Annals of dermatology · 2021
Immunohistochemical Analysis of Prurigo Nodularis in 209 Patients: Clinicopathological Analysis between Atopic and Non-Atopic Patients and between Treatment Response Groups.
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Byun Hyun Jeong, Jang Donghwi, Lee Dong-Youn, Yang Jun-Mo
Аннотация
BACKGROUND: Prurigo nodularis (PN) is a highly pruritic disease that significantly impairs patient quality of life. Although the mechanism that causes pruritus is not clear, one hypothesis argues that neural hyperplasia, mast cell, and Merkel cell neurite complexes may be associated with PN pathogenesis.
OBJECTIVE: The objective of this study was to analyze whether special staining outcomes differed depending on the presence of atopic dermatitis (AD) and treatment response.
METHODS: A total of 209 patients diagnosed with PN was analyzed retrospectively. Patients were divided into two groups according to presence or past history of AD and by treatment response. Histopathologic features were obtained using the following stains: Giemsa, S-100, neuron-specific enolase, cytokeratin (CK)-20, CAM5.2, and CK8/CK18.
RESULTS: A total of 126 patients (60.29%) had AD, and 68 (32.54%) showed clinical improvement. There were no statistically significant differences in the staining results between the PN groups with AD (PN c AD) and without AD (PN s AD). Additionally, there were no statistically significant differences in staining results between the improved and non-improved groups.
CONCLUSION: Implementing the special stains helped to identify PN pathogenesis. Because there were no statistically significant differences in the special stain results between the improved and non-improved groups, we conclude that mast cell proliferation, neural hyperplasia, and Merkel cell hyperplasia may not have a significant effect on treatment response.
OBJECTIVE: The objective of this study was to analyze whether special staining outcomes differed depending on the presence of atopic dermatitis (AD) and treatment response.
METHODS: A total of 209 patients diagnosed with PN was analyzed retrospectively. Patients were divided into two groups according to presence or past history of AD and by treatment response. Histopathologic features were obtained using the following stains: Giemsa, S-100, neuron-specific enolase, cytokeratin (CK)-20, CAM5.2, and CK8/CK18.
RESULTS: A total of 126 patients (60.29%) had AD, and 68 (32.54%) showed clinical improvement. There were no statistically significant differences in the staining results between the PN groups with AD (PN c AD) and without AD (PN s AD). Additionally, there were no statistically significant differences in staining results between the improved and non-improved groups.
CONCLUSION: Implementing the special stains helped to identify PN pathogenesis. Because there were no statistically significant differences in the special stain results between the improved and non-improved groups, we conclude that mast cell proliferation, neural hyperplasia, and Merkel cell hyperplasia may not have a significant effect on treatment response.