Faculty Bibliography

Infectious panniculitis from hematogenous spread is uncommon and usually occurs in immunocompromised patients. Dissemination of gram-positive organisms to the subcutaneous tissue is rare with only several reports of disseminated panniculitis caused by Streptococcal species. We report a case of an immunocompetent 2-year-old boy presenting with diffuse neutrophilic panniculitis arising from methicillin-resistant Staphylococcus aureus septicemia. This case represents a highly atypical manifestation of severe MRSA infection and serves as a reminder to consider MRSA as a cause of disseminated neutrophilic panniculitis, particularly in high-risk populations.

The erythrodermic patient is often challenging and requires careful evaluation. Work-up should include an extensive and careful medication history, histological and laboratory testing, and if necessary, molecular studies for the evaluation of underlying malignancy. Herein, we present an erythrodermic patient with repeated biopsies demonstrating a spongiotic process who was found to have circulating atypical T-cells concerning for an underlying erythrodermic T-cell leukemia, most closely related to Sézary syndrome.

Porphyria cutanea tarda (PCT) is the most common type of porphyria, presenting in middle-aged patients with a photodistributed vesiculobullous eruption, milia, and scars. Porphyria cutanea tarda occurs in relation to inhibition of uroporphyrinogen decarboxylase, a key enzyme in the heme biosynthesis pathway. A number of genetic and acquired factors increase susceptibility to PCT by reducing uroporphyrinogen decarboxylase activity. A handful of other vesiculobullous conditions may mimic PCT both clinically and histologically; therefore, both skin biopsy and laboratory evaluation are helpful in confirming the diagnosis. We report a case of PCT in the setting of cigarette usage and untreated hepatitis C infection.

BACKGROUND: With the advent of digital microscopy, learning analytics can be leveraged to advance teaching of dermatopathology in dermatology residency.

Dermatologists rely on dermatopathologists to assess the need for excision of atypical melanocytic nevi.¹ We observed an increase in the diagnosis of moderately and severely atypical nevi and the recommendation to excise in cases referred for a second opinion. This article is protected by copyright. All rights reserved.

Photolichenoid dermatitis is an uncommon eruptive dermatitis that often occurs in association with a photosensitizing drug. Photodermatitis, in general, is an uncommon clinical manifestation of human immunodeficiency virus (HIV), most often affecting patients of African and Native American descent. Photolichenoid dermatitis has infrequently been reported in patients with HIV who have not been exposed to a photosensitizing drug. We report a case of an African patient with a photodistributed depigmenting eruption without exposure to a photosensitizing drug. Histologic examination revealed a patchy perivascular and bandlike lymphocytic infiltrate with melanophages, interface changes, and dyskeratotic keratinocytes, consistent with photolichenoid dermatitis. Laboratory examination was significant for a positive HIV-2 antibody. Photolichenoid dermatitis may be a presenting sign of HIV infection and may not necessarily be associated with exposure to a photosensitizing drug. Testing for HIV should be done in patients who present with photodistributed depigmenting eruptions, even in the absence of exposure to a photosensitizing drug, and particularly in patients of African and Native American descent.

Squamous cell carcinoma (SCC) growth is governed by tumor propagating progenitor cells (TPCs) that self-renew and differentiate into SCC cells without proliferative potential. The molecular mechanisms controlling this fate choice within these tumors are still elusive. Here we identify PITX1 as a fate determining transcription factor in mouse and human SCCs. PITX1 co-localizes with SOX2 and TRP63 in nuclei of TPCs, but it is not detected in differentiated SCC cells. Conditional gene targeting combined with ChIP-sequencing and transcriptomics reveals PITX1 cooperates with SOX2 and TRP63 to sustain a SCC specific transcriptional feed forward circuit that maintain TPC-renewal, while they also inhibit Klf4transcription and KLF4 dependent squamous differentiation. Conversely, KLF4 represses PITX1, SOX2 and TRP63 expression to prevent their expansion into supra-basal layers. This bi-stable multi-input network motif provides a molecular framework that explains self-renewal, aberrant differentiation and SCC growth in mice and humans, revealing new clues for differentiation stimulating therapies for SCCs.