کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5685015 | 1597926 | 2017 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Observational retrospective study of vascular modulator changes during treatment in essential thrombocythemia
ترجمه فارسی عنوان
بررسی گذشته نگر از تغییرات مدولاتور عروقی در طی درمان در ترومبوسیتمی ضروری
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کلمات کلیدی
EMPPLTADMRMPET-1WCCCTRULVWFMPNSSCPPPFSCTSP-1ASAEDRFPMPAnagrelideadrenomedullin - آدرنومدولینAspirin - آسپرینAnnexin V - آنکسیان VANA - اصلیendothelin-1 - اندوتلین-1endothelium derived relaxing factor - اندوتلیوم عامل آرامش بخش مشتق شده استThrombospondin - ترومبوزپوندینessential thrombocythaemia - ترومبوسیتامین ضروریWhite cell count - تعداد سلول سفیدMicroparticles - ذرات کوچکWorld Health Organisation - سازمان بهداشت جهانیMyeloproliferative neoplasms - نئوپلاسم های میلوپرولیفراتیوNeutrophils - نوتروفیل هاNitric oxide - نیتریک اکسیدhaemoglobin - هموگلوبینHydroxyurea - هیدروکسی اورهforward scatter - پراکندگی رو به جلوside scatter - پراکندگی سمتPlatelet - پلاکتplatelet poor plasma - پلاکت پلاسمای ضعیفWHO - کهcontrol group - گروه کنترل
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
پزشکی و دندانپزشکی (عمومی)
چکیده انگلیسی
Essential thrombocythemia (ET) patients are at risk of developing thrombotic events. Qualitative platelet (PLT) abnormalities and activation of endothelial cells (ECs) and PLTs are thought to be involved. Microparticles (MPs) can originate from PLTs (PMPs), ECs (EMPs), or red cells (RMPs). Previous studies have indicated that MPs contribute to ET pathophysiology. Endothelial modulators (eg, nitric oxide [NO], adrenomedullin [ADM], and endothelin-1 [ET-1]) are also involved in the pathophysiology of this condition. We hypothesized that treatments for reducing PLT count might also indirectly affect MP generation and endothelial activity by altering endothelial modulator production. The rationale of this study was that hydroxyurea (HU), a cytostatic drug largely used in ET, induces the production of a potent vasoactive agent NO in ECs. An observational retrospective study was designed to investigate the relationship between MPs, NO, ADM, and ET-1 in ET patients on treatment with HU, anagrelide (ANA), aspirin (ASA), and a group of patients before treatment. A total of 63 patients with ET diagnosis: 18 on HUÂ +Â ASA, 15 on ANAÂ +Â ASA, 19 on ASA only, and 11 untreated patients, and 18 healthy controls were included in this study. Blood samples were analyzed for MP (absolute total values) and functional markers (percentage values) by flow cytometry. PLT-derived MPs were studied using CD61, CD62P, CD36, and CD63, whereas endothelial-derived MPs were studied using CD105, CD62E, and CD144. Endothelial modulator markers (NO, ADM, and ET-1) were measured by ELISA. Total MP count was higher in the group treated with ANAÂ +Â ASA (PÂ <Â 0.01). MP markers modified in ET patients returned to levels of healthy controls following treatment, in particular, in patients on ANA treatment. NO and ADM values were higher in the HU group (PÂ <Â 0.001). HU and ANA treatment also affected MP production in a cell origin-specific manner. HU and ANA, although acting via different pathways, have similar final effects. For instance, HU causes vasodilatation by increasing NO and ADM levels, whereas ANA impairs vasoconstriction by reducing ET-1. In conclusion, therapy with HU cytostatic drugs and ANA can reduce PLT count in ET, and also affect endothelial modulatory agents, with HU sustaining vasodilation and prothrombotic MP concentration, whereas ANA decreases vasoconstriction.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Translational Research - Volume 184, June 2017, Pages 21-34
Journal: Translational Research - Volume 184, June 2017, Pages 21-34
نویسندگان
Andrea Piccin, Michael Steurer, Clemens Feistritzer, Ciaran Murphy, Elva Eakins, Muriel Van Schilfgaarde, Daisy Corvetta, Angela Maria Di Pierro, Irene Pusceddu, Luigi Marcheselli, Roberto Gambato, Martin Langes, Dino Veneri, Omar Perbellini,