高嗜酸血癥課件

1、Eosinophils and Disease PathogenesisGeneralhighly specialized granulocytic effector cells;produce and store diverse biologically active molecules;Transmigrationinvasionsecretionrecruitmentmarked and persistent HEalterations in the microenvironment chronic (and potentially irreversible) organ damageB

2、ox 1. Major causes of hypereosinophilia Non-neoplastic reactive conditions (secondary/reactive HE) Helminth infections Scabies, other infestations Allergic bronchopulmonary aspergillosis Drug reactions (allergic or toxic) Other allergic reactions Atopic diseases Chronic graft-versus-host disease Chr

3、onic inflammatory disorders (e.g., IBD) Autoimmune diseasesHES Neoplastic conditions with secondary/reactive HE Hodgkis disease B- or T-cell lymphoma/leukemia Langerhans cell histiocytosis Solid tumors/malignancy Myeloid neoplasms and stem cell neoplasms (primary HE) Chronic eosinophilic leukemia NO

4、S Hematopoietic neoplasms with eosinophilia and abnormalities in PDGFRA Hematopoietic neoplasms with eosinophilia and abnormalities in FGFR1 CML with eosinophilia AML with inv(16) and eosinophilia (AML-M4-eo) JAK2 V617F+ MPN with eosinophilia ASM with eosinophilia MDS with eosinophilia MPN/MDS overl

5、ap syndromes with eosinophilia Idiopathic: HEUSEosinophil BiologyIL-5IL-3GM-CSFDisease PathogenesisTissue InfiltrationFibrosisHypercoagulabilityAllergic Mechanisms Depending on the underlying disease, HE and HES can be further subclassified. In hematologic neoplasms with HE, eosinophils are usually

6、clonal cells, although direct proof of eosinophil clonality is rarely obtained. Close clinical follow-up of HEUS is necessary to monitor for development of HES and/or an underlying disease. Treatment of HES depends on the underlying disease and on the presence of identified therapeutic targets. Comp

7、lete staging of all organ systems, including the skin, lung, heart, bone marrow and blood and GI tract, is essential in the evaluation of all patients with unexplained HE.Key issuesMedical News Therapies for Active Rheumatoid Arthritisafter Methotrexate FailureBackgroundconventional therapy VS biolo

8、gic agentsMethod48-weekdouble-blindnoninferiority trial353 participants with active rheumatoid despite methotrexate therapyDAS28etanerceptmethotrexate group sulfasalazine-hydroxychloroquine-methotrexate group Primary outcomesSecondary outcomesParticipants in the triple-therapy group had a mean progression of 0.54 Sharp score units；participants in the etanerceptmethotrexate group had a mean progression of 0.29 Sharp score uni