Background Alopecia areata (AA) is an autoimmune disease characterized by chronic inflammation, the pathogenesis of which is unknown. Stress is believed to play a role; however, evidence remains insufficient. A recent study showed that substance P (SP) damaged hair follicles by causing neurogenic inflammation, activating perifollicular mast cells, and inducing keratinocyte apoptosis. Objective We aimed at studying the role of SP in AA pathogenesis. We investigated the SP levels in the lesional scalp tissues and serum. We also studied the effect of SP on the inflammatory response and hair growth in the outer root sheath (ORS) cells. Methods We compared the serum levels of SP in 58 AA patients and 28 healthy subjects. Then, we checked the expression of SP and SP receptor, neurokinin-1 receptor (NK-1R) in the scalps of AA patients and healthy controls using immunohistochemical staining. Finally, we analyzed the mRNA expression of inflammatory cytokines and hair growth-related factors in ORS cells. Results SP and NK-1R expression were markedly higher in the hair follicles and interfollicular epidermis of the scalp lesions of AA patients. However, there was no statistically significant difference in serum SP levels between controls and patients, regardless of the type of alopecia. SP significantly increased the mRNA expression of inflammatory cytokines and decreased hair growth-related growth factors in ORS cells, but the results were not dramatic. Conclusion SP triggered a localized micro-inflammation in lesional hair follicles, provoked an inflammatory response, and inhibited hair growth, thereby confirming the pathogenic role of SP in AA.

Malignant melanoma (MM) may rarely exhibit divergent differentiation, in which melanocytic markers may be lost, leading to difficulty in diagnosis. A 64-year-old man recently diagnosed with myelodysplastic syndrome complained of development of a nodule in a melanocytic nevus on his scalp. On histopathologic examination, junctional nevus nests and diffuse cellular infiltrations with a sheet-like growth pattern of pleomorphic epithelioid cells were observed in the upper dermis. Junctional nevus cells were S-100 positive, and pleomorphic epithelioid cells extending from the junctional nests were weakly positive for S-100. Large polygonal cells with eccentric nuclei and intracytoplasmic hyaline inclusions were observed in the mid to deep dermis. These rhabdomyoblast-like polygonal cells diffusely expressed desmin and were focally positive for MyoD1. Some clusters of polygonal cells in the deep dermis expressed SOX10. Collectively, these clinical and histopathologic features suggested MM with rhabdomyosarcomatous differentiation. Desmin-and skeletal-musclespecific markers should be applied to melanocytic tumors with atypical epithelioid cells resembling rhabdomyoblasts, especially if these cells are negative for melanocytic markers.

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