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Eosinophil Granule Proteins in Cutaneous Disease
Published in Gerald J. Gleich, A. Barry Kay, Eosinophils in Allergy and Inflammation, 2019
Wells’ syndrome, or eosinophilic cellulitis, is characterized by recurrent cutaneous swellings (25). Lesions begin with prodromal burning or itching followed by redness and swelling, subsequently evolving in a few days into large areas of edema with violaceous borders. Individual lesions persist for days to weeks and gradually change from bright red to brown-red to finally a blue-gray. The lesions may be single or multiple, may occur in any cutaneous location, may recur, and bullae may develop over the surface. Urticarial lesions may also accompany the disease (26). Familial cases have been reported. The edematous and infiltrative plaques of Wells’ syndrome histologically are characterized by foci of dermal amorphous eosinophilic material called “flame figures.” When examined by immunofluorescence for MBP, the flame figures show bright extracellular staining, suggesting that extensive eosinophil degranulation has occurred (27).
Principles of Clinical Diagnosis
Published in Susan Bayliss Mallory, Alanna Bree, Peggy Chern, Illustrated Manual of Pediatric Dermatology, 2005
Susan Bayliss Mallory, Alanna Bree, Peggy Chern
Differential diagnosisNodular vasculitis (Bazin disease) from tuberculosisHenoch–Schönlein purpuraEosinophilic cellulitisInfectious cellulitisOther panniculitidesChild abuseTrauma
Hypereosinophilic syndrome
Published in Biju Vasudevan, Rajesh Verma, Dermatological Emergencies, 2019
HES conditions may present with varied cutaneous abnormalities [2,3,4]. Over 50% of HES patients have skin lesions of the trunk and/or extremities as the first manifestation of HES, including pruritic erythematous macules, papules, plaques, wheals, and nodules (Figures 39.1 and 39.2).Splinter hemorrhages and/or nail fold infarcts may herald the onset of thromboembolic disease [1].Eczematous lesions (involving hands, flexural areas, or dispersed plaques), erythroderma, and generalized thickening of the skin are also common.Urticaria and angioedema occur in all HES subtypes and are characteristic of certain variants, especially lymphocytic HES.Mucosal ulcers of the oropharynx and anogenital portend an aggressive clinical course, and death is likely within 2 years of presentation if the disorder is untreated. Mucosal ulcers may characterize myeloproliferative FIP1L1-PDGFRA-positive HES [14].Other various cutaneous disorders seen include erythema annulare centrifugum, necrotizing vasculitis, livedo reticularis, purpuric papules, and Wells syndrome (eosinophilic cellulitis). A diagnosis of HES may be delayed or missed because an association between skin findings and HES is not appreciated.Lymphocytic variant (L-HES) has predominant cutaneous features in the form of urticaria, erythroderma, and plaques. Patients with cutaneous symptoms should be investigated for the presence of abnormal T cells to exclude cutaneous T-cell lymphoma [15].The presence of lymphomatoid papulosis should prompt a search for FIPILI-PDGFRA mutation [16].
Clinical and immunologic differences in cellulitis vs. pseudocellulitis
Published in Expert Review of Clinical Immunology, 2021
Michael Goldenberg, Henry Wang, Trent Walker, Benjamin H Kaffenberger
It should be noted that a less common condition that can be mistaken for either allergic contact dermatitis or cellulitis is Eosinophilic Cellulitis, also called Well’s Syndrome [53]. This condition can present in various morphologies including burning, pruritic or tender, erythematous plaques that can be urticarial, as well as bullous, papulonodular, or papulovesicular lesions. The condition is especially prone to being mislabeled as bacterial cellulitis during the acute phase, which is often accompanied by systemic symptoms like fever and arthralgias. These plaques can present in numerous locations including the trunk, extremities, and face. The acute lesions typically involute after about six weeks and then become indurated, morphea-like lesions. The pathogenesis of Well’s Syndrome is not fully understood, but it is believed to be a hypersensitivity reaction triggered by arthropod bites, infections, vaccinations, medications, lymphoproliferative disease, and malignant tumors. The condition can be confirmed with a biopsy, which will initially show eosinophilic dermal edema during the acute phase. Subacute phase biopsies will show collagen fibers covered by fibrin and eosinophilic major basic protein. Chronic phase biopsies demonstrate palisading granulomas with giant cells and histiocytes without eosinophils. Up to half of affected patients will have peripheral eosinophilia as well. Treatment consists of corticosteroids or other immunosuppressive medications and addressing precipitating factors when found. However, patients often require repeated treatments given the common rate of recurrence [53].
Long-term effects of biologic therapies on peripheral blood eosinophils in patients with psoriasis: a 3-year single-center study
Published in Journal of Dermatological Treatment, 2020
Neslihan Akdogan, Sibel Dogan, Nilgun Atakan
Besides blood eosinophilia, eosinophilic pathologies were also associated with TNF-α inhibitors (20,21). Boura et al. revealed eosinophilic cellulitis after the 2nd adalimumab injection in a 72-year-old woman with a 30-year history of rheumatoid arthritis (RA) (20). Winfield et al. reported eosinophilic cellulitis-like reactions in a 57-year-old woman with RA after the 2nd dose of subcutaneous etanercept revealed on histopathologic examination (21). Eosinophilic infiltrates in solid organs owing to BT use are also shown in various reports (22). A 71-year-old man and a 67-year-old man with severe plaque-type psoriasis presented with eosinophilia and eosinophilic pneumonia during ustekinumab therapy after 7 months and 6 weeks, respectively, which were successfully treated with systemic corticosteroids (22,23).
A case report of recurrent Well’s syndrome masquerading as cellulitis
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
Anum Qureshi, Jasmine Manley, Tristan Flack, Mark H. Lowitt
A diagnosis of recurrent eosinophilic cellulitis of the perineal area was made. Treatment was instituted with solumedrol 40 mg twice daily for twodays. The skin dramatically improved within twodays with improvement of pain and erythema in the area. Solumedrol was replaced with prednisone 60 mg for 3 days followed by a 6-week taper. For breakthrough perianal pain, she was given clobetasol 0.05% cream twice daily for twoweeks and discharged on a tapering steroid dose. Minocycline was started as a steroid-sparing agent, but its use was limited by vertigo. Significant perineal itch continued, unresponsive to hydroxyzine, topical steroids, and topical lidocaine.