Mitral Valve Replacement in a Patient with Idiopathic Hypereosinophilic Syndrome and Pulmonary Arterial Hypertension

Kiriş, İlker; Okutan, Hüseyin; Peker, Tülay Tunçer; Aslan, Şükrü; Şahin, Mehmet; Bircan, Sema

doi:10.1111/j.1540-8191.2008.00639.x

Cited by 12 publications

(10 citation statements)

References 10 publications

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“…Advanced cardiac disease is less common today in patients with eosinophilic disease. Cardiac surgery can extend the life of patients with late‐stage heart disease manifested by endomyocardial fibrosis, mural thrombosis, and valvular insufficiency, Mitral and/or tricuspid valve repair or replacement and endomyocardectomy for late‐stage fibrotic heart disease can improve cardiac function. Bioprosthetic devices are generally preferred over their mechanical counterparts because of the reduced frequency of valve thrombosis.…”

Section: Risk‐adapted Therapymentioning

confidence: 99%

World Health Organization‐defined eosinophilic disorders: 2019 update on diagnosis, risk stratification, and management

2019

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Disease overview: The eosinophilias encompass a broad range of non-hematologic (secondary or reactive) and hematologic (primary or clonal) disorders with potential for end-organ damage.Diagnosis: Hypereosinophilia has generally been defined as a peripheral blood eosinophil count greater than 1.5 × 10 9 /L, and may be associated with tissue damage. After exclusion of secondary causes of eosinophilia, diagnostic evaluation of primary eosinophilias relies on a combination of various tests. They include morphologic review of the blood and marrow, standard cytogenetics, fluorescence in situ-hybridization, flow immunophenotyping, and T-cell clonality assessment to detect histopathologic or clonal evidence for an acute or chronic hematolymphoid neoplasm. Risk stratification: Disease prognosis relies on identifying the subtype of eosinophilia. After evaluation of secondary causes of eosinophilia, the 2016 World Health Organization endorses a semi-molecular classification scheme of disease subtypes. This includes the major category "myeloid/lymphoid neoplasms with eosinophilia and rearrangement of PDGFRA, PDGFRB, or FGFR1 or with PCM1-JAK2", and the MPN subtype, "chronic eosinophilic leukemia, not otherwise specified" (CEL, NOS). Lymphocyte-variant hypereosinophilia is an aberrant T-cell clone-driven reactive eosinophila, and idiopathic hypereosinophilic syndrome (HES) is a diagnosis of exclusion.Risk-adapted therapy: The goal of therapy is to mitigate eosinophil-mediated organ damage. For patients with milder forms of eosinophilia (eg, <1.5 × 10 9 /L) without symptoms or signs of organ involvement, a watch and wait approach with close-follow-up may be undertaken. Identification of rearranged PDGFRA or PDGFRB is critical because of the exquisite responsiveness of these diseases to imatinib. Corticosteroids are first-line therapy for patients with lymphocyte-variant hypereosinophilia and HES. Hydroxyurea and interferon-α have demonstrated efficacy as initial treatment and in steroid-refractory cases of HES. In addition to hydroxyurea, second line cytotoxic chemotherapy agents, and hematopoietic stem cell transplantation have been used for aggressive forms of HES and CEL, with outcomes reported for limited numbers of patients. The use of antibodies against interleukin-5 (IL-5) (mepolizumab), the IL-5 receptor (benralizumab), as well as other targets on eosinophils remains an active area of investigation.

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Section: Risk‐adapted Therapymentioning

confidence: 99%

World Health Organization‐defined eosinophilic disorders: 2019 update on diagnosis, risk stratification, and management

2019

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Section: Supportive Care and Surgerymentioning

confidence: 99%

World Health Organization‐defined eosinophilic disorders: 2017 update on diagnosis, risk stratification, and management

2017

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Disease overview: The eosinophilias encompass a broad range of nonhematologic (secondary or reactive) and hematologic (primary, clonal) disorders with potential for end-organ damage.Diagnosis: Hypereosinophilia has generally been defined as a peripheral blood eosinophil count greater than 1500/mm 3 and may be associated with tissue damage. After exclusion of secondary causes of eosinophilia, diagnostic evaluation of primary eosinophilias relies on a combination of morphologic review of the blood and marrow, standard cytogenetics, fluorescent in situ-hybridization, flow immunocytometry, and T-cell clonality assessment to detect histopathologic or clonal evidence for an acute or chronic myeloid or lymphoproliferative disorder.Risk stratification: Disease prognosis relies on identifying the subtype of eosinophilia. After evaluation of secondary causes of eosinophilia, the 2016 World Health Organization endorses a semimolecular classification scheme of disease subtypes which includes the major category "myeloid/ lymphoid neoplasms with eosinophilia and rearrangement of PDGFRA, PDGFRB, or FGFR1 or with PCM1-JAK2," and the "MPN subtype, chronic eosinophilic leukemia, not otherwise specified" (CEL, NOS). Lymphocyte-variant hypereosinophilia is an aberrant T-cell clone-driven reactive eosinophila, and idiopathic hypereosinophilic syndrome (HES) is a diagnosis of exclusion. Risk-adapted therapy:The goal of therapy is to mitigate eosinophil-mediated organ damage. For patients with milder forms of eosinophilia (e.g., < 1500/mm 3 ) without symptoms or signs of organ involvement, a watch and wait approach with close-follow-up may be undertaken. Identification of rearranged PDGFRA or PDGFRB is critical because of the exquisite responsiveness of these dis-

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“…Advanced cardiac disease is less common today in patients with eosinophilic disease. Cardiac surgery can extend the life of patients with late‐stage heart disease manifested by endomyocardial fibrosis, mural thrombosis, and valvular insufficiency , Mitral and/or tricuspid valve repair or replacement and endomyocardectomy for late‐stage fibrotic heart disease can improve cardiac function. Bioprosthetic devices are generally preferred over their mechanical counterparts because of the reduced frequency of valve thrombosis.…”

Section: Supportive Care and Surgerymentioning

confidence: 99%

World Health Organization‐defined eosinophilic disorders: 2015 update on diagnosis, risk stratification, and management

Gotlib¹

2015

American J Hematol

104

109

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Disease overview: The eosinophilias encompass a broad range of non‐hematologic (secondary or reactive) and hematologic (primary, clonal) disorders with potential for end‐organ damage. Diagnosis: Hypereosinophilia has generally been defined as a peripheral blood eosinophil count greater than 1,500/mm3 and may be associated with tissue damage. After exclusion of secondary causes of eosinophilia, diagnostic evaluation of primary eosinophilias relies on a combination of morphologic review of the blood and marrow, standard cytogenetics, fluorescent in situ‐hybridization, flow immunocytometry, and T‐cell clonality assessment to detect histopathologic or clonal evidence for an acute or chronic myeloid or lymphoproliferative disorder. Risk stratification: Disease prognosis relies on identifying the subtype of eosinophilia. After evaluation of secondary causes of eosinophilia, the 2008 World Health Organization establishes a semi‐molecular classification scheme of disease subtypes including ‘myeloid and lymphoid neoplasms with eosinophilia and abnormalities of PDGFRA, PDGFRB, or FGFR1’, chronic eosinophilic leukemia, not otherwise specified, (CEL, NOS), lymphocyte‐variant hypereosinophilia, and idiopathic hypereosinophilic syndrome (HES), which is a diagnosis of exclusion. Risk‐adapted therapy: The goal of the therapy is to mitigate eosinophil‐mediated organ damage. For patients with milder forms of eosinophilia (e.g. < 1,500/mm3) without symptoms or signs of organ involvement, a watch and wait approach with close‐follow‐up may be undertaken. Identification of rearranged PDGFRA or PDGFRB is critical because of the exquisite responsiveness of these diseases to imatinib. Corticosteroids are first‐line therapy for patients with lymphocyte‐variant hypereosinophilia and HES. Hydroxyurea and interferon‐alpha have demonstrated efficacy as initial treatment and steroid‐refractory cases of HES. In addition to hydroxyurea, second line cytotoxic chemotherapy agents and hematopoietic cell transplant have been used for aggressive forms of HES and CEL with outcomes reported for limited numbers of patients. Although clinical trials have been performed with anti IL‐5 (mepolizumab) and anti‐CD52 (alemtuzumab) antibodies, their therapeutic role in primary eosinophilic diseases and HES has yet to be established. Am. J. Hematol. 90:1077–1089, 2015. © 2015 Wiley Periodicals, Inc.

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Mitral Valve Replacement in a Patient with Idiopathic Hypereosinophilic Syndrome and Pulmonary Arterial Hypertension

Cited by 12 publications

References 10 publications

World Health Organization‐defined eosinophilic disorders: 2019 update on diagnosis, risk stratification, and management

World Health Organization‐defined eosinophilic disorders: 2019 update on diagnosis, risk stratification, and management

World Health Organization‐defined eosinophilic disorders: 2017 update on diagnosis, risk stratification, and management

World Health Organization‐defined eosinophilic disorders: 2015 update on diagnosis, risk stratification, and management

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