ABSTRACT Histiocytoid Sweet syndrome (H‐SS) is a variant of Sweet syndrome characterized by a dermal infiltrate of immature myeloid cells with histiocytoid morphology rather than mature neutrophils. These cells express myeloid markers including myeloperoxidase, lysozyme, CD15, and CD13. H‐SS has been associated with hematologic malignancies and demonstrates higher relapse rates compared with classic Sweet syndrome. This review synthesizes current evidence on the clinicopathologic features, immunophenotype, disease associations, and treatment of H‐SS, and examines its position within the broader spectrum of myeloid cutaneous infiltrates.
Background Dermal postinflammatory hyperpigmentation (PIH) is frequently refractory to treatment, and therapeutic response is thought to depend on the depth and distribution of dermal pigment. Key quantitative histopathologic features, however, remain poorly defined.Methods Ninety-five biopsy-proven cases of dermal PIH were analyzed. Fontana-Masson-stained sections underwent image analysis to quantify epidermal and dermal pigmentation intensity, melanophage density, cross-sectional area, and depth. Associations with inflammatory etiology, Fitzpatrick skin type (FST), and sun-exposure status of the biopsy site were assessed.Results Epidermal pigmentation intensity was significantly increased in spongiotic dermatitis, higher FST, and sun-exposed sites. Dermal pigmentation intensity was associated with sun exposure. Melanophage density increased with higher FST but was lower in spongiotic dermatitis compared with lichenoid and vacuolar interface dermatitis. In contrast, melanophage cross-sectional area and depth showed no significant associations with etiology, FST, or anatomic site. Median melanophage depth was 295.0 mu m (IQR, 220.0-407.0 mu m) from stratum corneum and 163.0 mu m (IQR, 111.2-235.5 mu m) from basement membrane, with consistent measurements across subgroups.Conclusion Despite variability in epidermal pigmentation and melanophage density, melanophage depth is uniform across dermal PIH. These findings refine the conventional epidermal-dermal PIH classification and support a quantitative, anatomy-based framework to inform depth-targeted treatment strategies.
ABSTRACT Background Mast cells are key regulators of cutaneous inflammation and are known to accumulate in response to various immunological stimuli. Although their role in several dermatological conditions has been established, their specific contribution to different forms of alopecia—particularly scarring versus nonscarring types—remains incompletely understood. This study aimed to compare the degree of mast cell infiltration across three distinct types of alopecia: androgenetic alopecia (AGA), fibrosing alopecia in a pattern distribution (FAPD), and lichen planopilaris (LPP). Method A total of 56 patients diagnosed with AGA, FAPD, or LPP were enrolled. Scalp biopsies were obtained from all participants, and diagnoses were confirmed through histopathological examination. Mast cell distribution and infiltration density were quantified and analyzed using SPSS and Stata software. The study was conducted with full ethical approval. Result The majority of participants (91%) were female, with a mean age of 44.3 years. FAPD was the most prevalent diagnosis (42.9%). LPP demonstrated the highest degree of mast cell infiltration, while AGA exhibited the lowest (ANOVA, p < 0.001). Post hoc analysis revealed significant differences between AGA and FAPD (−17.7%, p = 0.001) and between AGA and LPP (−20.1%, p = 0.001). Although mast cell infiltration was higher in patients over 40 years of age, this difference did not reach statistical significance. No significant association was identified between mast cell infiltration and patient sex. Conclusion Mast cell infiltration is significantly more pronounced in scarring alopecias (LPP and FAPD) compared to non‐scarring AGA, suggesting a shared immunopathological mechanism underlying follicular destruction in scarring subtypes. These findings also raise important questions regarding the potential inflammatory contribution of mast cells to AGA pathogenesis.
ABSTRACT Mechanical stress on the pilosebaceous unit can contribute to mechanical alopecia (MA) as seen with traction alopecia (TA) and trichotillomania (TTM). While some histological features that point to TA and TTM have been described, these may be absent in biopsies obtained at earlier stages of disease. Additional anomalies of the pilosebaceous unit have been observed that may assist in the histopathological detection of MA. A blinded, retrospective, qualitative, and semiquantitative study was performed comparing horizontally processed scalp biopsy sections of clinicopathologically confirmed TA ( n = 16) and TTM ( n = 9) to nearly matched controls ( n = 15). Translocation of sebocytes into the follicular canal was seen in both TA and TTM, supporting a shared underlying mechanism. Vectorially warped sebaceous lobules were observed predominately in TA ( p = 0.0002), while collapse of the inner root sheath of the lower follicular isthmus and surface lichenification were primarily seen in TTM ( p < 0.0002). Lateral impingement of the follicular canal was seen in both TA and TTM ( p < 0.0001), although more commonly in TA. These alterations were observed in the absence of other previously described features. Further validation studies in larger cohorts are warranted to assess their diagnostic utility in the recognition of MA.
