Localized Acquired Perforating Dermatosis on Scalp Presented With Acute and Diffuse Total Alopecia

Acquired perforating dermatosis (APD) is a group of skin disorders characterized by the transepidermal elimination of various dermal connective tissue components. The lesions typically present as hyperkeratotic papules and nodules, often developing on the extensor surfaces of the extremities. This study describes two cases of APD, consisting of acquired reactive perforating collagenosis (RPC) and perforating folliculitis (PF), which occurred exclusively on the scalp, accompanied by diffuse hair shedding. Case A: A 52-year-old woman with hypertension (HT), type 2 diabetes mellitus (T2DM), dyslipidemia (DLP), and end stage kidney disease (ESKD) on hemodialysis for 2 years presented with diffuse hair shedding, thinning of the lateral eyebrows, followed by the development of hyperkeratotic papules with central crust on the scalp over the past 2 months (Figure 1a). Physical examination revealed non-scarring alopecic patches across the scalp, along with discrete hyperkeratotic papules. A hair pull test was positive for dystrophic hairs. Trichoscopy showed black dots, broken hairs, and coiled hairs. Histopathology from punch biopsies confirmed alopecia areata (AA) and RPC (Figure 1c). Intramuscular triamcinolone injection monthly for a total of 4 months together with a topical combination of betamethasone dipropionate and salicylic acid led to lesion clearance, with no recurrence after 1 year. Case B: A 49-year-old woman with HT, T2DM, DLP, and ESKD undergoing peritoneal dialysis for 6 years presented with widespread hair loss and non-pruritic hyperkeratotic papules on her scalp for one month (Figure 2a). Trichoscopy revealed multiple black dots and broken hair. Biopsies were taken and confirmed the diagnoses of AA and PF. The treatment regimen included intramuscular injections of triamcinolone and topical therapy, which led to significant clinical improvement. The patient experienced reduced hair shedding and resolution of the hyperkeratotic papules without recurrence. APD has been proposed as a unifying term for most perforating disorders, including RPC, PF, and Kyrle disease. This proposal is based on the overlapping and mixed histological features observed [1]. APD typically presents as a chronic, pruritic dermatosis characterized by central keratotic crusts, which can develop anywhere on the body but are most found on the extensor surfaces of the limbs and trunk. Scalp involvement has been previously reported in six cases of APD, including four cases of RPC and two cases of Kyrle disease. To date, there has been no reported case of localized APD exclusively affecting the scalp [2]. The pathophysiology of APD remains incompletely understood. Microtrauma caused by scratching is considered one of the most significant triggers. Laser hair removal, which can induce microtrauma and inflammation, has also been reported to trigger RPC [3]. The two most common associated conditions are T2DM and ESKD, while inflammatory skin diseases such as atopic dermatitis [2] and psoriasis have also been noted [1]. Acute diffuse and total alopecia (ADTA) is a distinct subtype of AA, characterized by the acute onset of diffuse hair loss accompanied by perifollicular inflammation. Autoimmunity is believed to play a significant role in its pathogenesis. ADTA has a favorable prognosis, with spontaneous hair regrowth often occurring without treatment [4]. These two cases of APD occurring concomitantly with ADTA suggest a possible association between the two conditions. The exclusive localization of APD to the scalp, without involvement of other commonly affected sites, and its synchronous clinical course with ADTA—both in onset and resolution—support the hypothesis that perifollicular inflammation associated with ADTA may trigger APD. Notably, the favorable response of both diseases to dupilumab further underscores a shared immunopathogenic mechanism, highlighting the central role of type 2 inflammation as a potential common pathway [5]. The authors have nothing to report. The patients in this manuscript have given written informed consent to the publication of their case details. The authors declare no conflicts of interest. The data that support the findings of this study are available from the corresponding author upon reasonable request.