Lichen Planopilaris Treated With a Peroxisome Proliferator–Activated Receptor γ Agonist

Departments of Dermatology, The Permanente Medical Group, Vallejo, California, USA.
Archives of dermatology (Impact Factor: 4.79). 12/2009; 145(12):1363-6. DOI: 10.1001/archdermatol.2009.283
Source: PubMed


Primary cicatricial alopecias (PCAs), rare disorders that lead to permanent hair loss, have been poorly understood and are difficult to treat. Lichen planopilaris (LPP)is a prototypical PCA; patients often present with sudden onset of hair loss and clinically significant symptoms of itching, burning, and pain of the scalp. Examination reveals patchy alopecia or a more diffuse thinning of the scalp with characteristic perifollicular erythema and perifollicular scale at the margins of the areas of alopecia.Treatment typically includes use of antiinflammatory medications; although symptoms may improve,hair loss is often progressive.

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    • "Furthermore, investigations of PCA therapies should consider skin sterol levels as a potential therapeutic target and as a disease biomarker. A promising therapeutic strategy for PCA could be the restoration of cholesterol homeostasis in hair follicle cells by clinically available agonists of PPARγ or antagonists of LXR which are nuclear receptors that modulate this pathway [10], [43], [44]. "
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    ABSTRACT: Primary cicatricial alopecia (PCA) is a group of inflammatory hair disorders that cause scarring and permanent hair loss. Previous studies have implicated PPARγ, a transcription factor that integrates lipogenic and inflammatory signals, in the pathogenesis of PCA. However, it is unknown what triggers the inflammatory response in these disorders, whether the inflammation is a primary or secondary event in disease pathogenesis, and whether the inflammatory reaction reflects an autoimmune process. In this paper, we show that the cholesterol biosynthetic pathway is impaired in the skin and hair follicles of PCA patients. Treatment of hair follicle cells with BM15766, a cholesterol biosynthesis inhibitor, or 7-dehydrocholesterol (7-DHC), a sterol precursor, stimulates the expression of pro-inflammatory chemokine genes. Painting of mouse skin with 7-DHC or BM15766 inhibits hair growth, causes follicular plugging and induces the infiltration of inflammatory cells into the interfollicular dermis. Our results demonstrate that cholesterologenic changes within hair follicle cells trigger an innate immune response that is associated with the induction of toll-like receptor (TLR) and interferon (IFN) gene expression, and the recruitment of macrophages that surround the hair follicles and initiate their destruction. These findings reveal a previously unsuspected role for cholesterol precursors in PCA pathogenesis and identify a novel link between sterols and inflammation that may prove transformative in the diagnosis and treatment of these disorders.
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    • "A promising new treatment focus for lichen planopilaris is the abnormal peroxisome proliferator-activated receptor pathways, which leads to aberrant lipid metabolism in the sebaceous gland, a toxic buildup of lipids, and an inflammatory response.56 Improvement of lichen planopilaris following treatment with the oral peroxisome proliferator-activated receptor-γ agonist, pioglitazone hydrochloride at 15 mg/day was recently reported.57 "
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    ABSTRACT: Hair loss is a very common complaint. Patients may describe increased shedding and diffuse or localized alopecia. The differential diagnosis of hair loss includes a number of disorders causing cicatricial or noncicatricial alopecias. This paper describes the clinical approaches and diagnostic tests that are useful in the evaluation of patients presenting with alopecia. It also reviews treatments for noncicatricial alopecias, including androgenetic alopecia, alopecia areata, and telogen effluvium, as well as cicatricial alopecias, including lichen planopilaris, its clinical variant frontal fibrosing alopecia, and discoid lupus erythematosus.
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