Galectin-7 as a potential biomarker of Stevens-Johnson syndrome/toxic epidermal necrolysis: identification by targeted proteomics using causative drug-exposed peripheral blood cells

Hama, Natsumi; Nishimura, Keiko; Hasegawa, Akito; Yuki, Akihiko; Kume, Hideaki; Adachi, Jun; Kinoshita, Manao; Ogawa, Youichi; Nakajima, Saeko; Nomura, Takashi; Watanabe, Hideaki; Mizukawa, Yoshiko; Tomonaga, Takeshi; Shimizu, Hiroshi; Abe, Riichiro

doi:10.1016/j.jaip.2019.05.002

Cited by 16 publications

(14 citation statements)

References 17 publications

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“…There are a number of other potential biomarkers under investigation that may demonstrate specificity for SJS/TEN. In one study [ 61 ], peripheral blood mononuclear cells (PBMCs) from patients who had recovered from SJS/TEN were cultured and re-exposed to the causative drug. The supernatant of the culture fluid was analyzed using proteomics to identify potential biomarkers.…”

Section: Clinical Updatesmentioning

confidence: 99%

“…This protocol was also used to evaluate the molecules secreted by PBMCs in non-severe cutaneous adverse drug reactions (cADRs). When comparing the two groups, Hama et al [ 61 ] discovered one protein, galectin-7, exhibited higher levels in sera of SJS/TEN patients than in sera of non-severe cADRs ( p = 0.005). Serum galectin-7 also correlated with disease severity with significantly higher levels during the acute phase and decreased levels in the late phase of the disease (>7 days).…”

Section: Clinical Updatesmentioning

confidence: 99%

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Stevens–Johnson Syndrome and Toxic Epidermal Necrolysis: A Review of Diagnosis and Management

et al. 2021

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Stevens–Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN) are rare diseases that are characterized by widespread epidermal necrosis and sloughing of skin. They are associated with significant morbidity and mortality, and early diagnosis and treatment is critical in achieving favorable outcomes for patients. In this scoping review, Excerpta Medica dataBASE and PubMed were searched for publications that addressed recent advances in the diagnosis and management of the disease. Multiple proteins (galectin 7 and RIP3) were identified that are promising potential biomarkers for SJS/TEN, although both are still in early phases of research. Regarding treatment, cyclosporine is the most effective therapy for the treatment of SJS, and a combination of intravenous immunoglobulin (IVIg) and corticosteroids is most effective for SJS/TEN overlap and TEN. Due to the rare nature of the disease, there is a lack of prospective, randomized controlled trials and conducting these in the future would provide valuable insights into the management of this disease.

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Section: Clinical Updatesmentioning

confidence: 99%

Section: Clinical Updatesmentioning

confidence: 99%

Stevens–Johnson Syndrome and Toxic Epidermal Necrolysis: A Review of Diagnosis and Management

et al. 2021

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“…Further, serum soluble Fas-ligand (sFasL) levels (Posadas et al, 2002;Abe et al, 2003;Murata et al, 2008), granulysin (Chung et al, 2008;Porebski et al, 2013;Cho et al, 2014;Chung et al, 2015;Weinborn et al, 2016), IL-15 (Su et al, 2017), CD137 (Trubiano et al, 2017b) and the proapoptotic factor galectin-7 (Hama et al, 2019) have been described in the pathological processes of SJS/TEN with sFasL and galectin-7 being considered as biomarkers able to predict TEN progression but not SJS (Shiohara et al, 2015;Hama et al, 2019) and granulysin serum levels correlating with disease severity and mortality (Chung et al, 2008;Chung et al, 2015). In DRESS/DiHS, several markers were reported as indicators of disease progression and activity such as the serum thymus and activation-regulated chemokine (TARC) (Ogawa et al, 2013;Komatsu-Fujii et al, 2017;Komatsu-Fujii et al, 2018) and granulysin (Saito et al, 2012).…”

Section: Biomarkers In Adverse Drug Reactionsmentioning

confidence: 99%

An Updated Review of the Diagnostic Methods in Delayed Drug Hypersensitivity

Copaescu

Gibson

et al. 2021

Front. Pharmacol.

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Delayed drug hypersensitivity reactions are clinically diverse reactions that vary from isolated benign skin conditions that remit quickly with no or symptomatic treatment, drug discontinuation or even continued drug treatment, to the other extreme of severe cutaneous adverse reactions (SCARs) that are associated with presumed life-long memory T-cell responses, significant acute and long-term morbidity and mortality. Diagnostic “in clinic” approaches to delayed hypersensitivity reactions have included patch testing (PT), delayed intradermal testing (IDT) and drug challenges for milder reactions. Patch and IDT are, in general, performed no sooner than 4–6 weeks after resolution of the acute reaction at the maximum non-irritating concentrations. Functional in vitro and ex vivo assays have largely remained the province of research laboratories and include lymphocyte transformation test (LTT) and cytokine release enzyme linked ImmunoSpot (ELISpot) assay, an emerging diagnostic tool which uses cytokine release, typically IFN-γ, after the patient’s peripheral blood mononuclear cells are stimulated with the suspected drug(s). Genetic markers such as human leukocyte antigen have shown recent promise for both pre-prescription screening as well as pre-emptive and diagnostic testing strategies.

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“…Besides these, Hama et al used the mass spectrometry to analyze the supernatant in PBMCs from SJS/TEN patients after reexposure to causative drugs and found galectin-7 was strongly upregulated (Hama et al, 2019). Galectin-7 is a protein specifically expressed in keratinocytes and is moderately repressed by retinoic acid (Magnaldo et al, 1995).…”

Section: Other Cytokines or Moleculesmentioning

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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Galectin-7 as a potential biomarker of Stevens-Johnson syndrome/toxic epidermal necrolysis: identification by targeted proteomics using causative drug-exposed peripheral blood cells

Cited by 16 publications

References 17 publications

Stevens–Johnson Syndrome and Toxic Epidermal Necrolysis: A Review of Diagnosis and Management

Stevens–Johnson Syndrome and Toxic Epidermal Necrolysis: A Review of Diagnosis and Management

An Updated Review of the Diagnostic Methods in Delayed Drug Hypersensitivity

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

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