PMC10294281_01
Clinical images demonstrating evolution of lesions over time in 2016 (a) and 2022 (b).
cde530423_f01.jpg
PMC10294281_01_cde530423_f01.jpg
F1
At this point, the patient had developed over 100 lesions since their initial presentation, though many of the lesions had regressed with time (Fig. 1).
Histopathology for the skin biopsy, demonstrating epidermal hyperplasia and basal layer hyperpigmentation overlying a plate-like proliferation of fascicles of bland spindle cells in the upper reticular dermis (H&E, x40) (a). b Higher power image of (a) (H&E, x100). c Higher power image of (a) (H&E, x400). d Immunohistochemistry highlighting the SMA-positive myofibroblasts within the lesion. Note that the small vessels also stain positive, which demonstrates a positive internal control (SMA, x400). e Immunohistochemistry demonstrating scattered, non-specific positivity of factor XIIIa within the lesion (factor XIIIa, x400). SMA, smooth muscle actin.
cde530423_f02.jpg
PMC10294281_01_cde530423_f02.jpg
F2
Histopathological examination showed epidermal hyperplasia and basal layer hyperpigmentation overlying a plate-like proliferation of fascicles of bland spindle cells with eosinophilic cytoplasm in the upper reticular dermis (Fig. 2a-c). Immunohistochemistry showed that most lesional cells were weakly positive for smooth muscle actin (Fig. 2d) accompanied by focal positivity for factor XIIIa (Fig. 2e), but the lesions were negative for Sox-10 and desmin (images not included).