“…After 6 months of therapy, there was no hair growth, and the hair loss had progressed to alopecia totalis. 7 This patient's disease was already progressing rapidly when tacrolimus ointment was added, and no current treatment modality alters the course of AA. Five patients with long-standing, treatment-resistant alopecia universalis applied tacrolimus ointment 0.1% once daily for 6 months to a 6 cm 3 6 cm area on the scalp and no hair growth was stimulated.…”
“…After 6 months of therapy, there was no hair growth, and the hair loss had progressed to alopecia totalis. 7 This patient's disease was already progressing rapidly when tacrolimus ointment was added, and no current treatment modality alters the course of AA. Five patients with long-standing, treatment-resistant alopecia universalis applied tacrolimus ointment 0.1% once daily for 6 months to a 6 cm 3 6 cm area on the scalp and no hair growth was stimulated.…”
“…Several case reports have shown treatment failure of tacrolimus in severe AA/AU patients. [61][62][63] It may be that inadequate expression of FKBPs in a subset of AU patients contributes to therapeutic resistance to tacrolimus, revealing a potentially useful marker for therapeutic efficacy. Nevertheless, the limited number of patients within this study limits its direct translation to the bedside.…”
Alopecia areata (AA) is an autoimmune hair loss disorder in which systemic disturbances have been described, but are poorly understood. To evaluate disease mechanisms, we examined gene expression in the blood of defined clinical subgroups (patchy AA persistent type, AAP, n ¼ 5; alopecia universalis, AU, n ¼ 4) and healthy controls (unaffected relatives, UaR, n ¼ 5; unaffected non-relatives, UaNR, n ¼ 4) using microarrays. Unsupervised hierarchical clustering separates all four patient and control groups, producing three distinct expression patterns reflective of 'inheritance', 'disease' and 'severity' signatures. Functional classification of differentially expressed genes (DEGs) comparing disease (AAP, AU) vs normal (UaR) groups reveals upregulation in immune response, cytokine signaling, signal transduction, cell cycle, proteolysis and cell adhesionrelated genes. Pathway analysis further reveals the activation of several genes related to natural killer-cell cytotoxicity, apoptosis, mitogen activated protein kinase, Wnt signaling and B-and T-cell receptor signaling in AA patients. Finally, 35 genes differentially expressed in AA blood overlap with DEGs previously identified in AA skin lesions. Our results implicate innate and adaptive immune processes while also revealing novel pathways, such as Wnt signaling and apoptosis, relevant to AA pathogenesis. Our data suggest that peripheral blood expression profiles of AA patients likely carry new biomarkers associated with disease susceptibility and expression.
Many therapeutic modalities have been used to treat alopecia areata, with variable efficacy and safety profiles. Unfortunately, none of these agents is curative or preventive. Also, many of these therapeutic agents have not been subjected to randomized, controlled trials, and, except for topical immunotherapy, there are few published studies on long-term outcomes. The treatment plan is designed according to the patient’s age and extent of disease. In this paper, the therapeutic agents are organized according to their efficacy and safety profiles into first-line, second-line, and third-line options.
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