Type I pityriasis rubra pilaris treated with tumor necrosis factor inhibitors, ustekinumab, or secukinumab: A review

2018 ◽  
Vol 79 (3) ◽  
pp. 585-587
Author(s):  
Nolan J. Maloney ◽  
Lisa D. Hisaw ◽  
Scott Worswick
2010 ◽  
Vol 14 (4) ◽  
pp. 185-188 ◽  
Author(s):  
Yao-Hua Zhang ◽  
Youwen Zhou ◽  
Nigel Ball ◽  
Ming-Wan Su ◽  
Jin-Hua Xu ◽  
...  

Background: Pityriasis rubra pilaris (PRP) has unknown etiology and is often refractory to conventional therapies. Objective: To document a PRP patient's response to adalimumab therapy and to highlight the potential role of tumor necrosis factor (TNF) in the development of PRP skin lesions. Methods: A patient received adalimumab therapy at standard dosing intervals. In addition, the messenger ribonucleic acid (mRNA) of TNF in the lesional and perilesional normal skin was quantified in two patients with PRP. Results: The patient responded to adalimumab therapy and achieved clinical remission by 4 months. There was a significant elevation of TNF mRNA in the lesional skin of PRP. Conclusion: TNF upregulation is detected in PRP lesional skin, consistent with the observed clinical efficacy of TNF blockade for the treatment of PRP.


2012 ◽  
Vol 18 (11) ◽  
pp. 1502-1511 ◽  
Author(s):  
Mike J.L. Peters ◽  
Alper M. van Sijl ◽  
Alexandre E. Voskuyl ◽  
Naveed Sattar ◽  
Yvo M. Smulders ◽  
...  

2000 ◽  
Vol 20 (3) ◽  
pp. 912-918 ◽  
Author(s):  
Patricia Greenwel ◽  
Shizuko Tanaka ◽  
Dmitri Penkov ◽  
Wen Zhang ◽  
Michelle Olive ◽  
...  

ABSTRACT Extracellular matrix (ECM) formation and remodeling are critical processes for proper morphogenesis, organogenesis, and tissue repair. The proinflammatory cytokine tumor necrosis factor alpha (TNF-α) inhibits ECM accumulation by stimulating the expression of matrix proteolytic enzymes and by downregulating the deposition of structural macromolecules such as type I collagen. Stimulation of ECM degradation has been linked to prolonged activation of jun gene expression by the cytokine. Here we demonstrate that TNF-α inhibits transcription of the gene coding for the α2 chain of type I collagen [α2(I) collagen] in cultured fibroblasts by stimulating the synthesis and binding of repressive CCAAT/enhancer proteins (C/EBPs) to a previously identified TNF-α-responsive element. This conclusion was based on the concomitant identification of C/EBPβ and C/EBPδ as TNF-α-induced factors by biochemical purification and expression library screening. It was further supported by the ability of the C/EBP-specific dominant-negative (DN) protein to block TNF-α inhibition of α2(I) collagen but not TNF-α stimulation of the MMP-13 protease. The DN protein also blocked TNF-α downregulation of the gene coding for the α1 chain of type I collagen. The study therefore implicates repressive C/EBPs in the TNF-α-induced signaling pathway that controls ECM formation and remodeling.


2014 ◽  
Vol 41 (10) ◽  
pp. 2078-2084 ◽  
Author(s):  
Melissa L. Mannion ◽  
Fenglong Xie ◽  
Jeffrey R. Curtis ◽  
Timothy Beukelman

Objective.Using administrative data from a large commercial US health insurer, we investigated temporal trends in medication use among children diagnosed with juvenile idiopathic arthritis (JIA).Methods.Children with ≥ 1 physician diagnosis code for JIA in the calendar years 2005 through 2012 were included. Use of tumor necrosis factor inhibitors (TNFi), methotrexate (MTX), nonsteroidal antiinflammatory drugs (NSAID), and oral glucocorticoids (GC) was determined. Temporal changes in medication usage were evaluated with the Cochran-Armitage test for trend. We used paired t-tests to evaluate the use of NSAID and GC in the 6 months before and after new TNFi use.Results.We identified 4261 unique individuals with JIA. The proportion of patients receiving TNFi increased from 8.7% in 2005 to 22.4% in 2012 (p < 0.0001). MTX use increased from 18.4% to 23.2% (p = 0.02). NSAID use decreased from 49% to 40% (p = 0.02). GC use was relatively unchanged. Following new TNFi use, the mean number of NSAID prescriptions (among prevalent users) decreased from 2.8 to 2.0 (p < 0.0001), and the mean daily GC dose (among prevalent users) decreased from 7.3 mg/day to 3.9 mg/day (p < 0.0001). Many new TNFi users (57%) had not used MTX in the previous 6 months, and only 37% had any concurrent MTX use in the 6 months following new TNFi use.Conclusion.TNFi use in the treatment of JIA increased 2- to 3-fold over the last 8 years. New TNFi use was associated with decreased NSAID and GC use. TNFi may be replacing, rather than complementing, MTX in the treatment of many patients.


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