Tufted hair folliculitis: a pattern of scarring alopecia?

We present a patient with pemphigus vulgaris who, over the years, experienced the development of tufted hair folliculitis as a result of scalp involvement. Multiple hairs emerged from widely dilated follicular ostia surrounded by indurated, scarred skin. Histopathologic findings were typical for tufted hair folliculitis. We believe that because a specific host response to scalp injury might be crucial to the development of this rare disorder, it should be regarded as a type of scarring alopecia.     

Bilateral lagophthalmos in leprosy: is it a rare phenomenon?

Lagophthalmos is one of the well known complications of leprosy due to involvement of the facial nerve. Herein, we report three cases of bilateral lagophthalmos due to leprosy which presented to us within a span of just three months. In all these cases, lagophthalmos was not the presenting complaint and it was detected by the treating doctor during examination. This report is being presented to highlight the importance of cranial nerve examination in all cases of leprosy as at times early changes of lagophthalmos may go unnoticed by the patient.     

Fibrosing alopecia in a pattern distribution: patterned lichen planopilaris or androgenetic alopecia with a lichenoid tissue reaction pattern?

BACKGROUND: Androgenetic alopecia is characterized by a defined area of progressive nonscarring alopecia. The clinical and histological findings in 15 women and 4 men with progressive scarring alopecia in a pattern distribution were studied. The results were evaluated and compared with clinicopathologic entities that feature scarring of the central scalp area, specifically, lichen planopilaris, pseudopelade, and follicular degeneration syndrome. OBSERVATIONS: Patients developed progressive fibrosing alopecia of the central scalp, without the multifocal areas of involvement typical of lichen planopilaris and pseudopelade. Perifollicular erythema, follicular keratosis, and loss of follicular orifices were limited to a patterned area of involvement. Biopsy specimens of early lesions demonstrated hair follicle miniaturization and a lichenoid inflammatory infiltrate targeting the upper follicle region. Advanced lesions showed perifollicular lamellar fibrosis and completely fibrosed follicular tracts indistinguishable from end-stage lichen planopilaris, pseudopelade, or follicular degeneration syndrome. CONCLUSIONS: Some patients with androgenetic alopecia might have additional clinical and histological features of inflammation and fibrosis limited to the area of androgenetic hair loss. In these patients, the histological findings of early lesions are identical to those seen in lichen planopilaris. The lichenoid tissue reaction leading to follicular destruction in these patients might be pathogenetically related to the events underlying androgenetic alopecia.     

Is androgenetic alopecia a photoaggravated dermatosis?

Progressive thinning of the scalp hair in androgenetic alopecia (AGA) results in a gradual decline in natural protection of the scalp from ultraviolet radiation (UVR). A number of pathologic conditions of the scalp are evidently related to UVR, particularly photosensitive diseases and disorders of the chronically photodamaged bald scalp. The most important chronic effects of UVR are photocarcinogenesis and solar elastosis. Besides these, erosive pustular dermatosis and 'red scalp' are distinct disorders peculiar to the balding scalp. While the consequences of sustained UVR on the unprotected scalp are well appreciated, the effects of UVR on hair loss have widely been ignored. However, clinical observations and theoretical considerations suggest that UVR may have negative effects: acute telogen effluvium from UVR has been described, and the production of porphyrins by Propionibacterium sp. in the pilosebaceous duct, with photoactivation of porphyrins leading to oxidative tissue injury, has been implicated in follicular microinflammation. Alternatively, keratinocytes themselves may respond to physicochemical stress from UVR, besides irritants and pollutants, by producing radical oxygen species and nitric oxide and by releasing proinflammatory cytokines, eventually leading to injury of the putative site of follicular stem cells in the superficial portion of the hair follicle. Since all of these processes involved in hair loss share the common feature that they are induced or exacerbated by exposure to sunlight, it is proposed that AGA is a photoaggravated dermatosis that requires photoprotection.     

Diffuse alopecia with stem cell folliculitis: chronic diffuse alopecia areata or a distinct entity?

A 34-year-old woman presented with an 8-year history of slowly progressive diffuse nonscarring alopecia with loss of hair density. Scalp biopsy specimens showed increased miniaturized follicles and an asymmetric wedge-shaped lymphocytic infiltrate concentrated on the stem cell-rich region at the point of entry of sebaceous ducts and at bulge-like regions of multiple follicles. Several hair bulbs emerging at the stem cell compartment also were inflamed, but the hair bulbs in the deeper dermis and subcutis were spared. I speculate whether these findings may represent a stem cell folliculitis similar to the reaction pattern previously observed in graft versus host disease and in androgenetic alopecia. The additional presence of peribulbar lymphocytic inflammation could indicate that the patient had a variant of alopecia areata. The clinical presentation of a slowly progressive diffuse alopecia without progression to clinically recognizable alopecia areata and the prominent lymphocytic inflammation involving the stem cell compartment may prompt a reexamination of similar cases currently classified as chronic diffuse alopecia areata. The concept that lymphocytes can inhibit stem cell function without destroying the stem cells themselves needs consideration.