کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
3261470 1207694 2016 5 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Plasma ADAMTS-13 protein is not associated with portal hypertension or hemodynamic changes in patients with cirrhosis
ترجمه فارسی عنوان
پروتئین ADAMTS-13 پلاسما با فشار خون بالای پورتال و یا تغییرات همودینامیک در بیماران مبتلا به سیروز همراه نیست
کلمات کلیدی
نشانگر؛ بیماری های مزمن کبدی
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی غدد درون ریز، دیابت و متابولیسم
چکیده انگلیسی

BackgroundActivated hepatic stellate cells synthesize the matrix metalloprotease ADAMTS13, which may be involved in the development of liver cirrhosis and portal hypertension. Plasma ADAMTS13 activity has been reported as both increased and decreased in cirrhosis, but ADAMTS13 protein has not previously been examined.AimTo evaluate ADAMTS13 protein in the hepatic circulation and the relation to disease severity, portal pressure, and systemic hemodynamics in cirrhotic patients.MethodsSixty-one cirrhotic patients (Child class: A = 22; B = 21; C = 18) and nine healthy controls underwent a liver vein catheterization with measurement of splanchnic and systemic hemodynamics, and plasma ADAMTS13 protein concentration in a hepatic vein and the femoral artery.ResultsADAMTS13 protein concentrations were increased in cirrhotic patients compared with controls (774 ng/ml [IQR: 585–955] vs. 538 ng/ml [IQR: 484–631], p < 0.03). There were no significant correlations to MELD score, Child Pugh score, portal pressure, nor systemic vascular resistance or cardiac output.ConclusionsThe increased concentration of ADAMTS13 protein in the hepatic circulation may reflect an increased number of active hepatic stellate cells in cirrhosis. However, ADAMTS13 was unrelated to portal hypertension and systemic hemodynamics. In conclusion, ADAMTS13 does not appear to be associated to disease severity or the hemodynamic derangement in patients with cirrhosis.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Digestive and Liver Disease - Volume 48, Issue 4, April 2016, Pages 404–408
نویسندگان
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