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Abstract
Fibrosing Alopecia in a Pattern Distribution (FAPD), a rare condition predominantly in postmenopausal women, is characterized as primary as cicatricial alopecia. There is a great deal of difficulty diagnosing and treating this condition because it combines the features of both androgenetic alopecia and lichen planopilaris. This systematic review summarizes the current knowledge on FAPD, its clinical and histopathological features, diagnosis, and management.

Introduction
Fibrosing Alopecia in a Pattern Distribution (FAPD), with primary cicatricial alopecia characteristics, is reported to be similar in nature to androgenetic alopecia (AGA) and lichen planopilaris (LPP) in regards to its histopathological and clinical features [1]. Postmenopausal women are most commonly affected by this rare condition with progressive hair loss and scarring [2]. As a result of low reported cases and confusion in diagnostic criteria, the incidence and prevalence of FAPD are unknown. An overview of FAPD's clinical and histopathological features, diagnosis, and management will be presented in this systematic review.

Literature Findings
Clinical Features
Postmenopausal women are more likely to develop FAPD [3]. Although there have been a few cases reported in men and premenopausal women [4]. Between 30 and 80 years of age is the average age of onset for FAPD [3]. The typical presentation of FAPD is diffuse hair thinning or hair loss with a patterned distribution that resembles AGA; however, characteristics of LPP––perifollicular erythema, scaling, or follicular hyperkeratosis––are also associated with FAPD [1].

An atrophic or hypertrophic scar may appear on the affected areas, which typically display an oval or irregular shape [5]. In most cases, patients report no to mild symptoms, and hair loss occurs slowly and gradually or waxes and wanes [2]. There is no inflammation in FAPD, unlike LPP, and it does not progress rapidly either [2]. 

Histopathology
FAPD shares histopathological characteristics with LPP and AGA [1]. AGA and LPP share several characteristics of FAPD, including decreased hair follicle density, lamellar fibrosis, and inflammation dominated by lymphocytic infiltrates near the hair follicle bulge [1,6].

Biopsies may demonstrate inflammatory infiltrates that resemble those seen in LPP, as well as interstitial collagen deposition [3]. It is also possible to find focal immunoglobulin and complement deposits in the basement membrane zone using direct immunofluorescence on the affected scalp [3].

Diagnosis
Hematology, dermoscopy, and clinical examination are used to diagnose FAPD. AGA and LPP have overlapping clinical and histopathological features, making FAPD difficult to diagnose [3]. The presence of hair loss in the frontal and vertex regions of postmenopausal women and the presence of scarring are clinically suggestive of FAPD [2]. White areas, empty follicular openings, and tubular structures may help differentiate FAPD from AGA on the dermoscopic level [7].

Management
FAPD is currently treated based on published case reports and expert opinions, as there is no standard of care. Although there is no golden standard of care, preventing further scarring and preserving hair helps in early diagnosis and treatment [3].

Despite their histopathological similarity, both LPP and FAPD can be treated with intralesional corticosteroids, topical corticosteroids, hydroxychloroquine, mycophenolate mofetil, and oral retinoids. [8]. On the other hand, patients with FAPD who have similar characteristics to that of AGA may be treated with minoxidil, finasteride, and spironolactone [2].

Conclusion
The clinical and histopathological features of FAPD overlap with those of AGA and LPP, a rare form of primary cicatricial alopecia. Clinical evaluations, dermoscopy, and histopathological examinations are used to diagnose this disease. There are currently no proven effective treatments for treating this condition, which focus on reducing inflammation and preventing further scarring. For a better understanding of FAPD, further research is needed to investigate its pathogenesis, diagnostic criteria, and treatment strategies.