Síndrome de Schnitzler: presentación de un caso y revisión de la respuesta al tratamiento con anakinra

Gutiérrez, Laura Benítez; Pita, Susana Mellor; Ureta, Pablo Tutor de; Bango, M. Yebra

doi:10.1016/j.medcli.2012.09.003

Cited by 3 publications

(1 citation statement)

References 5 publications

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“…IL-1 blocking therapies are the most effective ones. Both the IL-Ra anakinra [ 3 , 11 , 12 , 14 , 16 , 18 , 27 , 29 , 33 , 35 , 39 – 41 , 45 , 47 , 50 , 55 , 58 , 59 , 63 , 68 – 71 , 76 , 77 , 83 , 92 – 94 , 104 , 106 , 113 , 115 , 119 – 121 , 127 , 129 , 131 – 133 , 135 , 136 , 140 , 153 ] (Van Hoof, Relas, Björk, Fox, Croot: p.c., and personal observations), which blocks IL-1α and IL-1β, and the anti-IL-1β antibody canakinumab [ 12 , 41 , 136 , 154 ] (Fox: p.c. ), which only inhibits IL-1β, induce a complete remission in more than 90% of cases.…”

Section: Reviewmentioning

confidence: 99%

Schnitzler's syndrome: lessons from 281 cases

Koning

2014

Clinical & Translational All

101

169

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Schnitzler’s syndrome is an autoinflammatory disorder characterized by the association of a monoclonal IgM (or IgG) gammopathy, a chronic urticarial rash, and signs and symptoms of systemic inflammation, including fever, arthralgias and bone pain. It was first described in 1972. This review summarizes the clinical features, efficacy of therapies, and follow-up data of the 281 cases that have been reported to date. Also, the results of skin histology, bone imaging, laboratory investigations, and studies of the pathogenesis will be discussed, including the pivotal role of interleukin-1 beta in this disorder.Electronic supplementary materialThe online version of this article (doi:10.1186/2045-7022-4-41) contains supplementary material, which is available to authorized users.

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Section: Reviewmentioning

confidence: 99%

Schnitzler's syndrome: lessons from 281 cases

Koning

2014

Clinical & Translational All

101

169

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Management of Schnitzler’s syndrome

Lipsker

Lenormand

2014

Expert Opinion on Orphan Drugs

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An Expanding Role for Interleukin-1 Blockade from Gout to Cancer

Dinarello

2014

Mol Med

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There is an expanding role for interleukin (IL)-1 in diseases from gout to cancer. More than any other cytokine family, the IL-1 family is closely linked to innate inflammatory and immune responses. This linkage is because the cytoplasmic segment of all members of the IL-1 family of receptors contains a domain, which is highly homologous to the cytoplasmic domains of all toll-like receptors (TLRs). This domain, termed "toll IL-1 receptor (TIR) domain," signals as does the IL-1 receptors; therefore, inflammation due to the TLR and the IL-1 families is nearly the same. Fundamental responses such as the induction of cyclo-oxygenase type 2, increased surface expression of cellular adhesion molecules and increased gene expression of a broad number of inflammatory molecules characterizes IL-1 signal transduction as it does for TLR agonists. IL-1β is the most studied member of the IL-1 family because of its role in mediating autoinflammatory disease. However, a role for IL-1α in disease is being validated because of the availability of a neutralizing monoclonal antibody to human IL-1α. There are presently three approved therapies for blocking IL-1 activity. Anakinra is a recombinant form of the naturally occurring IL-1 receptor antagonist, which binds to the IL-1 receptor and prevents the binding of IL-1β as well as IL-1α. Rilonacept is a soluble decoy receptor that neutralizes primarily IL-1β but also IL-1α. Canakinumab is a human monoclonal antibody that neutralizes only IL-1β. Thus, a causal or significant contributing role can be established for IL-1β and IL-1α in human disease.

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Síndrome de Schnitzler: presentación de un caso y revisión de la respuesta al tratamiento con anakinra

Cited by 3 publications

References 5 publications

Schnitzler's syndrome: lessons from 281 cases

Schnitzler's syndrome: lessons from 281 cases

Management of Schnitzler’s syndrome

An Expanding Role for Interleukin-1 Blockade from Gout to Cancer

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