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Pulmonary Arterial Hypertension from Hepatic HHT

Yutian Sun1, Jinyi Wu2 and Xiaowei Li2*
1Pharmaceutical Department, China-Japan Union Hospital, Jilin University, Changchun 130033, PR China
2Cardiovacular Department, China-Japan Union Hospital, Jilin University, Changchun 130033, PR China
Corresponding Author : Xiaowei Li
Cardiovascular Department
China-Japan Union Hospital
Jilin University, Changchun 130033
PR China
E-mail: [email protected]
Received: September 01, 2015 Accepted: September 20, 2015 Published: September 27, 2015
Citation: Sun Y, Wu J, Li X (2015) Pulmonary Arterial Hypertension from Hepatic HHT. InternMed 5:109. doi:10.4172/2165-8048.1000i109
Copyright: © 2015 Sun Y, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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A 42-year female was admitted to our hospital complaining of repeated cough and pant for 2 years. The patient had intermittent nasal bleeding, and her family (including her mother, her aunt) had also similar medical history. Many capillary blood vessels were dilated in her finger and tongue (Figures 1 and 2).
No heart murmur or rhonchi was audible on the chest auscultation. Hepatosplenomegaly was not noted on abdominal field palpation. Echocardiography suggested right atrium enlargement, right ventricle enlargement, and pulmonary arterial hypertension. Abdominal ultrasound suspected hepatic hemangioma.
Chest radiography showed mild cardiomegaly with increasing pulmonary vascular markings (Figure 3). Contrast-enhanced CT of chest revealed the same cardiac alterations as echocardiography (Figure 4). Hepatic contrast-enhanced CT revealed parenchymal perfusion disorders, arteriosystemic shunts and arterioportal shunts (Figures 5 and 6).
Hereditary Hemorrhagic Telangiectasia (HHT) is mucocutaneous or visceral angiodysplastic lesions, which may be distributed throughout cardiovascular system. Currently, the pathogeneses of the disease could result from genetic mutations that interfere with angiogenesis and its control mechanisms [1].
Hepatic involvement occurs in 30% to 73% of patients with HHT; most of them are symptomatic or have a slight elevation of r-GGT [2]. Hepatic vascular lesions range from tiny telangiectases to transient perfusion abnormalities and large confluent focal vascular masses.
Three different and often concurrent types of intrahepatic shunts are responsible for the parenchymal, vascular and bile duct signs. An arteriovenous shunt can, on rare occasions, be responsible for highoutput heart failure as described in our case.
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