Fibrosing alopecia in a pattern distribution (FAPD) is an infrequent presentation of primary cicatricial alopecia with clinical, histopathological, and trichoscopic features of both Androgenetic Alopecia (AGA) and Lichen Planopilaris (LPP) (1, 2). It was first described by Zinkernagel and Trüeb in 2000, when they mentioned that FAPD is related to AGA in its pathogenesis and distribution, with a diffuse hair loss pattern that progresses to a cicatricial and lichenoid reaction (3). Their findings were supported by clinical response with an antiandrogen that decreased hair loss and reduced inflammation (3). This alopecia is more prevalent among women than men, but while males manifest it at an earlier age, females tend to manifest it in the postmenopausal period (1–3). Our objective was to describe the clinical, trichoscopic, and histopathological features of 46 Hispanic male patients with FAPD.

FAPD is a rare form of primary cicatricial alopecia with a lichenoid inflammation pattern, sharing clinical, trichoscopic, and histological features of both AGA and LPP. This distinctive condition was initially described by Zinkernagel and Trüeb in 2000 (1–3).

Most case series exhibit a marked female predominance but an earlier age of onset among males, who are typically affected in their fifth decade. This was outlined in the original paper, where only 4 out of 19 patients were men, with a mean age of 54 years old (the mean age among women was 59 years). Another international multicenter study had similar findings: 11% were men (n = 57), with a mean age of 57 vs. 59 in women (4). A case series of 13 patients from Chile, however, described an even lower mean age of 37 years among the four men included (ranging from 28 to 46 years) (5). Similarly, a Japanese publication on FAPD affecting 7 males (from a sample of 24) found a mean age of 26.57 years (ranging from 17 to 40 years) (6). Such results correlate with ours and suggest that male patients in Latin America, perhaps similar to the Asian population, may have an earlier age of presentation than Europeans and North Americans (1, 3–6).

The pathogenesis of FAPD is not fully understood, with some experts considering it a variant of lichen planopilaris or a type of primary lymphocytic cicatricial alopecia (1, 2). The latter is characterized by a lichenoid reaction to the upper part of the hair follicle, triggering perifollicular inflammation and fibrous follicular tracts (1, 2). It is also theorized that in immunogenetically susceptible patients, hair follicles altered by the progression of AGA may produce a lichenoid reaction when exposed to an antigenic stimulus (1).

Contrary to what was published by Zinkernagel and Trüeb, who identified 13 cases of FPHL and only 6 of MPHL, MPHL predominated in our sample (3). This is important since FPHL affecting the centroparietal area is considered the most common presentation (1–3). In their paper, 75% of the men with MPHL had a Hamilton—Norwood scale stages III and IV (3). It also indicates that, despite being less common in males than females, FAPD resembles AGA with progressive bitemporal, frontal, and vertex recession as described in other publications (1–3).

Griggs et al. (1) proposed a specific set of criteria to diagnose FAPD in suspected cases of cicatricial alopecia. It requires a combination of clinical, trichoscopic, and histologic data (1). We believe this approach fully applies to our population and facilitates the appraisal of differential diagnosis (Figure 2) (1). According to those criteria, all subjects in our sample presented a symmetrical pattern of hair loss in androgen-dependent areas of the scalp (1). Our trichoscopic findings were perifollicular scale and follicular keratosis, loss of follicular openings, hair diameter variability, single hairs per follicular unit, and perifollicular erythema, which correspond to all the listed trichoscopic criteria (Figure 3) (1). Finally, all histologic criteria, virtually the same as those used for AGA and LPP, were fulfilled in our study from one or two 4 mm-punch biopsies (1). The vertical/horizontal sections revealed concentric perifollicular lamellar fibrosis, lymphohistiocytic infiltrate (predominantly in the upper region of the hair follicle), fibrotic follicular tracts, follicular miniaturization, and interface dermatitis (1–3). In the present study, concentric perifollicular lamellar fibrosis was considered an absolute diagnostic criterion for inclusion. Despite the heterogeneity in biopsy orientation, diagnostic confidence was maintained because this hallmark histopathological feature was identified in 100% of cases, allowing consistent clinicopathological correlation across all participating centers. The optimal treatment for FAPD is yet to be determined. The information available is based on case reports and retrospective studies, with unclear conclusions about follow-up and prognosis (1, 2, 4). The treatment aims to halt inflammation, prevent disease progression and scarring alopecia, and reverse the miniaturization of the hair follicle, an apparent trigger in genetically predisposed subjects (1, 4). In our study, we observed the use of several therapies including topical, intralesional, and systemic anti-inflammatory agents, growth-stimulating agents, and anti-androgenic agents, all of which are involved in the pathophysiology of this entity.

Table 1 shows a clinical, trichoscopic and histological comparison as well as demographic values from our study and from some of the case series reviewed in this article.

The limitations of this study are related to its retrospective design. The sample processing techniques for histopathological evaluation were not fully standardized across centers: only 24% of patients had both vertical and horizontal sections available, while the remaining cases were assessed using a single biopsy orientation, predominantly vertical sections. To our knowledge, this represents the largest case series on male FAPD to date, and the largest composed exclusively of Latin American patients.

In summary, fibrosing alopecia in a pattern distribution (FAPD) remains a condition with limited epidemiological characterization. Our findings suggest a trend toward an earlier age of onset among Latin American men with FAPD, showing similarities to reports in Asian populations rather than those from European and North American cohorts. However, this observation should be interpreted with caution, as it may be influenced by differences in referral patterns, diagnostic awareness, and access to health care. We acknowledge the challenge of diagnosing male patients with FAPD, as they often clinically resemble AGA in their classic loss pattern. The diagnostic criteria proposed by Griggs et al. (1) proved valuable in assessing the clinical, trichoscopic, and histological presentation of the patients in this study.

To our knowledge, this study represents the largest case series of male FAPD documented thus far. Our exploration of the epidemiological details of this challenging condition aims to contribute to a better understanding of FAPD and potentially improve patients’ quality of life.