Jerry Shapiro

Alopecia areata update: Part I. Clinical picture, histopathology, and pathogenesis

UNLABELLED Alopecia areata (AA) is an autoimmune disease that presents as nonscarring hair loss, although the exact pathogenesis of the disease remains to be clarified. Disease prevalence rates from 0.1% to 0.2% have been estimated for the United States. AA can affect any hair-bearing area. It often presents as well demarcated patches of nonscarring alopecia on skin of overtly normal appearance. Recently, newer clinical variants have been described. The presence of AA is associated with a higher frequency of other autoimmune diseases. Controversially, there may also be increased psychiatric morbidity in patients with AA. Although some AA features are known poor prognostic signs, the course of the disease is unpredictable and the response to treatment can be variable. Part one of this two-part series on AA describes the clinical presentation and the associated histopathologic picture. It also proposes a hypothesis for AA development based on the most recent knowledge of disease pathogenesis. LEARNING OBJECTIVES After completing this learning activity, participants should be familiar with the most recent advances in AA pathogenesis, recognize the rare and recently described variants of AA, and be able to distinguish between different histopathologic stages of AA.

Alopecia areata investigational assessment guidelines

From Duke University Medical Center, Durhama; University of Minnesota, Minneapolisb; Pontefract General Infirmaryc; University of California at San Franciscod; Northwest Cutaneous Research Specialists, Portlande; The University of British Columbia, Vancouverf; and Johnson & Johnson, Skin Biology Research Center, Skillman.g Reprint requests: Elise A. Olsen, MD, Professor of Medicine, Duke University Medical Center, Box 3294, Durham, NC 27710. J Am Acad Dermatol 1999;40:242-6. *Developed from the Alopecia Areata Consensus meeting sponsored by the National Alopecia Areata Foundation at the First Tricontinental Meeting of the Hair Research Societies, Brussels, Belgium, Oct 8, 1995. Participants are listed at the end of the guidelines. Copyright

Alopecia areata: pathogenesis and potential for therapy.

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.

Alopecia areata update: Part II. Treatment

UNLABELLED Various therapeutic agents have been described for the treatment of alopecia areata (AA), but none are curative or preventive. The aim of AA treatment is to suppress the activity of the disease. The high rate of spontaneous remission and the paucity of randomized, double-blind, placebo-controlled studies make the evidence-based assessment of these therapies difficult. The second part of this two-part series on AA discusses treatment options in detail and suggests treatment plans according to specific disease presentation. It also reviews recently reported experimental treatment options and potential directions for future disease management. LEARNING OBJECTIVES After completing this learning activity, participants should be able to compare the efficacy and safety of various treatment options, formulate a treatment plan tailored to individual patients, and recognize recently described treatments and potential therapeutic approaches.

Hair care products: waving, straightening, conditioning, and coloring

Hair is a very important and distinctive feature that plays a major role in self perception. To some extent, it expresses our personality and who we are. Hair is one of the few physical features that we can easily change. Its length, color, and shape can be modified to create a totally different style. All those different styles can be used to seduce, conform, or even make a statement. Although hair has no vital function, its immeasurable importance is usually brutally discovered by those affected by alopecia. Although hair cosmetics are widely available, the medical literature is rather scarce, and specialized literature is not readily accessible to most of us. The aim of this article is to give a practical and simple overview of the different hair cosmetic treatments available. Knowing how they affect the hair will enable the physician to better assess different problems secondary to cosmetic treatments and will also provide some answers to commonly asked questions.

HAIR REGROWTH: Therapeutic Agents

Today there are new classes of hair growth promotors with proven efficacy. This article reviews the current state of the art agents for treatment of two of the most common forms of hair loss encountered in clinical practice, androgenetic alopecia and alopecia areata. Current therapeutic strategies are based on recent advances in the understanding of disordered hair growth. Practical treatment protocols are presented.

CXCR3/Ligands Are Significantly Involved in the Tumorigenesis of Basal Cell Carcinomas

Basal cell carcinoma (BCC) is the most common skin malignancy encountered worldwide. We hypothesized that CXC chemokines, small cytokines involved in inducing directed leukocyte chemotaxis, could play a key role in the modulation of BCC growth. In this study, quantitative RT-PCR revealed that the chemokines CXCL9, 10, 11, and their receptor CXCR3 were significantly upregulated by an average 22.6-fold, 9.2-fold, 26.6-fold, and 4.9-fold, respectively in BCC tissue samples as compared with nonlesional skin epithelium. Immunohistochemistry analysis revealed that CXCR3, CXCL10, and CXCL11, but not CXCL9, colocalized with cytokeratin 17 (K17) in BCC keratinocytes. In addition, CXCR3 and its ligands were expressed in cells of the surrounding BCC stroma. The chemokines and K17 were also expressed in cultured human immortalized HaCaT keratinocytes. Exposure of HaCaT cells or primary BCC-derived cells to CXCL11 peptides in vitro significantly increased cell proliferation. In primary BCC-derived cell cultures, addition of CXCL11 progressively selected for K17+/CXCR3+ co-expressing cells over time. The expression of CXCR3 and its ligands in human BCC keratinocytes, the enhancement of keratinocyte cell proliferation by CXCL11, and the homogeneity of K17+ BCC cells in human BCC-isolated cell population supported by CXCR3/CXCL11 signaling all suggest that CXCR3 and its ligands may be important autocrine and/or paracrine signaling mediators in the tumorigenesis of BCC.

Topical photodynamic therapy with 5‐aminolaevulinic acid does not induce hair regrowth in patients with extensive alopecia areata

Background Photodynamic therapy (PDT) is a new modality involving the administration of a photosensitizer, or photosensitizer precursor, followed by its activation with light to generate a therapeutic effect. 5‐Aminolaevulinic acid (ALA) is a photosensitizer precursor that is transformed by cells into protoporphyrin IX (PpIX), which can in turn be activated by red light.

Calcipotriol plus Betamethasone Dipropionate Scalp Formulation Is Effective and Well Tolerated in the Treatment of Scalp Psoriasis: A Phase II Study

Background: There is a need for more effective therapy for scalp psoriasis. Objective: To assess the efficacy and safety of a 2-compound scalp formulation including calcipotriol and betamethasone dipropionate in the treatment of scalp psoriasis. Methods: Patients (n = 218) with scalp psoriasis were randomized to treatment with the 2-compound scalp formulation (n = 108) or betamethasone dipropionate in the same vehicle (n = 110). The treatments were applied once daily on the scalp for up to 8 weeks. Results: The 2-compound scalp formulation showed a significantly higher efficacy than betamethasone dipropionate on the total sign score at the end of treatment (p = 0.042) and after 2 weeks (p = 0.005). Conclusion: The calcipotriol plus betamethasone dipropionate scalp formulation was superior to betamethasone dipropionate in the same vehicle when used once daily for up to 8 weeks in the treatment of scalp psoriasis.

Systemic cyclosporine and low-dose prednisone in the treatment of chronic severe alopecia areata: A clinical and immunopathologic evaluation

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