread via used furniture as well as travelers (clothing, baggage). They feed at night for 4 to 12 minutes and typically cause a painless bite of which the host is unaware. Bed bugs are detected via human inspection, bed bug sniffing dogs, and CO2-emitting monitoring systems. In conjunction with chemical treatment of the home, the following strategies can be used to prevent further infestation: a sealed, plastic cover for the mattress, moving the mattress away from the wall, keeping blankets off the floor, petrolatum applied to the legs of the bed, plastic cups under the legs of the beds, white sheets to make the bed bugs and/or blood more visible, removing loose wallpaper, and filling in cracks in floorboards, furniture, walls, and windowsills. Travelers should examine the bed, avoid using hotel drawers, keep suitcases zipped, and launder clothes with heated drying upon return. The exact cause of PU is often not found and thus it is a diagnosis of exclusion. Common causes are bed bugs, scabies, lice (all types), fleas, chiggers, and mosquitoes. Important differential diagnoses to consider are prurigo nodularis, allergic contact dermatitis, id reaction, atopic dermatitis, drug rash, urticaria, sarcoidosis, early varicella, pityriasis lichenoides, miliaria rubra, papulovesicular polymorphous light eruption, papular acrodermatitis of childhood (Gianotti–Crosti syndrome), linear IgA bullous dermatosis, folliculitis, delusions of parasitosis, and neurotic excoriations. We suggest a therapeutic ladder based on simultaneously addressing: (1) a presumed arthropod assault; (2) the pathophysiology of the allergic and inflammatory response; and (3) the severity of the inflammation at presentation. Most important is the identification and removal of the offending arthropod, which may require intense investigation as to the possible sources. Because the risks are minimal and the benefit great, empiric therapy for scabies should be given. This can be achieved with permethrin cream 5% or malathion lotion 0.5% done once and repeated 3 to 7 days later. In the case of suspected bed bugs and fleas, fumigation of the home is required using professional services. Fumigation of the home should also be considered in recurrent cases of PU. Clothes and bedding should be laundered before and after treatment; specifically, placed in a dryer at 60°C for 10 minutes to dehydrate and kill scabies and bed bugs. In persistent cases, application of DEET before bed may help. If there are pets in the home, aggressive flea control and veterinary evaluation may be necessary. If the exposure is thought to be from the outdoors, prevention can be achieved through protective clothing and insect repellents. While the cause of PU is being investigated and treated, symptomatic therapy should be implemented immediately for patient comfort and to reduce and prevent inflammation. For mild cases, topical steroids should be prescribed, with choice of class depending on the severity of lesions. For individual refractory or severe lesions, intralesional triamcinolone is often helpful. When steroids fail or if inflammation is severe on initial presentation, proceed to systemic immunosuppression; for example, a 10-day oral prednisone taper starting at 1 mg/kg or 1 mg/kg of intramuscular triamcinolone. When PU becomes chronic in the context of two failed courses of systemic steroids and negative pest control investigations, other diagnoses and/or systemic immunosuppressants should be considered, e.g., phototherapy, cyclosporine, or methotrexate. Antihistamines often control pruritus. In milder cases, non-sedating antihistamines such as loratadine, desloratidine, fexofenadine, cetirizine, or levocetirizine can help. Doses above those given on the product labeling may be necessary. With more severe itching, diphenhydramine and hydroxyzine are favored. In chronic or recurrent cases, T-cell mediated lesions, in contrast to the histamine-mediated lesions of early PU, may render antihistamines ineffective. In that case, topical agents, such as camphor/menthol, calamine lotion, crotamiton, lidocaine, and pramoxine, can help. Secondary infection, often from scratching, is a concern, especially in children, and appropriate topical or oral antibiotics should be used. Specific investigations Complete blood count with differential Serum IgE Skin biopsy (if systemic treatment is being given) Environmental evaluation Scratch test for dermographism Papular urticaria: a histopathologic study of 30 patients. Jordaan HF, Schneider JW. Am J Dermatopathol 1997; 19: 119–26. Over half the cases had mild acanthosis, mild spongiosis, exocytosis of lymphocytes, mild subepidermal edema, extravasation of erythrocytes, a superficial and deep mixed inflammatory cell infiltrate of moderate intensity with interstitial eosinophils. Four subtypes are described: lymphocytic, eosinophilic, neutrophilic, and mixed. The authors conclude that a type I hypersensitivity reaction is part of the pathogenesis of PU based on immunohistochemical evidence. Only gold members can continue reading. Log In or Register to continue Share this:Click to share on Twitter (Opens in new window)Click to share on Facebook (Opens in new window) Related Related posts: Cat scratch disease Hemangiomas Drug eruptions Erythropoietic protoporphyria Necrolytic migratory erythema Nevoid basal cell carcinoma syndrome Stay updated, free articles. Join our Telegram channel Join Tags: Treatment of Skin Disease Comprehensive Therapeutic Strategies Aug 7, 2016 | Posted by admin in Dermatology | Comments Off on Papular urticaria Full access? Get Clinical Tree Get Clinical Tree app for offline access Get Clinical Tree app for offline access
171 Papular urticaria Dana Turker and Jacob O. Levitt Evidence Levels: A Double-blind study B Clinical trial ≥ 20 subjects C Clinical trial < 20 subjects D Series ≥ 5 subjects E Anecdotal case reports Papular urticaria (PU) is a common disease characterized by chronic or recurrent eruptions of 3–10 mm pruritic papules, wheals, and/or vesicles caused by hypersensitivity to the bites of arthropods, including fleas, mosquitoes, scabies, and bedbugs. Not all individuals who are bitten by an offending arthropod develop a reaction to the bite. However, when a bite reaction resulting in a papular skin eruption does occur, this is defined as papular urticaria. Although the antigenic stimulus cannot be identified in all cases, an eosinophilic infiltrate on histology supports that etiology. Papules tend to appear on extensor surfaces of the extremities and may have a central punctum; lesions last between 2 and 10 days. Excoriations, lichenification, and secondary infection are often noted. Cases are generally seen in children between the ages of 2 and 7 and in adults, with a predilection for the spring and summer months. Bed bugs (Cimex lectularius) are an increasingly common cause of PU. They live in wallpaper, mattress seams, couches, and headboards but can also be found in luggage, vehicles, and clothing. Importantly, they can live off of the host up to 1 year after just one blood meal and can be spread via used furniture as well as travelers (clothing, baggage). They feed at night for 4 to 12 minutes and typically cause a painless bite of which the host is unaware. Bed bugs are detected via human inspection, bed bug sniffing dogs, and CO2-emitting monitoring systems. In conjunction with chemical treatment of the home, the following strategies can be used to prevent further infestation: a sealed, plastic cover for the mattress, moving the mattress away from the wall, keeping blankets off the floor, petrolatum applied to the legs of the bed, plastic cups under the legs of the beds, white sheets to make the bed bugs and/or blood more visible, removing loose wallpaper, and filling in cracks in floorboards, furniture, walls, and windowsills. Travelers should examine the bed, avoid using hotel drawers, keep suitcases zipped, and launder clothes with heated drying upon return. The exact cause of PU is often not found and thus it is a diagnosis of exclusion. Common causes are bed bugs, scabies, lice (all types), fleas, chiggers, and mosquitoes. Important differential diagnoses to consider are prurigo nodularis, allergic contact dermatitis, id reaction, atopic dermatitis, drug rash, urticaria, sarcoidosis, early varicella, pityriasis lichenoides, miliaria rubra, papulovesicular polymorphous light eruption, papular acrodermatitis of childhood (Gianotti–Crosti syndrome), linear IgA bullous dermatosis, folliculitis, delusions of parasitosis, and neurotic excoriations. We suggest a therapeutic ladder based on simultaneously addressing: (1) a presumed arthropod assault; (2) the pathophysiology of the allergic and inflammatory response; and (3) the severity of the inflammation at presentation. Most important is the identification and removal of the offending arthropod, which may require intense investigation as to the possible sources. Because the risks are minimal and the benefit great, empiric therapy for scabies should be given. This can be achieved with permethrin cream 5% or malathion lotion 0.5% done once and repeated 3 to 7 days later. In the case of suspected bed bugs and fleas, fumigation of the home is required using professional services. Fumigation of the home should also be considered in recurrent cases of PU. Clothes and bedding should be laundered before and after treatment; specifically, placed in a dryer at 60°C for 10 minutes to dehydrate and kill scabies and bed bugs. In persistent cases, application of DEET before bed may help. If there are pets in the home, aggressive flea control and veterinary evaluation may be necessary. If the exposure is thought to be from the outdoors, prevention can be achieved through protective clothing and insect repellents. While the cause of PU is being investigated and treated, symptomatic therapy should be implemented immediately for patient comfort and to reduce and prevent inflammation. For mild cases, topical steroids should be prescribed, with choice of class depending on the severity of lesions. For individual refractory or severe lesions, intralesional triamcinolone is often helpful. When steroids fail or if inflammation is severe on initial presentation, proceed to systemic immunosuppression; for example, a 10-day oral prednisone taper starting at 1 mg/kg or 1 mg/kg of intramuscular triamcinolone. When PU becomes chronic in the context of two failed courses of systemic steroids and negative pest control investigations, other diagnoses and/or systemic immunosuppressants should be considered, e.g., phototherapy, cyclosporine, or methotrexate. Antihistamines often control pruritus. In milder cases, non-sedating antihistamines such as loratadine, desloratidine, fexofenadine, cetirizine, or levocetirizine can help. Doses above those given on the product labeling may be necessary. With more severe itching, diphenhydramine and hydroxyzine are favored. In chronic or recurrent cases, T-cell mediated lesions, in contrast to the histamine-mediated lesions of early PU, may render antihistamines ineffective. In that case, topical agents, such as camphor/menthol, calamine lotion, crotamiton, lidocaine, and pramoxine, can help. Secondary infection, often from scratching, is a concern, especially in children, and appropriate topical or oral antibiotics should be used. Specific investigations Complete blood count with differential Serum IgE Skin biopsy (if systemic treatment is being given) Environmental evaluation Scratch test for dermographism Papular urticaria: a histopathologic study of 30 patients. Jordaan HF, Schneider JW. Am J Dermatopathol 1997; 19: 119–26. Over half the cases had mild acanthosis, mild spongiosis, exocytosis of lymphocytes, mild subepidermal edema, extravasation of erythrocytes, a superficial and deep mixed inflammatory cell infiltrate of moderate intensity with interstitial eosinophils. Four subtypes are described: lymphocytic, eosinophilic, neutrophilic, and mixed. The authors conclude that a type I hypersensitivity reaction is part of the pathogenesis of PU based on immunohistochemical evidence. Only gold members can continue reading. Log In or Register to continue Share this:Click to share on Twitter (Opens in new window)Click to share on Facebook (Opens in new window) Related Related posts: Cat scratch disease Hemangiomas Drug eruptions Erythropoietic protoporphyria Necrolytic migratory erythema Nevoid basal cell carcinoma syndrome Stay updated, free articles. Join our Telegram channel Join Tags: Treatment of Skin Disease Comprehensive Therapeutic Strategies Aug 7, 2016 | Posted by admin in Dermatology | Comments Off on Papular urticaria Full access? Get Clinical Tree
