Martin A. Menter M.D.

Menter, A., B. E. Strober, D. H. Kaplan, D. Kivelevitch, E. F. Prater, B. Stoff, A. W. Armstrong, C. Connor, K. M. Cordoro, D. M. R. Davis, B. E. Elewski, J. M. Gelfand, K. B. Gordon, A. B. Gottlieb, A. Kavanaugh, M. Kiselica, N. J. Korman, D. Kroshinsky, M. Lebwohl, C. L. Leonardi, J. Lichten, H. W. Lim, N. N. Mehta, A. S. Paller, S. L. Parra, A. L. Pathy, R. N. Rupani, M. Siegel, E. B. Wong, J. J. Wu, V. Hariharan and C. A. Elmets (2019). “Joint AAD-NPF guidelines of care for the management and treatment of psoriasis with biologics.” J Am Acad Dermatol Feb 13. [Epub ahead of print].

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Psoriasis is a chronic, inflammatory multisystem disease that affects up to 3.2% of the US population. This guideline addresses important clinical questions that arise in psoriasis management and care, providing recommendations based on the available evidence. The treatment of psoriasis with biologic agents will be reviewed, emphasizing treatment recommendations and the role of the dermatologist in monitoring and educating patients regarding benefits as well as associated risks.

Elmets, C. A., C. L. Leonardi, D. M. R. Davis, J. M. Gelfand, J. Lichten, N. N. Mehta, A. W. Armstrong, C. Connor, K. M. Cordoro, B. E. Elewski, K. B. Gordon, A. B. Gottlieb, D. H. Kaplan, A. Kavanaugh, D. Kivelevitch, M. Kiselica, N. J. Korman, D. Kroshinsky, M. Lebwohl, H. W. Lim, A. S. Paller, S. L. Parra, A. L. Pathy, E. F. Prater, R. Rupani, M. Siegel, B. Stoff, B. E. Strober, E. B. Wong, J. J. Wu, V. Hariharan and A. Menter (2019). “Joint AAD-NPF guidelines of care for the management and treatment of psoriasis with awareness and attention to comorbidities.” J Am Acad Dermatol Feb 7. [Epub ahead of print].

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Psoriasis is a chronic, inflammatory, multisystem disease that affects up to 3.2% of the US population. This guideline addresses important clinical questions that arise in psoriasis management and care, providing recommendations on the basis of available evidence.

Guttman-Yassky, E., R. Bissonnette, B. Ungar, M. Suarez-Farinas, M. Ardeleanu, H. Esaki, M. Suprun, Y. Estrada, H. Xu, X. Peng, J. I. Silverberg, A. Menter, J. G. Krueger, R. Zhang, U. Chaudhry, B. Swanson, N. M. H. Graham, G. Pirozzi, G. D. Yancopoulos and D. H. JD (2019). “Dupilumab progressively improves systemic and cutaneous abnormalities in patients with atopic dermatitis.” J Allergy Clin Immunol 143(1): 155-172.

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BACKGROUND: Dupilumab is an IL-4 receptor alpha mAb inhibiting signaling of IL-4 and IL-13, key drivers of type 2-driven inflammation, as demonstrated by its efficacy in patients with atopic/allergic diseases. OBJECTIVE: This placebo-controlled, double-blind trial (NCT01979016) evaluated the efficacy, safety, and effects of dupilumab on molecular/cellular lesional and nonlesional skin phenotypes and systemic type 2 biomarkers of patients with moderate-to-severe atopic dermatitis (AD). METHODS: Skin biopsy specimens and blood were evaluated from 54 patients randomized 1:1 to weekly subcutaneous doses of 200 mg of dupilumab or placebo for 16 weeks. RESULTS: Dupilumab (vs placebo) significantly improved clinical signs and symptoms of AD, was well tolerated, and progressively shifted the lesional transcriptome toward a nonlesional phenotype (weeks 4-16). Mean improvements in a meta-analysis-derived AD transcriptome (genes differentially expressed between lesional and nonlesional skin) were 68.8% and 110.8% with dupilumab and -10.5% and 55.0% with placebo (weeks 4 and 16, respectively; P < .001). Dupilumab significantly reduced expression of genes involved in type 2 inflammation (IL13, IL31, CCL17, CCL18, and CCL26), epidermal hyperplasia (keratin 16 [K16] and MKi67), T cells, dendritic cells (ICOS, CD11c, and CTLA4), and TH17/TH22 activity (IL17A, IL-22, and S100As) and concurrently increased expression of epidermal differentiation, barrier, and lipid metabolism genes (filaggrin [FLG], loricrin [LOR], claudins, and ELOVL3). Dupilumab reduced lesional epidermal thickness versus placebo (week 4, P = .001; week 16, P = .0002). Improvements in clinical and histologic measures correlated significantly with modulation of gene expression. Dupilumab also significantly suppressed type 2 serum biomarkers, including CCL17, CCL18, periostin, and total and allergen-specific IgEs. CONCLUSION: Dupilumab-mediated inhibition of IL-4/IL-13 signaling through IL-4 receptor alpha blockade significantly and progressively improved disease activity, suppressed cellular/molecular cutaneous markers of inflammation and systemic measures of type 2 inflammation, and reversed AD-associated epidermal abnormalities.

Strober, B., J. Crowley, R. G. Langley, K. Gordon, A. Menter, C. Leonardi, D. Arikan and W. C. Valdecantos (2018). “Systematic review of the real-world evidence of adalimumab safety in psoriasis registries.” J Eur Acad Dermatol Venereol 32(12): 2126-2133.

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Long-term safety of adalimumab in psoriasis clinical studies has been established. The objective of this research was to review real-world evidence of adalimumab safety from registries of adult patients with psoriasis treated in clinical practice. Databases (BIOSIS Previews, Current Contents Search, Derwent Drug File, EMBASE, EMBASE Alert, EMCare, MEDLINE, SciSearch) were searched for psoriasis registries with adalimumab safety data. Eligible papers were English language manuscripts (conference abstracts excluded) from psoriasis registries presenting safety data for adult patients with psoriasis receiving adalimumab. The incidence and rate (events/100 patient-years [PY]) of adverse events (AEs), serious AEs (SAEs) and AEs of special interest are reported. Abstracts of 425 publications were screened, and 401 publications excluded (208 conference abstracts; 193 papers). Remaining manuscripts were fully screened; 14 were excluded (no adalimumab data, n = 10; no safety data, n = 2; no on-treatment data, n = 1; not English, n = 1), and 10 selected. Overall rates of AEs (4273 [22.2/100PY]) and SAEs (827 [4.3/100PY]) were reported in the ESPRIT registry (N = 6059). Rates of infections (7.7-14.7/100PY) and serious infections (<0.6-2.0/100PY) were reported in four studies. Cardiovascular-related events were reported in three studies:

Silfvast-Kaiser, A., S. Y. Paek and A. Menter (2018). “Anti-IL17 therapies for psoriasis.” Expert Opin Biol Ther Nov 30. [Epub ahead of print].

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INTRODUCTION: Interleukin-17 (IL-17) is a proinflammatory cytokine considered to play a significant role in the immunopathogenesis of plaque psoriasis. As a result, focus in clinical trials has undergone a shift towards disease specific targets, with the goals of more effective treatment and reduction in the incidence of serious adverse events. Areas Covered: Two monoclonal antibodies targeting IL-17A (secukinumab, ixekizumab) and one against the IL-17 receptor (brodalumab) are approved for the treatment of moderate-to-severe plaque psoriasis. Herein, the clinical efficacy, safety and tolerability of each is reviewed by summarizing the existing literature (found via PubMed database). Expert Commentary: The development and approval of the IL-17 inhibitor agents secukinumab, ixekizumab, and brodalumab has expanded psoriatic treatment with effective options, validating the importance of the pro-inflammatory role of IL-17 psoriatic pathophysiology. Biologic treatment options for psoriasis will continue to grow, especially IL-17 and IL-23 related agents, with an increasing specificity of agents to be available in the future.