The Hypereosinophilic Syndrome: Clinical Features, Laboratory Findings and Treatment

Spry, C. J. F.

doi:10.1111/j.1398-9995.1982.tb02339.x

Cited by 115 publications

(79 citation statements)

References 90 publications

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“…Idiopathic CEP is a clinicopathologic entity characterized by systemic and pulmonary manifestations, such as fever, weight loss, cough, dyspnoea, blood eosinophilia, peripheral opacities on chest X-ray, and a prompt response to corticosteroid therapy [1][2][3] . Idiopathic HES is also a clinical disease entity of unknown aetiology characterized by severe eosinophilia and a range of clinical problems, including cardiovascular, thromboembolic, respiratory, skin and/or nervous system complications [11,12]. External causes of eosinophilia, such as drug reaction and infections, were ruled out in this patient, and vasculitis was not found histologically.…”

Section: Discussionmentioning

confidence: 99%

Chronic eosinophilic pneumonia progressing to lung fibrosis

Yoshida¹,

Shijubo²,

Koba³

et al. 1994

Eur Respir J

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C Ch hr ro on ni ic c e eo os si in no op ph hi il li ic c p pn ne eu um mo on ni ia a p pr ro og gr re es ss si in ng g t to o l lu un ng g f fi ib br ro os si is s ABSTRACT: A 65 year old Japanese man was hospitalized with fever. Opacities distributed mainly in the subpleural regions were found on chest computed tomographic scan (CT), and these promptly cleared with corticosteroid therapy.Four years later, he presented with severe eosinophilia. Both chest X-ray and high resolution CT scan showed ground-glass opacities and honeycombing, suggesting lung fibrosis. A lung biopsy demonstrated intra-alveolar eosinophil infiltration, interstitial thickening with eosinophil infiltration, and a widely-distributed desquamative interstitial pneumonia-like reaction. With corticosteroid therapy, the ground-glass opacities decreased with a corresponding clinical improvement, although lung honeycombing and blood eosinophilia remained.In this case, circulating intercellular adhesion molecule-1 and circulating and bronchoalveolar lavage fluid eosinophil granule proteins were felt to be more effective markers for evaluating disease activity than the blood eosinophil number.

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Section: Discussionmentioning

confidence: 99%

Chronic eosinophilic pneumonia progressing to lung fibrosis

Yoshida¹,

Shijubo²,

Koba³

et al. 1994

Eur Respir J

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“…Stillman 1912), it was not until 1974 that the idiopathic hypereosinophilic syndrome was separated as a distinct entity (see Spry 1982). Before then, patients with this syndrome had been thought to have eosinophilic leukaemia or eosinophilic leukaemoid reactions.…”

Section: Eosinophil Secretionmentioning

confidence: 99%

“…We still know relatively little about the properties of each individual protein, and there may be some surprises in the future, once each of these constituents has been tested in a highly pure form in a wide range of assay systems. These should include studies on brain cells, vascular endothelium, platelets and fibroblasts, as neurological disease (Moore et al 1985), thromboembolic disease , and fibrosis are all features of the hypereosinophilic syndrome (Spry 1982), for which there is, as yet, no explanation.…”

mentioning

confidence: 99%

New Properties and Roles for Eosinophils in Disease: Discussion Paper

Spry¹

1985

J R Soc Med

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“…From five reports that included CSF examination, only two out of eight IHS patients had increased CSF eosinophil counts (53,142,155,194,279). In some cases, the distinction between IHS and leukemia is problematic, and infiltration of the meninges with eosinophils suggests a diagnosis of malignancy (269). Besides the classical criteria initially proposed in 1975, absence of clonality and rearrangements in genes like PDGFRA (the gene for platelet-derived growth factor receptor, alpha polypeptide), should be included in the diagnostic workup (56).…”

Section: Neoplastic Diseasesmentioning

confidence: 99%

Update on Eosinophilic Meningoencephalitis and Its Clinical Relevance

2009

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SUMMARY Eosinophilic meningoencephalitis is caused by a variety of helminthic infections. These worm-specific infections are named after the causative worm genera, the most common being angiostrongyliasis, gnathostomiasis, toxocariasis, cysticercosis, schistosomiasis, baylisascariasis, and paragonimiasis. Worm parasites enter an organism through ingestion of contaminated water or an intermediate host and can eventually affect the central nervous system (CNS). These infections are potentially serious events leading to sequelae or death, and diagnosis depends on currently limited molecular methods. Identification of parasites in fluids and tissues is rarely possible, while images and clinical examinations do not lead to a definitive diagnosis. Treatment usually requires the concomitant administration of corticoids and anthelminthic drugs, yet new compounds and their extensive and detailed clinical evaluation are much needed. Eosinophilia in fluids may be detected in other infectious and noninfectious conditions, such as neoplastic disease, drug use, and prosthesis reactions. Thus, distinctive identification of eosinophils in fluids is a necessary component in the etiologic diagnosis of CNS infections.

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The Hypereosinophilic Syndrome: Clinical Features, Laboratory Findings and Treatment

Cited by 115 publications

References 90 publications

Chronic eosinophilic pneumonia progressing to lung fibrosis

Chronic eosinophilic pneumonia progressing to lung fibrosis

New Properties and Roles for Eosinophils in Disease: Discussion Paper

Update on Eosinophilic Meningoencephalitis and Its Clinical Relevance

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