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- Kolm, Isabel, et al.
(författare)
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Lichen aureus with pseudolymphomatous infiltrate
- 2021
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Ingår i: Journal of cutaneous pathology. - : Wiley-Blackwell. - 0303-6987 .- 1600-0560. ; 48:5, s. 669-673
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Tidskriftsartikel (refereegranskat)abstract
- Lichen aureus is a variant of pigmented purpuric dermatoses. The usual histopathology of lichen aureus is characterized by a subepidermal dense, band-like lymphocytic infiltrate, extravasated erythrocytes, and hemosiderin deposits. We report three patients with lichen aureus on the extremities with similar clinical, dermoscopic, and histopathological findings characterized by a dense band-like relatively deep dermal infiltrate accompanied by extravasation of erythrocytes and hemosiderin deposits occasioning a resemblance to a lymphoproliferative disorder.
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- Mitteldorf, C., et al.
(författare)
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PD-1 and PD-L1 in neoplastic cells and the tumor microenvironment of Merkel cell carcinoma
- 2017
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Ingår i: Journal of cutaneous pathology. - : Blackwell Publishing Ltd. - 0303-6987 .- 1600-0560. ; 44:9, s. 740-746
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Tidskriftsartikel (refereegranskat)abstract
- Background: Merkel cell carcinoma (MCC) is an aggressive neoplasm, which is often associated with Merkel cell polyomavirus (MCPyV). Programmed death-1 (PD-1) and its ligand PD-L1 are key players of the tumor microenvironment (TME). Methods: Fourteen paraffin-embedded tissue samples of MCC were stratified by their MCPyV detection. Apart from PD-L1 and PD-1, the TME was further characterized for the expression of CD33, FOXP3 and MxA. Results: We observed PD-1 in 2 of 12 tumors. PD-L1 expression by tumor cells was found in 7 of 8 MCPyV(+) samples and was detected particularly in the periphery. The tumor cells were surrounded by a shield of PD-L1/CD33 immune cells. Expression of PD-L1 by the tumor cells was higher in areas with a denser immune infiltrate. CD33(+) cells without direct tumor contact were PD-L1 negative. Only a low number of FOXP3(+) regulatory T-cells was admixed. Tumor cells of MCPyV(−) samples were mostly PD-L1 negative. Conclusions: Our data demonstrate that PD-L1 expression occurs in tumor and immune cells, in areas in which they are close in contact. Interferon seems to play a role in this interaction. We postulate that PD-L1(+)/CD33(+) cells shield the tumor against attacking PD-1(+) immune cells. Therefore, next to anti-PD-1/PD-L1 antibodies, blockade of CD33 seems to be a promising therapeutic approach. © 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
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- Tocco-Tussardi, Ilaria, et al.
(författare)
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Microbiological findings and antibacterial therapy in Stevens-Johnson syndrome/toxic epidermal necrolysis patients from a Swedish Burn Center
- 2017
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Ingår i: Journal of cutaneous pathology. - : Wiley. - 0303-6987 .- 1600-0560. ; 44:5, s. 420-432
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Superimposed infections/sepsis are the major cause of morbidity/mortality in Stevens-Johnson syndrome/Toxic Epidermal Necrolysis (SJS/TEN). It is a delicate balance between avoiding new pharmaceuticals and prophylactically treat an incipient infection. The objective of this study was to investigate the rates and types of infection-microbials and antibiotics involved in SJS/TEN patients.MATERIALS AND METHODS: Microbiology and clinical data were collected for SJS/TEN patients admitted to our Burn Center from January 2010 through January 2016.RESULTS: A total of 24 patients were admitted over the study period. There were 303 bacterial cultures taken whereof 113 (37.3%) were positive (median of 4.4 per patient). Twenty-two (91.7%) patients had at least 1 positive sample recorded. Fifteen (62.5%) patients had a confirmed episode of sepsis with skin being the most common source of colonization (77.8%). Eleven (45.8%) patients received empiric antibiotic therapy at referral facility/prior to admission to our Center. Patients who grew a higher number of different species were significantly less likely to have received early empiric antimicrobial therapy (P < .001).CONCLUSION: Secondary bacterial infection and sepsis were a highly common finding in our patient population. Despite the risk of resistance and further immunological provocation, empirical antibiotic treatment might have a place in clinical management.
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