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Systemic Diseases and the Skin
Published in Ayşe Serap Karadağ, Lawrence Charles Parish, Jordan V. Wang, Roxburgh's Common Skin Diseases, 2022
Jana Kazandjieva, Razvigor Darlenski, Nikolai Tsankov
Laboratory studies: The histologic findings from a skin biopsy include acanthosis, hyperkeratosis, and hypergranulosis without parakeratosis or spongiosis. The diagnosis of the associated esophageal malignancy is made by performing an esophagogastroscopy and biopsy.
The skin
Published in C. Simon Herrington, Muir's Textbook of Pathology, 2020
There is compact hyperkeratosis overlying an acanthotic epidermis with focal wedge-shaped hypergranulosis. Areas of hyperkeratosis overlying the foci of hypergranulosis are believed to correspond to Wickham's striae noted clinically. The rete ridges have a saw-toothed outline. There is a band of inflammation, predominantly lymphocytic with occasional histiocytes, at the dermal aspect of the dermoepidermal junction. Damage to the basal cell layer manifests as vacuolar degeneration (minute, discrete vacuoles on membranous aspect of keratinocytes) and results in keratinocyte apoptosis (Figure 19.9B). The latter appears microscopically as rounded, homogenous eosinophilic, bodies (colloid/Civatte bodies) within the epidermis or papillary dermis.
Disorders of keratinization and other genodermatoses
Published in Ronald Marks, Richard Motley, Common Skin Diseases, 2019
This is a rare, autosomal recessive disorder of keratinization, characterized by a striking degree of hyperkeratosis but not much erythema. As with NBIE and epidermolytic hyperkeratosis, some patients develop the condition after being born in a collodion membrane. The hyperkeratosis may be discoloured brown, for reasons that are unclear (Fig. 18.11). As with the other severe disorders of keratinization, there may be marked ectropion and ear deformities (Fig. 18.12). Histologically, there is marked hyperkeratosis and hypergranulosis.
Squamous cell carcinoma arising in an epidermal inclusion cyst
Published in Baylor University Medical Center Proceedings, 2022
Suzanne Alkul, Christopher N. Nguyen, Nisha S. Ramani, Mahmud Alkul, Ida Orengo, Ikue Shimizu, Bhuvaneswari Krishnan
The pathologic differential diagnostic considerations of a dermal cystic lesion lined by squamous epithelium include an inclusion cyst of epidermal or pilar type. The epidermal type shows squamous lining epithelium with preserved granular layer and lumen with epidermal-type keratinous material. The pilar type cyst epithelium shows squamous cells with absence of granular layer, and lumen with eosinophilic pilar-type keratinous material with cholesterol clefts/calcification. Squamous lined cysts secondary to human papillomavirus infection have been reported18–20 and are more commonly on the palms and soles and rarely the scalp. These cysts show squamous lining epithelia with papillomatosis, hypergranulosis, parakeratosis, and, rarely, cytoplasmic inclusions. Proliferative changes in the cyst wall occupying the cyst lumen can be seen in proliferating trichilemmal or epidermal cysts, or malignancy arising in epithelial cysts. Proliferating trichilemmal tumors, commonly seen in the scalp, show a wide spectrum of squamous proliferation. Epithelial proliferation with pleomorphism and surrounding stromal invasion is seen in carcinomas arising in trichilemmal cyst. A proliferating epidermal cyst shows squamous proliferation with epidermal-type keratinization. Atypia of the squamous cells can be seen.
Therapeutic potential of biologics in prurigo nodularis
Published in Expert Opinion on Biological Therapy, 2022
Svenja Müller, Thomas Bieber, Sonja Ständer
Nonspecific histological findings in CNPG consist of pseudoepithelimatous epidermal hyperplasia, focal parakeratosis and hypergranulosis, fibrosis of the collagen fibers of the papillary dermis, increase of capillaries and fibroblasts as well as a perivascular and interstitial inflammatory infiltrate predominantly consisting of T cells, lymphocytes, eosinophils, mast cells, neutrophils, and macrophages [5,13,28,33]. In the epidermis, the density of intraepidermal nerve fibers is decreased [9]. Nerve fibers in the dermis appear thickened and hyperplastic, often positive for protein gene product 9.5, substance P, which is secreted by neurons and adheres to the neurokinin-1 receptor in the skin as well, calcitonin gene-related peptide and p 75 nerve growth factor (NGF) [5,6,9,13,26]. These neuropeptides may be responsible for the development and chronicity of the cutaneous neurogenic inflammation [6,32]. Calcitonin gene-related peptide can affect pruritus modulating mu and kappa opioid receptors [26].
Pathophysiology, diagnosis, and pharmacological treatment of prurigo nodularis
Published in Expert Review of Clinical Pharmacology, 2021
Kyle A. Williams, Youkyung S. Roh, Isabelle Brown, Nishadh Sutaria, Pegah Bakhshi, Justin Choi, Sylvie Gabriel, Rajeev Chavda, Shawn G. Kwatra
For specific subsets of patients, further testing may be warranted. Although PN is a clinical diagnosis, skin biopsies may be indicated for atypical clinical presentations. Skin biopsies, though not routinely done in the workup of PN, can provide useful information, particularly when considering other primary dermatoses as the cause of PN [4,54]. Histologically, lesions of PN typically display orthohyperkeratotis, irregular epidermal hyperplasia, hypergranulosis, fibrosis of the papillary dermis, and an increased number of fibroblasts and capillaries [4,55]. These changes correlate with scratch-induced injuries from the perpetual itch-scratch cycle seen in PN. As a caveat, while these changes can support PN diagnosis, they are also seen in other pruritic conditions and therefore are not pathognomonic [4]. As aforementioned, there are decreases in epidermal nerve fiber density and increases in dermal nerve fiber density within lesional PN skin. In the elderly population with PN and urticaria, direct immunofluorescence (DIF) may also be indicated to identify any underlying autoimmune blistering disorders such as bullous pemphigoid [4,55].