Combination therapy: Etanercept and intravenous immunoglobulin for the acute treatment of Stevens-Johnson syndrome/toxic epidermal necrolysis

Gillenwater, T Justin; Nagengast, Eric S.; McCullough, Meghan; Peng, David H.; Garner, W.L.

doi:10.1016/j.burns.2018.12.018

Cited by 27 publications

(19 citation statements)

References 30 publications

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“…injection of il-1α could block the function of il-1β and significantly reduce the expression of NF-κB in the medial prefrontal cortex, thus significantly improving depressive behaviors in rats (68). Previous studies have shown that etanercept can be used in the treatment of serum-positive ra and Stevens-Johnson syndrome/toxic epidermolysis triggered by carbamazepine, and play a key role in cardiovascular safety in patients with ra (69)(70)(71). However, there are few cases of clinical treatment of Pe with etanercept.…”

Section: Discussionmentioning

confidence: 99%

Effects and mechanism of the etanercept on pancreatic encephalopathy

Jing

Zhu

et al. 2020

Mol Med Report

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Pancreatic encephalopathy (Pe) is a common fatal complication of acute pancreatitis (aP). Proinflammatory cytokines such as tumor necrosis factor (TnF)-α and interleukin (il)-6 are generated during aP, and act synergistically to promote Pe and multisystem failure. caerulein-induced aP provides a convenient model to explore the role of proinflammatory cytokines in PE. The aim of the present study was to examine the effect of the TnF-α inhibitor etanercept in Pe models and elucidate the regulatory mechanisms. To model Pe in vitro, rat hippocampal H19-7/iGF-ir neuronal cells were treated with 10 nmol/ml caerulein alone or in combination with etanercept (1, 10 or 100 µmol/ml). To model Pe in vivo, rats were injected with 50 µg/kg caerulein alone or combined with 10 mg/kg etanercept. at 6 h after administration, it was noted that etanercept downregulated expression of TnF-α, il-1β and il-6 by negatively regulating nF-κB (a master regulator of cytokine expression) signaling, and prevented the accumulation of reactive oxygen species. conversely, etanercept promoted the expression of the neurotrophic and anti-inflammatory hypoxia-inducible factor 1 α . in rat hippocampus, etanercept also reduced the levels of expression and inhibited the inflammatory response to reduce edema and neural necrosis. Together, these data suggested that etanercept could attenuate caerulein-induced Pe, at least in part via suppression of nF-κB signaling and alleviation of oxidative stress.

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Section: Discussionmentioning

confidence: 99%

Effects and mechanism of the etanercept on pancreatic encephalopathy

Jing

Zhu

et al. 2020

Mol Med Report

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“…Excitingly, TNF-α antagonists are translated into clinical therapeutics for SJS/TEN in recent years. Tons of evidence supports TNF antagonists halt SJS/TEN (Paradisi et al, 2014;Gavigan et al, 2018;Shear et al, 2018;Trujillo-Trujillo et al, 2018;Chafranska et al, 2019;Coulombe et al, 2019;Pham et al, 2019;Zhang et al, 2020). A randomized controlled trial compared etanercept (a TNF inhibitor) with systemic corticosteroid treatment in adult SJS/TEN patients and showed a decreased SCORTEN-predicted mortality rate, reduced skin healing time, and less gastrointestinal hemorrhage in the etanercept group.…”

Section: Tnf-α-related Apoptosismentioning

confidence: 99%

Current Pharmacogenetic Perspective on Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis

Cheng

2021

Front. Pharmacol.

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Adverse drug reactions are a public health issue that draws widespread attention, especially for Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) which have high mortality and lack of efficacious treatment. Though T-cell-mediated HLA-interacted immune response has been extensively studied, our understanding of the mechanism is far from satisfactory. This review summarizes infection (virus, bacterial, and mycoplasma infection), an environmental risk factor, as a trigger for SJS/TEN. The mutations or polymorphisms of drug metabolic enzymes, transporters, receptors, the immune system genes, and T-cell-mediated apoptosis signaling pathways that contribute to SJS/TEN are discussed and summarized. Epigenetics, metabolites, and mobilization of regulatory T cells and tolerogenic myeloid precursors are emerged directions to study SJS/TEN. Ex vivo lymphocyte transformation test has been exploited to aid in identifying the causative drugs. Critical questions on the pathogenesis of SJS/TEN underlying gene polymorphisms and T cell cytotoxicity remain: why some of the patients carrying the risky genes tolerate the drug and do not develop SJS/TEN? What makes the skin and mucous membrane so special to be targeted? Do they relate to skin/mucous expression of transporters? What is the common machinery underlying different HLA-B alleles associated with SJS/TEN and common metabolites?

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“…Although there was no difference in mortality (15.4 vs. 10%), and lower ICU stay (6.9 vs. 15.1 days) and lower total LOS (9.8 vs. 16.4 days) were without statistical significance, compared with their previous cohort review of IVIG alone, the SCORTEN, affected total body surface area and disease presentation were worse than those in the IVIG alone group. This indicates that there is also little improvement in the treatment effect of a combination of IVIG and other immunomodulators ( 34 ).…”

Section: Ivig Therapy For Sjs/tenmentioning

confidence: 99%

Recent Dermatological Treatments for Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis in Japan

2021

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Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are serious conditions characterized by necrosis of the skin and mucus membranes, and are mainly caused by medication and infections. Although the exact pathomechanism of SJS/TEN remains unclear, keratinocyte death is thought to be triggered by immune reactions to these antigens. While there is no established therapy for SJS/TEN, corticosteroids and intravenous immunoglobulin (IVIG) have been utilized as immunomodulator. We previously conducted a study to evaluate the efficacy of IVIG therapy in Japanese patients with SJS/TEN. IVIG was administered at a dosage of 400 mg/kg/day for 5 consecutive days as an additional therapy with systemic steroids. Prompt amelioration was observed in seven of the eight patients. All patients survived without sequelae. Recently, we retrospectively analyzed 132 cases of SJS/TEN treated in our two hospitals. The mortality rates in the patients treated with methylprednisolone pulse were 0% (0/31) for SJS and 7.0% (3/43) for TEN, and 0% (0/10) in the TEN patients treated with methylprednisolone pulse in combination with IVIG. These results suggest that early treatment with high-dose steroids, including methylprednisolone pulse therapy, and IVIG together with corticosteroids are possible therapeutic options to improve the prognosis of SJS/TEN.

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Combination therapy: Etanercept and intravenous immunoglobulin for the acute treatment of Stevens-Johnson syndrome/toxic epidermal necrolysis

Cited by 27 publications

References 30 publications

Effects and mechanism of the etanercept on pancreatic encephalopathy

Effects and mechanism of the etanercept on pancreatic encephalopathy

Current Pharmacogenetic Perspective on Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis

Recent Dermatological Treatments for Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis in Japan

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