Chad Jessup

Histopathology of Vascular Anomalies

Vascular anomalies may be appropriately classified into two broad categories, vascular tumors and vascular malformations, which are distinguished by the presence of cellular proliferation in contrast to aberrations in morphogenesis, respectively. This system of classification is based upon histological features that may in large part be differentiating, but nevertheless, may show morphological overlap. Advances in immunophenotyping allow for more precise diagnoses as well as further delineation of cell origins. In the discussion, we present the clinical, histological, and, when applicable, the immunophenotypic presentation of vascular anomalies commonly seen in infancy and early childhood.

Pityriasis rubra pilaris exacerbation with topical use of imiquimod

The role of immune response modifiers is increasing in the treatment of dermatologic diseases. Imiquimod, a toll‐like receptor agonist, results in up‐regulation of proinflammatory cytokines for improved immune surveillance. Although topical use is generally well‐tolerated, imiquimod can potentially result in systemic effects and exacerbate generalized inflammatory papulosquamous diseases of the skin. We report the case of a 67‐year‐old man who was treated with imiquimod for actinic keratosis and developed fever and a progressive erythematous papulosquamous eruption that was histologically consistent with pityriasis rubra pilaris.

De novo intraepidermal epithelioid melanocytic dysplasia: a review of 263 cases

Background: De novo intraepidermal epithelioid melanocytic dysplasia (DNIEMD) is a newly characterized lesion that is associated with a personal and/or family history of malignant melanoma (MM) and/or dysplastic nevi (DN). However, the biological significance is still uncertain and the persons predisposed to this lesion have not been adequately described.

Importance of universal mismatch repair protein immunohistochemistry in patients with sebaceous neoplasia as an initial screening tool for Muir-Torre syndrome☆☆☆

Muir-Torre syndrome, a Lynch syndrome variant, is characterized by sebaceous neoplasia plus one or more malignancies, typically colon cancer. The significance of DNA mismatch repair (MMR) deficiency detection by immunohistochemistry (IHC) in colorectal carcinomas is well established and is recommended as a screening tool for Lynch syndrome in newly diagnosed colorectal carcinomas. In comparison, literature on IHC application to detect MMR proteins (MLH1, MSH2, MSH6, and PMS2) in sebaceous neoplasia has been less studied and has been derived almost exclusively from tertiary care centers. Herein we describe the largest series to date characterizing MMR deficiency in sebaceous neoplasms, as well as the relative frequencies of each deficiency. Two hundred sixteen consecutive sebaceous neoplasms (216 patients) were analyzed from a community practice setting (133 sebaceous adenomas, 68 sebaceomas, 15 sebaceous carcinomas). One hundred forty-three were MMR deficient (66%), of which 90 were MSH2/MSH6 deficient (63%), 27 MLH1/PMS2 deficient (19%), 22 MSH6 deficient (15%), and 4 PMS2 deficient (3%). MMR deficiency was significantly associated with site, with tumors off of the head and neck more likely to be MMR deficient (specificity 96%). In contrast to prior reports, no significant trend in MMR-deficient versus -nondeficient tumors was seen in age at presentation (median age, 68 versus 66), tumor-infiltrating lymphocytes, or tumor type. Given the low sensitivity of age < 60 years (30%), location off of the head and neck (41%), or presence of tumor-infiltrating lymphocytes (29%) in MMR deficiency detection, IHC screening programs should test all sebaceous neoplasms for MMR deficiency, regardless of their clinicopathological features.

Primary cutaneous amyloidosis of the external ear: a clinicopathological and immunohistochemical study of 17 cases

Primary cutaneous amyloidosis includes several forms of localized amyloidosis characterized by superficial amyloid deposits occurring at or near the dermal–epidermal junction in the absence of systemic involvement. Primary cutaneous amyloidosis of the auricular concha and external ear represents a rarely described variant. There have been 27 cases reported in the English language literature, and herein we report 17 additional cases. This article demonstrates that the amyloid observed in this context is generally positive for Congo red, crystal violet and thioflavin T. It also expresses cytokeratin 34ßE12 via immunohistochemistry. Our immunohistochemical results and review of the literature suggest that the amyloid in amyloidosis of the external ear is the result of basal keratinocyte degeneration and does not signify deposition from a systemic or generalized process.

Neural and Neuroendocrine Neoplasms

Clinical: Benign reactive proliferation of nerves and fibroblasts in response to trauma. Often presents as a small, firm painful lesion typically associated with trauma found at any age or body site.

Vascular Neoplasms and Malformations

This chapter will cover vascular anomalies according to the subcategories of vascular neoplasms (benign and malignant), vascular neoplasms of uncertain behavior, vascular malformations and vascular dilatations. Importantly vascular neoplasms are regarded as lesions, which undergo cellular proliferations, while vascular malformations are the result of aberrations in morphogenesis.

Primary Cutaneous Melanomas Seen as Inflamed Pigmented Lesions in Patients Undergoing Adjuvant Interferon Treatment A Possible Diagnostic Clue for Physicians

BACKGROUND In addition to a complete skin examination every few months, adjuvant interferon treatment is often recommended for patients with high-risk melanomas. Therefore, dermatologists play an important role in detecting multiple primary melanomas and may be required to attempt to identify the primary melanoma in patients with metastatic disease. OBSERVATIONS We describe 3 patients with a diagnosis of melanoma who were diagnosed as having a new primary cutaneous melanoma within weeks of initiating interferon treatment. All 3 melanomas were inflamed clinically, prompting excisional biopsy. Histopathologic analysis of the melanomas revealed thin (<1.0 mm Breslow thickness) invasive tumors, as well as the presence of tumor-infiltrating lymphocytes and/or regression. CONCLUSIONS Inflamed melanocytic lesions in patients undergoing interferon treatment should be further evaluated to investigate the possibility of primary cutaneous melanomas. This observation may enable earlier detection and treatment of melanomas in patients with multiple tumors or metastatic melanoma with an unknown primary site.

Vasculitic and Vasculopathic Disorders

This chapter is organized according to large, medium and small vessel vasculitis as proposed by the Chapel Hill Consensus Conference on the nomenclature of systemic vasculitis. The subset of small vessel vasculitic lesions will be addressed according to the predominant inflammatory cell infiltrate or feature (neutrophilic, urticarial, fibrosing, lymphocytic and granulomatous). The final section will address neutrophilic dermatoses and vasculopathies.

Drug Reaction Patterns

Reactions to drugs can vary quite a bit clinically as well as histopathologically. The different types of drug reactions will be grouped below according to their clinical name or histological pattern. Although they will be listed by histological reactions pattern(s), an attempt has been made to list them in decreasing order of incidence. The four most common drug reactions in the skin are morbilliform (exanthematous), urticarial, fixed drug, and the erythema multiforme/Stevens-Johnson syndrome/toxic epidermal necrolysis spectrum.