CD10 immunohistochemistry in prurigo nodularis

Fernández-Flores, Ángel

doi:10.1111/j.1365-2559.2008.02981.x

Cited by 5 publications

(3 citation statements)

References 12 publications

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“…Few authors analyzed a series of patients, such as Lindley et al (n = 23) and Mattila et al (n = 43) 21,25,26 . Several papers investigated single features such as changes in anatomy and distribution of dermal nerve fibers, mast cells, Merkel cells, dendritic cells, eosinophils and endothelial cells using specific immunohistochemical and immunofluorescence staining methods 21,24,31–50 . In sum, previous studies failed to give a consistent description and definition of routine histological findings in PN.…”

Section: Prurigo Nodularis (Pn): Previously Described Histopathologicmentioning

confidence: 99%

Prurigo nodularis: systematic analysis of 58 histological criteria in 136 patients

2010

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Section: Prurigo Nodularis (Pn): Previously Described Histopathologicmentioning

confidence: 99%

Prurigo nodularis: systematic analysis of 58 histological criteria in 136 patients

2010

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“…Thus, PN is sometimes considered to be a clinical pattern induced by chronic pruritus and repeated scratching 5 and common histopathologic presentations include orthohyperkeratosis, acanthosis, parakeratosis, papillary dermal fibrosis with perivascular inflammatory infiltrations, and characteristic neural hypertrophy 12 13 . Several previous studies have reported changes in nerve, Merkel, and mast cells 12 14 15 . Although the mechanism of pruritus is not clear, one hypothesis suggests that neural hyperplasia, mast cell, and Merkel cell neurite complexes may be associated with PN pathogenesis 1 15 16 17 18 19 20 .…”

Section: Introductionmentioning

confidence: 91%

Immunohistochemical Analysis of Prurigo Nodularis in 209 Patients: Clinicopathological Analysis between Atopic and Non-Atopic Patients and between Treatment Response Groups

et al. 2021

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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 AD) and without AD (PN 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.

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“…This importance is highlighted when in the face of chronic skin diseases because of their unknown or complex mechanisms. Skin diseases that are the subject of proteomic research are: AD, psoriasis, prurigo nodularis, eczema, scarring, aging and skin cancer [42,44,[52][53][54][55][56][57][58][59][60][61][62][63][64][65]. Proteomic (and genomic) study of AD is popular because it is a chronic skin disorder of unknown cause.…”

Section: Proteomics Studies Of Skin Diseasementioning

confidence: 99%

Atopic dermatitis-associated protein interaction network lead to new insights in chronic sulfur mustard skin lesion mechanisms

Amiri

Jafari

Jamalkandi

et al. 2013

Expert Review of Proteomics

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Chronic sulfur mustard skin lesions (CSMSLs) are the most common complications of sulfur mustard exposure; however, its mechanism is not completely understood.According to clinical signs, there are similarities between CSMSL and atopic dermatitis (AD). In this study, proteomic results of AD were reviewed and the AD-associated protein-protein interaction network (PIN) was analyzed. According to centrality measurements, 16 proteins were designated as pivotal elements in AD mechanisms. Interestingly, most of these proteins had been reported in some sulfur mustard-related studies in late and acute phases separately. Based on the gene enrichment analysis, aging, cell response to stress, cancer, Toll- and NOD-like receptor and apoptosis signaling pathways have the greatest impact on the disease. By the analysis of directed protein interaction networks, it is concluded that TNF, IL-6, AKT1, NOS3 and CDKN1A are the most important proteins. It is possible that these proteins play role in the shared complications of AD and CSMSL including xerosis and itching.

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CD10 immunohistochemistry in prurigo nodularis

Cited by 5 publications

References 12 publications

Prurigo nodularis: systematic analysis of 58 histological criteria in 136 patients

Prurigo nodularis: systematic analysis of 58 histological criteria in 136 patients

Immunohistochemical Analysis of Prurigo Nodularis in 209 Patients: Clinicopathological Analysis between Atopic and Non-Atopic Patients and between Treatment Response Groups

Atopic dermatitis-associated protein interaction network lead to new insights in chronic sulfur mustard skin lesion mechanisms

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