Faculty Bibliography

Although the complete picture for alopecia areata (AA) pathogenesis has yet to be determined, recent research has made much progress in our understanding of the disease mechanism. Numerous circumstantial evidence supports the notion that AA is fundamentally a disease mediated by inflammatory cells and may be autoimmune in nature. Recent research has shown the hair-loss phenotype is precipitated predominantly by CD8+ lymphocytes, but the disease mechanism is driven by CD4+ lymphocytes. Although genetic susceptibility is a key contributor to disease development, disease onset and phenotypic presentation are probably modified by complex environmental interplay. On the basis of our current understanding of AA disease pathogenesis, several experimental and theoretical therapeutic approaches might be possible. However, the pathogenetic disease mechanism is particularly robust and the development of a cure for AA will be a significant challenge

OBJECTIVE: Hair removal using lasers or broadband intense pulsed light has become one of the most ubiquitous medical procedures. At our center a small proportion of patients have spontaneously reported what they believed to be increased hair growth at sites of previous laser epilation. We sought to retrospectively review the prevalence and features of this paradoxical effect. METHODS: This was a single center, retrospective study that included all patients who underwent laser hair removal during a 4-year period with a long-pulsed alexandrite laser. All cases of laser-induced hypertrichosis were assessed clinically by history, examination, and laboratory tests, and confirmed by review of serial clinical photographs taken during the course of the laser treatments. The clinical features of patients with postlaser hypertrichosis were compared with 50 patients randomly selected from among all those who had undergone laser hair removal at our center (n = 489). RESULTS: Of 489 patients, 3 (0.6%, 95% confidence interval: 0.01-1.9%) treated with the long-pulsed alexandrite laser (755 nm) reported increased hair after laser hair epilation. There was a trend for this adverse effect to occur in darker skin phototypes (IV) and with black hair as compared with the unaffected comparison group (n = 50). However, the small number of cases (n = 3) did not provide sufficient power to adequately test factors such as age, sex, treatment settings, and number of treatments statistically. CONCLUSION: Postlaser hair removal hypertrichosis is a real but rare occurrence in our experience

The cicatricial alopecias encompass a diverse group of disorders characterized by permanent destruction of the hair follicle and irreversible hair loss. Destruction of the hair follicle can result from primary, folliculocentric disease or as a secondary result. This article focuses on the former, or primary cicatricial alopecias. The cause and pathogenesis of many of these disorders are largely unknown. Although unique clinicopathologic features allow for accurate diagnosis in some cases, diagnostic certainty is often elusive and reflects the limits of present understanding. Classification of the primary cicatricial alopecias on the basis of pathology provides a diagnostic and investigational framework and, it is hoped, will facilitate future enlightenment. Details of classification, etiopathogenesis, clinicopathologic features, differential diagnosis, and practical management of the primary cicatricial alopecias will be discussed. LEARNING OBJECTIVES: Upon completion of this learning activity, participants should be familiar with the following aspects of the primary cicatricial alopecias: (1) the new, consensus-issued classification scheme, (2) current understanding about etiopathogenesis, (3) salient clinicopathologic features, (4) differential diagnosis, and (5) therapeutic management

The management of patients with hair loss requires a customized plan. Diagnosis, prognosis, psychosocial impact, treatment options, and patient preference are key determinants. This article discusses current agents for the treatment of three commonly encountered nonscarring alopecias: male- and female-pattern hair loss, telogen effluvium, and alopecia areata. Algorithmic approaches to management are provided

Alopecia areata (AA) is a hair loss disease marked by a focal inflammatory infiltrate of dystrophic anagen stage hair follicles by CD4+ and CD8+ lymphocytes. Although AA is thought to be an autoimmune disorder, definitive proof is lacking. Moreover, characterization of the primary pathogenic mechanisms by which hair loss is induced in AA is limited. In this context, animal models may provide a vital contribution to understanding AA. Recent research using animal models of AA has focused on providing evidence in support of a lymphocyte-mediated pathogenic mechanism consistent with AA as an autoimmune disease. In the future, research with both humans and animal models shall likely concentrate on identifying the primary antigenic epitopes involved in AA and the genetics of AA susceptibility. With a comprehensive understanding of the key elements in AA pathogenesis, new avenues for therapeutic research and intervention will be defined

BACKGROUND: There is currently no quantitative tool for evaluating vitiligo treatment response using parametric methods. OBJECTIVE: To develop and apply a simple clinical tool, the Vitiligo Area Scoring Index (VASI), to model the response of vitiligo to narrowband UV-B (NB-UV-B) phototherapy using parametric tests. DESIGN: Prospective, randomized, controlled, bilateral left-right comparison trial. SETTING: North American tertiary care, university-affiliated phototherapy center. PATIENTS: Patients older than 18 years with stable vitiligo involving at least 5% of their total body surface in a symmetric distribution. INTERVENTION: Treatment with NB-UV-B was given 3 times a week to half of the body on all patients for either 60 treatments or 6 months. The contralateral side served as a no-treatment control. MAIN OUTCOME MEASURE: Repigmentation was assessed using the VASI, which was based on a composite estimate of the overall area of vitiligo patches at baseline and the degree of macular repigmentation within these patches over time. The VASI was validated separately against physician and patient global assessments. The overall reductions in VASI for NB-UV-B and control groups were modeled by multilevel regression with random effects and compared parametrically. RESULTS: The VASI scoring correlated well with both patient and physician global assessments (P =.05 and P<.001, respectively, using ordinal logistic regression). The extent of repigmentation after 6 months on the treated side was 42.9% (95% confidence interval, 26.7%-59.0%) vs 3.3% (95% confidence interval -19.3% to 30.0%) on the untreated side (P<.001). A significant difference between control and NB-UV-B groups was apparent within the first 2 months of therapy. The legs, trunk, and arms were much more likely to repigment than the feet and hands. CONCLUSIONS: The VASI is a quantitative clinical tool that can be used to evaluate vitiligo parametrically. Patients treated with NB-UV-B can be expected to achieve approximately 42.9% repigmentation of their vitiligo after 6 months of treatment, with the greatest response being achieved over the trunk and nonacral portions of the extremities