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The Medical Letter on Drugs and... Sep 2022
Topics: Alopecia Areata; Azetidines; Humans; Purines; Pyrazoles; Sulfonamides
PubMed: 36094552
DOI: No ID Found -
The Journal of Investigative... Nov 2020The C3H/HeJ model has long dominated basic alopecia areata (AA) in vivo research and has been used as proof-of-principle that Jak inhibitors are suitable agents for AA... (Comparative Study)
Comparative Study Review
The C3H/HeJ model has long dominated basic alopecia areata (AA) in vivo research and has been used as proof-of-principle that Jak inhibitors are suitable agents for AA management in vivo. However, its histologic features are not typical of human AA, and it is questionable whether it is sufficiently clinically predictive for evaluating the therapeutic effects of candidate AA agents. Instead, the humanized mouse model of AA has been used to functionally demonstrate the role of key immune cells in AA pathogenesis and to discover human-specific pharmacologic targets in AA management. Therefore, we advocate the use of both models in future preclinical AA research.
Topics: Alopecia Areata; Animals; Disease Models, Animal; Drug Evaluation, Preclinical; Humans; Mice; Mice, Inbred C3H
PubMed: 33099377
DOI: 10.1016/j.jisp.2020.05.001 -
The Journal of Allergy and Clinical... Feb 2018Treatments for alopecia areata (AA) have evolved over the decades from broad and nonspecific therapies to those that are now more targeted and rationally selected. This... (Review)
Review
Treatments for alopecia areata (AA) have evolved over the decades from broad and nonspecific therapies to those that are now more targeted and rationally selected. This was achieved by means of close cooperation and communication between clinicians and basic scientists, which resulted in the elucidation and understanding of the unique pathophysiology of AA. In this review we discuss this evolution and how novel therapies for AA have changed over the decades, what we have in our current arsenal of drugs for this potentially devastating disease, and what the future holds.
Topics: Alopecia Areata; Drug Development; Humans
PubMed: 29155099
DOI: 10.1016/j.jaci.2017.10.028 -
Der Hautarzt; Zeitschrift Fur... Nov 2013The epidemiology of alopecia areata as well as murine models of this disease and genome-wide association studies support the concept of alopecia areata as an autoimmune...
The epidemiology of alopecia areata as well as murine models of this disease and genome-wide association studies support the concept of alopecia areata as an autoimmune disease. In addition, the genome-wide association studies have led to the identification of new potential therapeutic targets such as CTLA4; these results have already led to the initiation of clinical studies, for example, with abatacept. Currently topical and intralesional corticosteroids as well as immunotherapy with diphenylcyclopropenone are most common therapeutic approaches.
Topics: Adrenal Cortex Hormones; Alopecia Areata; Dermatologic Agents; Humans; Immunologic Factors; Immunotherapy; Prevalence
PubMed: 24177663
DOI: 10.1007/s00105-013-2576-3 -
International Journal of Rheumatic... Oct 2023
Topics: Humans; Alopecia Areata
PubMed: 37807618
DOI: 10.1111/1756-185X.14815 -
Dermatology Nursing Apr 2007
Topics: Adult; Alopecia Areata; Biopsy; Diagnosis, Differential; Female; Humans; Immunosuppressive Agents; Minoxidil; Nurse's Role; Patient Education as Topic; Risk Factors; Vasodilator Agents
PubMed: 17526309
DOI: No ID Found -
Journal of the American Academy of... Jul 2004
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The Medical Letter on Drugs and... Nov 2023
Topics: Humans; Alopecia Areata; Protein Kinase Inhibitors; Janus Kinase Inhibitors; Immunologic Factors
PubMed: 37983117
DOI: 10.58347/tml.2023.1690a -
Advances in Therapy Jul 2017Alopecia areata (AA), a prevalent inflammatory cause of hair loss, lacks FDA-approved therapeutics for extensive cases, which are associated with very poor rates of... (Review)
Review
Alopecia areata (AA), a prevalent inflammatory cause of hair loss, lacks FDA-approved therapeutics for extensive cases, which are associated with very poor rates of spontaneous hair regrowth and major psychological distress. Current treatments for severe cases include broad immune-suppressants, which are associated with significant adverse effects, precluding long-term use, with rapid hair loss following treatment termination. As a result of the extent of the disease in severe cases, topical contact sensitizers and intralesional treatments are of limited use. The pathogenesis of AA is not yet fully understood, but recent investigations of the immune activation in AA skin reveal Th1/IFN-γ, as well as Th2, PDE4, IL-23, and IL-9 upregulations. Tissue analyses of both animal models and human lesions following broad-acting and cytokine-specific therapeutics (such as JAK inhibitors and ustekinumab, respectively) provide another opportunity for important insights into the pathogenesis of AA. As reviewed in this paper, numerous novel therapeutics are undergoing clinical trials for AA, emphasizing the potential transformation of the clinical practice of AA, which is currently lacking. Dermatologists are already familiar with the revolution in disease management of psoriasis, stemming from better understanding of immune dysregulations, and atopic dermatitis will soon follow a similar path. In light of these recent developments, the therapeutic arena of AA treatments is finally getting more exciting. AA will join the lengthening list of dermatologic diseases with mechanism-targeted drugs, thus changing the face of AA.
Topics: Alopecia Areata; Animals; Dermatologic Agents; Drug-Related Side Effects and Adverse Reactions; Humans; Immunosuppressive Agents
PubMed: 28646393
DOI: 10.1007/s12325-017-0542-7 -
Expert Reviews in Molecular Medicine Jun 2006Although 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... (Review)
Review
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.
Topics: Alopecia Areata; Animals; Antigen Presentation; Autoimmune Diseases; CD4-Positive T-Lymphocytes; CD8-Positive T-Lymphocytes; Disease Models, Animal; Female; Humans; Immunosuppressive Agents; Inflammation; Lymphocyte Activation; Male; Mice; Phenotype
PubMed: 16787552
DOI: 10.1017/S146239940601101X