Idiopathic hypereosinophilic syndrome associated with elevated plasma levels of interleukin‐10 and soluble interleukin‐2 receptor

Kanbe,; Kurosawa,; Igarashi,; Tamura,; Yamashita,; Kurimoto,; Miyachi,

doi:10.1046/j.1365-2133.1998.02525.x

Cited by 10 publications

(7 citation statements)

References 9 publications

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“…In one patient, anaplastic T‐cell lymphoma subsequently developed. Other patients with HES have been reported in whom soluble IL‐2 receptor levels were high (Kanbe et al , 1998). The successful treatment of patients with hypereosinophilic syndrome with cyclosporine (Akiyama et al , 1997; Nadarajah et al , 1997) and of others where remission was induced by the use of chlorodeoxyadenosine (2CDA), which is known to suppress helper T cells (Ueno et al , 1997), is further supportive evidence of the role of helper T cells in HES.…”

Section: Aetiology Of Hes: Is It a T‐cell Disorder?mentioning

confidence: 99%

The eosinophilias, including the idiopathic hypereosinophilic syndrome

2003

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Section: Aetiology Of Hes: Is It a T‐cell Disorder?mentioning

confidence: 99%

The eosinophilias, including the idiopathic hypereosinophilic syndrome

2003

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“…25 Serum IL-8 and IL-10 levels were also significantly elevated in HES patients compared to healthy controls. This has been reported previously [28][29][30] and is of unknown clinical significance, However, since neither the IL-8 nor the IL-10 receptor has been described on eosinophils, it is unlikely that the elevated serum levels of these two cytokines would have a direct effect on eosinophil survival or response to GC.…”

Section: Dysregulated Expression Of a Variety Of Th2 And Inflammatorymentioning

confidence: 55%

Mechanisms of glucocorticoid resistance in hypereosinophilic syndromes

Stokes

Yoon

Makiya

et al. 2019

Clin Experimental Allergy

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Background Glucocorticoids (GC) are considered first‐line therapy for most patients with hypereosinophilic syndrome (HES). Although response rates are generally high, many patients require moderate to high doses for control of eosinophilia and symptoms, and up to 15% of patients do not respond at all. Despite this, little is known about the mechanisms of GC resistance in patients with HES. Objective To explore the aetiology of GC resistance in HES. Methods Clinical data and samples from 26 patients with HES enrolled on a prospective study of GC responsiveness and 23 patients with HES enrolled on a natural history study of eosinophilia for whom response to GC was known were analysed retrospectively. Expression of GC receptor isoforms was assessed by quantitative RT‐PCR in purified eosinophils. Serum cytokine levels were quantified by suspension array assay in multiplex. Results Despite an impaired eosinophil response to GC after 7 days of treatment, the expected rise in absolute neutrophil count was seen in 7/7 GC‐resistant patients, suggesting that GC resistance in HES is not a global phenomenon. Eosinophil mRNA expression of glucocorticoid receptor (GR) isoforms (α, β, and P) was similar between GC‐sensitive (n = 20) and GC‐resistant (n = 9) patients with HES. Whereas geometric mean serum levels were also comparable between GC‐r (n = 11) and GC‐s (n = 19) for all cytokines tested, serum IL‐5 levels were >100 pg/mL only in GC‐r patients. Conclusions and Clinical Relevance These data suggest that the mechanism of GC resistance in HES is not due to a global phenomenon affecting all lineages, but may be due, at least in some patients, to impairment of eosinophil apoptosis by increased levels of IL‐5.

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“…Collectively, TNFα, IL-5, and eotaxin-3 appeared to play an important role in generating peripheral hypereosinophilia, while IL-10 was most closely correlated with prolonged APTT and anticoagulant. Indeed, eosinophilic diseases have been associated with TNFα [32,33], IL-5 [34], IL-10 [35], and eotaxin-3 [36,37], while IL-10 was overexpressed in IgG4RD [38,39]. The causal relationship between these cytokines, eosinophilia, IgG4, and clinical manifestations remains to be elucidated.…”

Section: Discussionmentioning

confidence: 99%

A patient with hypereosinophilic syndrome that manifested with acquired hemophilia and elevated IgG4: a case report

2012

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IntroductionHypereosinophilic syndrome is defined as a prolonged state (more than six months) of eosinophilia (greater than 1500 cells/μL), without an apparent etiology and with end-organ damage. Hypereosinophilic syndrome can cause coagulation abnormalities. Among hypereosinophilic syndrome types, the lymphocytic variant (lymphocytic hypereosinophilic syndrome) is derived from a monoclonal proliferation of T lymphocytes. Here, we describe the case of a patient with lymphocytic hypereosinophilic syndrome who presented with a coagulation abnormality. To the best of our knowledge, this is the first such report including a detailed clinical picture and temporal cytokine profile.Case presentationA 77-year-old Japanese man presented to our facility with massive hematuria and hypereosinophilia (greater than 2600 cells/μl). His eosinophilia first appeared five years earlier when he developed femoral artery occlusion. He manifested with multiple hematomas and prolonged activated partial thromboplastin time. His IgG4 level was remarkably elevated (greater than 2000 mg/dL). Polymerase chain reaction tests of peripheral blood and bone marrow identified lymphocytic hypereosinophilic syndrome. His prolonged activated partial thromboplastin time was found to be due to acquired hemophilia. Glucocorticoids suppressed both the hypereosinophilia and coagulation abnormality. However, tapering of glucocorticoids led to a relapse of the coagulation abnormality alone, without eosinophilia. Tumor necrosis factor α, interleukin-5, and/or eotaxin-3 may have caused the hypereosinophilia, and interleukin-10 was correlated with the coagulation abnormality.ConclusionsTo the best of our knowledge, this is the first case in which lymphocytic hypereosinophilic syndrome and IgG4-related disease have overlapped. In addition, our patient is only the second case of hypereosinophilic disease that manifested with acquired hemophilia. Our patient relapsed with the coagulation abnormality alone, without eosinophilia. This report shows that the link between eosinophilia, IgG4, and clinical manifestations is not simple and provides useful insight into the immunopathology of hypereosinophilic syndrome and IgG4-related disease.

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Idiopathic hypereosinophilic syndrome associated with elevated plasma levels of interleukin‐10 and soluble interleukin‐2 receptor

Abstract: Idiopathic hypereosinophilic syndrome associated with elevated plasma levels of interleukin-10 and soluble interleukin-2 receptor CORRESPONDENCE 917

Cited by 10 publications

References 9 publications

The eosinophilias, including the idiopathic hypereosinophilic syndrome

The eosinophilias, including the idiopathic hypereosinophilic syndrome

Mechanisms of glucocorticoid resistance in hypereosinophilic syndromes

A patient with hypereosinophilic syndrome that manifested with acquired hemophilia and elevated IgG4: a case report

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