In patients with multiple naevi sequential dermoscopy imaging is a useful strategy to avoid missing melanomas while minimizing unnecessary excision of benign lesions. For better compliance, the first re-examination should be scheduled at 3 months after the baseline visit. Regular annual follow-up monitoring is also needed to detect slow-growing melanomas in which subtle changes may become apparent only over time.
Eccrine poroma (EP) may clinically mimic a number of benign and malignant skin tumors. Dermoscopy improves the clinical diagnosis of many pigmented and nonpigmented skin tumors, but to date little is known about the impact of dermoscopy in the diagnosis of EP. We report 2 patients with EP and discuss the diagnostic significance of the observed dermoscopic findings.
We describe 3 cases of desmoplastic nevus with special emphasis on some repetitive dermoscopic and histopathologic features, which-if confirmed on larger series-could allow to identify desmoplastic nevus as a specific clinicopathologic entity within the spectrum of acquired melanocytic nevi.
Serum antibodies against desmoglein 1 (Dsgl) are known to induce the clinical and histological manifestations of pemphigus foliaceus (PF), autoimmune bullous disease targeting skin. The basic pathophysiological phenomenon of PF blistering is the disruption of epithelial integrity in the granular layer of the epidermis due to separation of keratinocytes from one another, or acantholysis. In this report we investigate the changes in subcellular distribution of Dsgl in response to serum of patients with PF by using an in vitro model of PF. Immunofluorescence analysis on HaCaT cells indicates that non-clustered Dsgl is markedly internalized after exposure to serum. However, binding of PF IgG to Dsgl-rich adhesion complexes (desmosomes) does not cause disruption of such structures nor depletion of clustered Dsgl, as revealed by colocalization ofPF IgG and Dsgl in a punctate staining on cell membrane 24 hours after treatment. Furthermore, morphological studies demonstrate that the dramatic alterations induced by PF sera are not the result of apoptotic programs. Taken together, our data strongly suggest that antiDsgl antibodies from PF serum could cause the internalization of non-clustered Dsgl and perturb the formation of new desmosomes but not directly disrupt Dsgl-containing junctions when stable contacts are already formed.
Dermoscopy and digital follow up might be the key factors to improve the knowledge about the natural evolution of nevi and melanoma and the spectrum of undefined melanocytic proliferations.
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