A case-control study addressing the population of epidermal and dermal inflammatory infiltrate including neural milieu in primary prurigo nodularis using S-100 and toluidine blue stain and its therapeutic implications

Diksha Agrawal; Kabir Sardana; Sinu Rose Mathachan; Minakshi Bhardwaj; Arvind Ahuja; Swasti Jain; Sanjeet Panesar

doi:10.1111/ijd.16834

A case-control study addressing the population of epidermal and dermal inflammatory infiltrate including neural milieu in primary prurigo nodularis using S-100 and toluidine blue stain and its therapeutic implications

Int J Dermatol. 2023 Nov;62(11):1352-1358. doi: 10.1111/ijd.16834. Epub 2023 Sep 27.

Authors

Diksha Agrawal¹, Kabir Sardana², Sinu Rose Mathachan², Minakshi Bhardwaj³, Arvind Ahuja³, Swasti Jain³, Sanjeet Panesar⁴

Affiliations

¹ Department of Dermatology, Venereology and Leprosy, Venkateshwara Institute of Medical Sciences, Amroha, Uttar Pradesh, India.
² Department of Dermatology and STDs, Dr RML Hospital and ABVIMS, New Delhi, India.
³ Department of Pathology, Dr. RML Hospital and ABVIMS, New Delhi, India.
⁴ Department of Community Medicine, Dr. RML Hospital and ABVIMS, New Delhi, India.

PMID: 37753716
DOI: 10.1111/ijd.16834

Abstract

Background: The pathogenesis of prurigo nodularis (PN) is considered to be multifactorial, with numerous cells and cytokines confabulating to produce an aberrant immune response.

Methods: A cross-sectional observational study was done in cases of untreated primary prurigo nodularis cases with histopathological assessment in 49 cases from lesional and nonlesional skin with assessment of epidermal and dermal changes, dermal infiltrate, S-100 and toluidine blue staining to assess the expression of nerve and mast cells.

Results: The most common histological changes seen in lesional skin were hyperkeratosis (98%), irregular hyperplasia (69.4%), hypergranulosis (69.4%), subepidermal clefting (6%), vertical collagen bundles (51.0%), and dermal fibrosis (48.9%). Chronic inflammatory infiltrate was seen in all cases (100%) predominantly of lymphocytes (100%) followed by eosinophils (18.4%), plasma cells (8.2%), and neutrophils (2.0%). There was a marked increase in the expression of S-100 (6.92 ± 3.40 vs. 3.94 ± 2.15, P < 0.001) and toluidine blue (4.99 ± 4.47 vs. 1.22 ± 1.28, P < 0.001) in the lesional skin as compared to the nonlesional skin.

Conclusion: We can infer that the epidermal and dermal pathology in PN is related to the infiltrate of lymphocytes, mast cells, and neural hyperplasia which perpetuate the pathogenesis by triggering the itch-inflammation cycle. Thus, apart from immunosuppressive agents that target lymphocytes and their cytokines, therapy targeted at mast cells and neural proliferation may be needed to treat prurigo nodularis.