28367 A case of chronic prurigo nodularis, angiolymphoid hyperplasia with eosinophilia, and reactive lymphadenopathy: Intersection of multiple processes, or a novel clinical entity?
Kurland E, Myers B, Friedman B, and Rambhatla P. 28367 A case of chronic prurigo nodularis, angiolymphoid hyperplasia with eosinophilia, and reactive lymphadenopathy: Intersection of multiple processes, or a novel clinical entity? J Am Acad Dermatol 2021; 85(3):AB185.
J Am Acad Dermatol
Background: Prurigo nodularis (PN) is a chronic skin disease characterized by intensely pruritic, hyperkeratotic nodules that can have significant deleterious effects on patient quality of life and are often difficult to treat. Various etiologies have been shown to trigger the development of PN lesions by initiating the itch-scratch cycle. Angiolymphoid hyperplasia with eosinophilia (AHLE) is a rare benign vascular tumor which may cause pain, bleeding or pruritus. We present a case of PN-like lesions with features of AHLE on pathology, which has been recalcitrant to several topical and systemic therapies.
Case: A 64-year-old female with a past medical history of breast cancer presented for management of long-standing PN resistant to several topical therapies, antihistamines, systemic medications (including methotrexate, mycophenolate mofetil, flutamide, minocycline, allopurinol, infliximab, cyclosporine, etanercept, oral prednisone) and phototherapy. On physical examination, she had diffusely scattered hyperpigmented, excoriated papules and nodules over her arms, legs, chest, and upper back. Multiple lesional biopsies revealed superficial and deep lymphoid infiltrate with multiple eosinophils, consistent with AHLE. Additionally, left axillary lymph node biopsy demonstrated reactive lymphoid hyperplasia with focal dermatopathic changes. Future systemic treatment options for this patient include dupilumab, thalidomide, apremilast and omalizumab.
Conclusion: To our knowledge, PN associated with AHLE has not been reported. This case emphasizes the utility of clinicopathological correlations and the importance of a systemic approach to investigate the underlying etiology of PN especially in treatment-resistant cases.