Follicular vitiligo: A report of 8 cases

Vitiligo-like lesions in patients receiving anti–programmed cell death-1 therapies are distinct from spontaneously occurring active vitiligo

“…4 Another distinct clinical sign that has not been reported in our study is the rapid involvement of hair follicles (Fig 1, B), which is not classically observed in vitiligo (at early stages), except in the rare clinical subtype follicular vitiligo. 5 Biologically, while we do agree with Fukuda et al that vitiligo-like lesions induced by antiePD-1 and vitiligo share a similar TH1/Tc1 driven immune response involving C-X-C motif chemokine receptor 3 (CXCR3 1 ) T cells producing interferon-, we could speculate, based on our results, that the reinvigorated immune response induced by antiePD-1 is much stronger than in vitiligo. Moreover, it is important to consider that compared to vitiligo, which affects melanocytes with intrinsic abnormalities, vitiligo-like lesions are rather the consequence of incidental attack of normal melanocytes.…”

Predictive Model for Response Rate to Narrowband Ultraviolet B Phototherapy in Vitiligo: A Retrospective Cohort Study of 579 Patients

“…There are a few types of vitiligo that do not fall into this classification. Follicular vitiligo, recently described, is a primary vitiligo of the hair, in which hair whitening precedes leukoderma (7). Mucosal vitiligo refers to the exclusive involvement of oral or genital mucosa (8).…”

The enigma and challenges of vitiligo pathophysiology and treatment

“…Although depigmentation commonly involves sites subjected to repeated trauma, pressure, or friction, the degree to which these stimuli, termed chronic koebnerization factors, contribute to the development of vitiligo remains an area of active research (Ezzedine et al, 2012). Leukotrichia, or depigmentation of the hair shaft, can affect anywhere between 10% to greater than 60% of patients with vitiligo (Gan et al, 2016). The presence of leukotrichia negatively affects the chance of repigmentation in response to treatment, presumably due to the loss of the melanocyte stem cell reservoir in the epithelium of the folliculosebaceous unit (Ezzedine et al, 2012).…”