A thorough history and physical exam in patients with GLPLS is a core component of a satisfactory diagnosis. Determining if a patient has experienced significant hair loss, psychosocial stress, or endocrinological abnormalities can lead you to other potential causations of alopecia that may exclude GLPLS as a final diagnosis. Physical examination should include a full body skin check with additional attention paid towards the perineum and axillae for signs of non-cicatricial alopecia. Examination of the trunk and extremities for signs of hyperkeratotic papules with surrounding perifollicular erythema also is a key component of GLPLS. Investigation of the scalp in GLPLS should reveal a multifocal, patchy, and cicatricial alopecia of the scalp. In addition, an anagen hair pull is often positive in GLPLS because of the relatively weak stabilization of the hair follicles of affected individuals.

Skin biopsy in conjunction with physical exam findings are the primary methods of diagnosis in GLPLS. Histology of the cicatricial areas and the hyperkeratotic papules reveals features of lichen planopilaris. Biopsy shows areas of perifollicular inflammation leading to pilosebaceous destruction, with late-stage GLPLS causing corruption of arrector pili muscles. Clinical evaluation of GLPLS shows erythematous follicular papules varying in size from 1 to 4 mm, non-cicatricial alopecia of the perineum and axillae, and patchy cicatricial alopecia on the scalp. Hyperkeratotic papules are typically present on the trunk, thighs, inner arms, outer arms, and wrists with or without pruritus. Initial onset of the hyperkeratotic papules can precede the development of alopecia on the scalp. However, there is no set chronological order of symptoms.[15]

The management of GLPLS remains elusive with no current therapeutic regimen highlighted to be dominant. Treatment focuses on reducing the immunological response before the development of follicular scarring. Novel research has shown that JAK inhibition with tofacitinib leads to the normalization of interferon-mediated T-cell chemotaxis, thus preventing infundibular inflammation. A case series of 8 lichen planopilaris patients treated with a twice a day 5mg dose of tofacitinib reported a 30-94% improvement of disease severity.[11] Zegarska et al. reported a case of a prednisone 30 mg dosage for two weeks then a subsequent reduction to 20 mg of prednisone with psoralen and ultraviolet light A at a dosage of 12 joules. This treatment regimen led to the moderate improvement of the follicular hyperkeratosis of the trunk and extremities. While reduction of the follicular papules occurred, there was no reduction in the cicatricial alopecia of the scalp or the non-cicatricial alopecia in the axillae and perineum.[16] Besides these modalities, there have been reports of the following therapies; intralesional glucocorticoids, topical glucocorticoids, systemic glucocorticoids, cyclosporine, tacrolimus ointment, and systemic retinoids. Most treatment methods lead to a reduction of perifollicular erythema and inflammation without effect on the cicatricial alopecia, or perineal and axillary non-cicatricial alopecia.[4][9][16]

Differential diagnosis in GLPLS includes classical lichen planopilaris, pseudopelade of Brocq, frontal fibrosing alopecia, lichen spinulosus, androgen insensitivity syndrome, discoid lupus erythematosus, secondary syphilis, and Addison disease.[17][18][19][20]

The course of GLPLS is often drawn-out and may improve with treatment, however full resolution of alopecic symptoms with current modalities of treatment is rare. Limited data is present to determine the average duration of disease with some cases extending for over 20 years. However, Zegarska et al. report a range of 6 months to 10 years.[16] Prognosis of GLPLS may see a significant improvement in the reduction of hyperkeratotic papules on the trunk and extremities with adequate medical management.

While GLPLS can bring about significant psycho-social stress from the superficial alteration to appearance, there are no known systemic manifestations of the disease. Further study of the INCENP protein and its role in overall mitotic function may lead to the discovery of concomitant morbidities in GLPLS, yet no such comorbidity is present at this moment. The primary lasting complication present in GLPLS is the existence of the follicular scarring that occurs after the infundibular inflammation. This cicatricial portion of the disease manifests on the scalp and leads to permanent damage of the pilosebaceous unit.

Patients suffering from GLPLS require a thorough explanation of prognosis and treatment options to lead them towards realistic expectation for the management of their disease. With current therapy often not affecting the alopecic portion of the disease, many patients forego treatment. While treatment modalities cannot cause improvement towards the prior cicatricial damage, early initiation of a therapeutic agent may lead to a reduction in further progression of the non-cicatricial alopecia, cicatricial alopecia of the scalp, and hyperkeratotic papule formation. Giving patients a clear insight into the goals of GLPLS therapy can improve compliance and lead to better patient-physician relationships.

an interprofessional approach at the initial evaluation of patients with GLPLS is the key to providing optimal care and improved outcomes. Multiple medical specialties can assist in the diagnostic and long-term care processes including dermatologists, dermatopathologists, pharmacists, hair-loss support groups, and psychologists.  Satisfactory diagnosis is of utmost importance followed by psycho-social assistance from trained professionals and alopecia support groups. Support groups of patients with alopecia can lead to increased feelings of belonging and reduce psycho-social stress associated with the diagnosis of GLPLS.[21][level V]