Idiopathic Eosinophilic Synovitis: Case Report and Review of the Literature

A, Atanes Sandoval; Fernández, Valpuesta; Núñez, Rosa; Galed, I; Blanco, F.J.; Garcı́a-Porrúa, Carlos; Freire, Mayka; Graña, Jose Maria; Galdo, F.

doi:10.3109/03009749609080013

Cited by 22 publications

(7 citation statements)

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“…Lyme's disease (1) tuberculosis, parasitism (2, 3) rheumatoid arthritis (4,5)familiarallergya nd dermographism( 4, 6, 7), hypereosinophilic syndrome, eosinophilic fasciitis (8)G ougerot-Sjogren syndrome, and neoplasias amongstothers) (4). HumanES hasb een also relatedt on on immune processes (e.g.r adiation therapy,p ostarthrography(dyeorair) (9), sclerosing infiltration of varix, andhemarthrosis)(4) andit hasb een also considereda sa ni diopathic problem (10). Acase of idiopathiclocalized ES wasreported in acat (11).…”

Section: Introductionmentioning

confidence: 99%

Eosinophilic synovitis of the tarsocrural joint in a horse

Climent

Carmona²,

Cuenca³

et al. 2007

Vet Comp Orthop Traumatol

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SummaryEosinophilic synovitis (ES) is a rare disease described in human and veterinary medicine. Only three cases have been reported in the horse. A case of tarsocrural synovitis in an Hispano-Arabian gelding is presented in this report. The patient presented with severe joint effusion and lameness of the right tarsocrural joint on admission. Synovial fluid analysis revealed an increased WBC of 12800 leukocytes/microliter with 76% of eosinophils. Lavage of the diseased joint and medical treatment with antibiotics and non-steroidal anti-inflammatory drugs produced remission of the clinical problem.

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Section: Introductionmentioning

confidence: 99%

Eosinophilic synovitis of the tarsocrural joint in a horse

Climent

Carmona²,

Cuenca³

et al. 2007

Vet Comp Orthop Traumatol

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“…The best-characterized examples in the FrenchAmerican-British classification of AML are M4Eo inv (16) Musculoskeletal N/A Arthritis, 79,80 effusions, 80 bursitis, 81 synovitis, 82 Raynaud phenomena, 83 digital necrosis, 84 polymyositis/myopathy 85,86 Renal N/A Acute renal failure with Charcot-Leyden crystalluria, 87 nephrotic syndrome, 88 immunotactoid glomerulopathy, 89 crescentic glomerulonephritis 90 Modified from Weller and Bubley 21 and from Brito-Babapulle 17 with permission from Elsevier. N/A indicates not available.…”

Section: Cytogenetic and Molecular Features Of Hematologic Malignancimentioning

confidence: 99%

The FIP1L1-PDGFRα fusion tyrosine kinase in hypereosinophilic syndrome and chronic eosinophilic leukemia: implications for diagnosis, classification, and management

Gotlib

Cools

Malone

et al. 2004

Blood

262

205

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Idiopathic hypereosinophilic syndrome (HES) and chronic eosinophilic leukemia (CEL) comprise a spectrum of indolent to aggressive diseases characterized by unexplained, persistent hypereosinophilia. These disorders have eluded a unique molecular explanation, and therapy has primarily been oriented toward palliation of symptoms related to organ involvement. Recent reports indicate that HES and CEL are imatinib-responsive malignancies, with rapid and complete hematologic remissions observed at lower doses than used in chronic myelogenous leukemia (CML). These BCR-ABL-negative cases lack activating mutations or abnormal fusions involving other known target genes of imatinib, implicating a novel tyrosine kinase in their pathogenesis. A bedside-to-benchtop translational research effort led to the identification of a constitutively activated fusion tyrosine kinase on chromosome 4q12, derived from an interstitial deletion, that fuses the platelet-derived growth factor receptor-␣ gene (PDGFRA) to an uncharacterized human gene FIP1-like-1 (FIP1L1). However, not all HES and CEL patients respond to imatinib, suggesting disease heterogeneity. Furthermore, approximately 40% of responding patients lack the FIP1L1-PDGFRA fusion, suggesting genetic heterogeneity. This review examines the current state of knowledge of HES and CEL and the implications of the FIP1L1-PDGFRA discovery on their diagnosis, classification, and management. IntroductionProtean biologic and clinical presentations characterize idiopathic hypereosinophilia (HES). HES is similar to other diseases given the moniker "diagnosis of exclusion," in that limited understanding of the pathogenesis of the disease has hampered therapeutic advances. The demonstration of increased myeloblasts or clonality or the development of either granulocytic sarcoma or acute myeloid leukemia helps clarify the origin of some cases of chronic eosinophilic leukemia. 1 In a subset of patients, hypereosinophilia is related to excessive secretion of eosinophilopoietic cytokines from a clonal population of lymphocytes. 2 The identification of FIP1-like-1-platelet-derived growth factor receptor-␣ (FIP1L1-PDGFRA) in cases of HES/CEL adds to a growing list of activated fusion tyrosine kinases linked to the pathogenesis of chronic myeloproliferative disorders. 3 It is unique, however, because it is the first description of a gain-of-function fusion protein resulting from a cryptic interstitial deletion between genes rather than a reciprocal chromosomal translocation. The FIP1L1-PDGFR␣ fusion protein transforms hematopoietic cells, and its kinase activity is inhibited by imatinib at a cellular 50% inhibitory concentration (IC 50 ) 100-fold lower than BCR-ABL. 3 Acquisition of an imatinib resistance mutation in the adenosine triphosphate (ATP)-binding domain of PDGFRA in a relapsed patient previously responsive to imatinib supports a critical role for FIP1L1-PDGFR␣ in the pathogenesis of disease and demonstrates that FIP1L1-PDGFR␣ is the therapeutic target of imatinib. 3 The identification of t...

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“…Immediate, subacute, and delayed hypersensitivity reactions may generate eosinophil chemotactic and chemokinetic factors. IgE‐mediated hypersensitivity responses cause aggregation of eosinophils at the site, where they contribute to the localization and regulation of the event 13–15 . Eosinophils have a selective response to histamine and other chemotactic mediators, such as sensitized lymphocytes, peptides of low to intermediate molecular weight, and arachidonic acid derivatives 16 .…”

Section: Discussionmentioning

confidence: 99%

Idiopathic Localized Eosinophilic Synovitis in a Cat

Silverstein

Almy

Zinkl

et al. 2000

Veterinary Clinical Pathol

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A 4-year-old male castrated Seal Point Himalayan cat was presented for evaluation of right thoracic limb lameness of 6 weeks duration. Synovial fluid analysis of the swollen right carpal joint revealed a mixed cell synovitis, with a total nucleated cell count of 13,200/microliter and 34% eosinophils. A diagnosis of idiopathic localized eosinophilic arthritis was made. Additional clinical and diagnostic findings included mild lymphadenopathy with lymphoid hyperplasia and an antinuclear antibody titer of 1:320. Lack of multisystem involvement made systemic lupus erythematosis unlikely. Immunosuppressive therapy with oral prednisone alleviated the lameness. Eosinophilic synovitis has not previously been reported in cats. An immune-mediated mechanism was likely in this case; however, the exact etiology remains unknown.

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Idiopathic Eosinophilic Synovitis: Case Report and Review of the Literature

Cited by 22 publications

References 10 publications

Eosinophilic synovitis of the tarsocrural joint in a horse

Eosinophilic synovitis of the tarsocrural joint in a horse

The FIP1L1-PDGFRα fusion tyrosine kinase in hypereosinophilic syndrome and chronic eosinophilic leukemia: implications for diagnosis, classification, and management

Idiopathic Localized Eosinophilic Synovitis in a Cat

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