Introduction: Lichen planopilaris (LPP) is a lymphocytic primary cicatricial alopecia presenting with scarring hair loss and variable degrees of perifollicular erythema and scaling. Pustules are infrequent and may mimic folliculitis decalvans (FD) and other forms of neutrophilic alopecia. We present a series of LPP cases with pustules and discuss the importance of differentiating them from primary neutrophilic folliculitis. Materials and Methods: Demographic, clinical, histopathological, and follow-up data of 13 cases of LPP with pustules followed at the Department of Dermatology of the University of São Paulo Medical School were described. Results: Seven females and 6 males were included. Onset of signs and symptoms ranged from 23 to 61 years of age. Previous diagnoses were FD in 3 patients, pityriasis amiantacea in 2 cases, and folliculitis keloidalis nuchae in 1 case. Other 7 cases presented typical clinical features of LPP. Discussion: There is limited data concerning LPP with pustules. Our analysis shows that LPP should be considered a differential diagnosis in patients with refractory folliculitis. Cautious examination of the entire scalp with dermoscopy and/or reevaluation after a course of antibiotics can avoid misdiagnosis. Further studies are required to establish the etiology of pustules in the setting of LPP.

Eosinophilic spongiosis is a histological feature shared by some distinct inflammatory disorders, and is characterized by the presence of intraepidermal eosinophils associated with spongiosis. Most often, isolated eosinophilic spongiosis indicates the early stages of a subjacent autoimmune bullous dermatosis, such as the pemphigus group and bullous pemphigoid. Herein, the main causes of eosinophilic spongiosis are discussed, as well as the supplementary investigation needed to elucidate its etiology.

There is not enough scientific evidence to support neutrophilic urticaria as a solid, separate entity.

Background Pemphigus herpetiformis (PH) is a rare clinical subtype of pemphigus with the presence of urticarial plaques, severe pruritus, rare acantholysis and eosinophilic spongiosis. Objectives The aim of this study was to investigate the influence of IL-31 and pro-inflammatory cytokines/chemokines in the pathogenesis of PH. Methods Twenty-five patients with PH and three groups: pemphigus foliaceus (PF = 14), pemphigus vulgaris (PV = 15) and healthy controls (HC = 20) were selected for this study. The groups were analysed by immunohistochemistry utilizing IL-31, IL-31RA, IL-4, IL-17 and TNF-a antibodies. Serum levels of IL-4, IL-13, TNF, CXCL8, CCL5 and CCL2 were evaluated by cytometric bead array. Results Analysis of IL-31 family of PH patients revealed the following findings: (i) Enhanced in situ expression of IL-31 in PH samples, compared to PF and to PV (epidermis); (ii) Cutaneous IL-31RA expression in PH samples was higher than in PF, PV and HC groups (epidermis and dermis); (iii) PF patients that evolved to PH showed significant increased IL-31RA epidermal expression during the PH phase. Profile of pro-inflammatory cytokines (IL-4, IL-17 and TNF-a) in PH patients' skin exhibited: (i) Enhanced IL-4 expression, when compared to patients with PF (epidermis and dermis) and with PV (epidermis); (ii) Augmented IL-17 expression than PF and PV patients (epidermis); (iii) Augmented expression of TNF-a when compared to PF at the epidermal level. Evaluation of circulating cytokines and chemokines showed higher levels of CXCL8 and CCL2 in PH sera compared to HC group. Conclusions IL-31 and IL-31RA, cytokines related to pruritus, and pro-inflammatory chemokines (CXCL8 and CCL2) seem to exert a role in the pathogenesis of PH. These findings support future studies to clarify the role of IL-31 pathway as a potential therapeutic target for patients with PH.

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