Infliximab: Efficacy in psoriasis

Arsiwala, Shehnaz

doi:10.4103/0378-6323.115525

Cited by 8 publications

(6 citation statements)

References 49 publications

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“…Notably, one patient was also receiving concomitant compound glycyrrhizin, an agent that is thought to block production of IL-8. 43 , 68 Methotrexate has been combined with several other agents for the treatment of EP, including with infliximab 55 , 69 – 71 ; with etretinate reporting satisfactory results 72 ; and with cyclosporine or etanercept reporting excellent results. 64 , 73 …”

Section: Systemic Agentsmentioning

confidence: 99%

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Erythrodermic psoriasis: pathophysiology and current treatment perspectives

Singh¹,

Lee²,

Uçmak³

et al. 2016

PTT

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Erythrodermic psoriasis (EP) is a rare and severe variant of psoriasis vulgaris, with an estimated prevalence of 1%–2.25% among psoriatic patients. The condition presents with distinct histopathologic and clinical findings, which include a generalized inflammatory erythema involving at least 75% of the body surface area. The pathogenesis of EP is not well understood; however, several studies suggest that the disease is associated with a predominantly T helper 2 (Th2) phenotype. Given the morbidity and potential mortality associated with the condition, there is a need for a better understanding of its pathophysiology. The management of EP begins with a comprehensive assessment of the patient's presentation and often requires multidisciplinary supportive measures. In 2010, the medical board of the US National Psoriasis Foundation published consensus guidelines advocating the use of cyclosporine or infliximab as first-line therapy in unstable cases, with acitretin and methotrexate reserved for more stable cases. Since the time of that publication, additional information regarding the efficacy of newer agents has emerged. We review the latest data with regard to the treatment of EP, which includes biologic therapies such as ustekinumab and ixekizumab.

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Section: Systemic Agentsmentioning

confidence: 99%

“… 92 – 96 Infliximab has also successfully been combined with other systemic agents, such as methotrexate and acitretin, with excellent clinical results. 58 , 69 , 70 , 97…”

Section: Biologicsmentioning

confidence: 99%

Erythrodermic psoriasis: pathophysiology and current treatment perspectives

Singh¹,

Lee²,

Uçmak³

et al. 2016

PTT

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“…It is a ~149kDa protein that has IgG1 kappa chain that binds specifically to soluble TNFα and transmembrane TNFα to inhibit the pro-inflammatory functions of TNFα [48]. Remicade binds to TNFα with ~44pM affinity [49]. In addition, Remicade has an in vivo half-life of roughly 8.5 days [49].…”

Section: Remicade (Infliximab) Is a Mouse-human Chimeric Anti-tnfαmentioning

confidence: 99%

“…Remicade binds to TNFα with ~44pM affinity [49]. In addition, Remicade has an in vivo half-life of roughly 8.5 days [49]. Psoriatic patients take Remicade through IV; with 4 mg/kg patient at initial weeks and then 2 to 6 mg/kg every 8 weeks thereafter [49].…”

Section: Remicade (Infliximab) Is a Mouse-human Chimeric Anti-tnfαmentioning

confidence: 99%

“…In addition, Remicade has an in vivo half-life of roughly 8.5 days [49]. Psoriatic patients take Remicade through IV; with 4 mg/kg patient at initial weeks and then 2 to 6 mg/kg every 8 weeks thereafter [49]. Remicade is also an effective biological treatment for psoriatic patients due to its ability to specifically inhibit TNFα, which is a pro-inflammatory cytokine found up-regulated within psoriatic patients.…”

Section: Remicade (Infliximab) Is a Mouse-human Chimeric Anti-tnfαmentioning

confidence: 99%

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Advances in Treatment Options for Psoriasis

Raju¹

2015

Int J Dermatol Clin Res

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Psoriasis is a skin disease that is evidenced primarily by plaques which can be seen throughout the body. Genetic predisposition that combines with an environmental trigger of the immune system is believed to be the root cause of psoriasis. This leads to signaling factors which coordinate the progression of inflammation and psoriatic plaques. Psoriatic patients commonly use topical agents, phototherapy, and systemic agents; however, biological therapies have become increasingly popular. This is primarily due to recent advances in the study of psoriasis which have shown that monoclonal antibodies and dimeric fusion proteins inhibit key signaling molecules within the inflammatory cascade such as TNFa, IL-12 and IL-23. This article reviews the advances made to understand the role of TNFa in the progression of psoriasis, discusses treatment options such as topical agents, phototherapy and systemic agents, and then compares a variety of monoclonal antibodies and dimeric fusion proteins as biological therapies. penetrate the lymphatic system, activate T cells, and engender the secretion of cytokines which induce the inflammatory cascade and psoriatic skin plaques [11,12]. However, in the innate immune system there are more identifiable mediators. For instance, toll-like receptors (TLRs) which are type 1 membrane glycoproteins that recognize pathogen associated molecular patterns (PAMPs), are important in the inflammatory cascade [13]. Within this cascade the keratinocyte barrier can be disturbed, NK lymphocytes can be activated, and natural killer receptors can be expressed. Interferon gamma (IFNγ), released by NK lymphocytes, and TNFα, released by keratinocytes, work together to create inflammation, which is a physical characteristic of plaque psoriasis [14,15]. Another prevalent characteristic of plaque psoriasis is epidermal hyperplasia. Within this condition, keratinocytes proliferate and within the focal regions Type 1 effectors accumulate and induce cytokines such as IFNγ, and TNFα [16,17]. Specifically, IL-12 and IL-23 are related to T cell differentiation and activation of T helper 1 cells phenotypes. Signaling molecules and role of TNFαAdditional cytokines play critical roles in adhesion, sub-type specific influx, trafficking and compartmentalization of leukocytes [18]. These include TARC and MDC, which preferentially recruit skin-homing memory T cells via the stimulation of integrin-ICAM-1 adhesive interactions [19]. T cells and Langerhans skin cells also express chemokine receptor GPR-1 (CCR10) for the ligand CTACK (CCL27), which significantly contributes to epidermal localization. Keratinocytes can also induce MIP-3α, which is another proinflammatory cytokine [20]. In addition, the epidermis accumulates neutrophils (Munro's microabscesses), which are extremely prevalent in psoriasis [21]. Within the psoriatic scales, there is high content of IL-8 and GRO-α, which are neutrophil-attracting chemokines [21]. IL-8 down regulates IL-10 receptor such that there is a loss of immune-regulation within psoriatic les...

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