Background and Objectives: Neurogenic rosacea is a clinically useful, but not yet standardized, sensory-weighted presentation within the rosacea spectrum. This narrative review evaluates its clinical features, differential diagnosis, proposed mechanisms, and reported therapeutic approaches while distinguishing direct human evidence from indirect and experimental findings. Materials and Methods: PubMed/MEDLINE, Scopus, Web of Science, and Google Scholar were searched through 30 June 2026 using predefined combinations of terms related to rosacea, facial dysesthesia, neurogenic inflammation, sensory pathways, mast cells, and treatment. English-language clinical and experimental publications were selected by relevance; reference lists were also screened. Evidence was grouped as phenotype-specific human evidence, human evidence from rosacea populations or related conditions, case-based evidence, and animal or cellular evidence. Results: Direct evidence specific to neurogenic rosacea is limited mainly to small observational series and case reports. Human rosacea studies support neurovascular involvement, whereas many TRP-channel, protease, LL-37-MRGPRX2, and mast cell links remain indirect or experimental. No validated diagnostic criteria or phenotype-specific treatment algorithms exist. Conclusions: Neurogenic rosacea is best regarded as a clinically useful but not yet standardized sensory-weighted presentation within the rosacea spectrum, as current evidence does not establish it as an independent phenotype. The clinical features summarized in this review may support recognition of this presentation and its differentiation from relevant mimics, while diagnostic and treatment decisions should remain individualized. Prospective cohorts, validated sensory measures, biomarkers, and controlled phenotype-stratified trials are needed.

A middle-aged man presented with asymptomatic multiple grouped papules present bilaterally symmetrically on the face. Histopathology revealed peri-follicular, predominantly B-cell lymphoid aggregates with germinal center formation and occasional tingible body macrophages. Immunohistochemistry for Bcl-2 was positive in the peripheral mantle zone while sparing the follicle center, suggesting a reactive lymphoid follicle. Clinical differential diagnosis of facial papules can be broad, encompassing sarcoidosis, granulomatous rosacea, lupus miliaris disseminatus faciei, acneiform eruption, and eruptive benign appendageal tumors, among others. We report a rare case of pseudolymphoma clinically presenting as multiple facial papules, diagnosed through combined histopathological and immunohistochemical evaluation.

Rosacea is a chronic central face dermatosis caused by a combination of dysregulated innate and adaptive immunity and hyperreactive cutaneous neurovasculature. Although classically associated with lighter skin phototypes, rosacea may affect up to 2-4% of Black, Asian, Pacific Islander, and Hispanic/Latino American populations and its prevalence is likely underestimated given our current diagnostic reliance on phenotypic expression (e.g., fixed erythema with or without intermittent exacerbations, flushing, and/or telangiectasias) that may be difficult to appreciate in more heavily pigmented skin. In patients with richly pigmented skin, a careful history of symptoms to assess the minor/secondary criteria (i.e., burning or stinging, edema, dryness, flushing, low tolerance for over-the-counter products, symptoms with classic 'triggers', family history and/or ocular symptoms), along with patient participation during the physical exam to establish their baseline skin tone, may facilitate diagnosis. Rosacea treatment regimens are centered around presentation and can include over-the-counter agents, lifestyle modifications, prescription topical, systemic, and procedural therapies. Optimal regimens may be tailored to best address patient-perceived disease severity and concerns and to minimize any further irritation/inflammation which may drive pigmentary alteration.

TRPV1 is a non-selective cation channel that is widely expressed in multiple skin cell types, including sensory nerve fibers, keratinocytes, immune cells and fibroblasts. It can be activated by noxious heat, acidic conditions, capsaicin and a range of endogenous inflammatory mediators. Upon activation, TRPV1 mediates Ca[2+] influx, leading to neuropeptide release and the initiation of neurogenic inflammation. Under physiological conditions, in addition to its well-established roles in nociception and pruritus transmission, TRPV1 contributes to several aspects of cutaneous homeostasis, including epidermal barrier repair, wound healing and hair follicle biology. Under pathological conditions, aberrant TRPV1 expression or dysfunction has been closely associated with the development of various skin disorders, such as psoriasis, atopic dermatitis, rosacea, skin aging and melanoma. In recent years, therapeutic strategies targeting TRPV1 have shown promising potential in alleviating cutaneous hypersensitivity, suppressing pruritus and delaying skin aging. This review provides an in-depth discussion of the expression profile and activation mechanism of TRPV1 in the skin, with a particular focus on its multifaceted roles in maintaining skin homeostasis and driving disease pathogenesis and further discusses the opportunities and challenges of targeting TRPV1 for clinical translation.

Rhinophyma is a benign, slowly progressive, disfiguring condition of the nose characterized by sebaceous gland hypertrophy, fibrosis, and follicular plugging, generally regarded as the end stage of phymatous rosacea. It predominantly affects middle-aged to elderly men and can cause significant cosmetic and psychosocial morbidity and, in advanced cases, nasal airway obstruction. We report a 71-year-old hypertensive man who presented with progressive, painless nasal enlargement involving the nasal tip and alar crests bilaterally. Incisional biopsy confirmed rhinophyma, showing sebaceous hyperplasia with cystic dilatation of the follicular infundibula and keratinous plugging. He underwent tangential excision using a cold blade combined with monopolar electrocautery, with hemostasis achieved by monopolar diathermy, and the wound was left to heal by secondary intention under a silver-based dressing. Healing was uneventful, with complete re-epithelialization and a satisfactory cosmetic outcome. This case supports tangential excision with monopolar electrocautery as a simple, effective, and reproducible technique for rhinophyma. Beyond the outcome itself, this report documents the intraoperative depth-control and symmetry cues used, the technical difficulties encountered during subunit contouring, and a staged postoperative wound-care protocol, so that an established but often summarily described technique can be reproduced in centres without access to laser or hydrosurgical platforms. A single case cannot establish superiority over alternative modalities, and comparative studies using standardized aesthetic outcome measures remain needed.