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Case Report
- Non-cirrhotic portal hypertension in an ankylosing spondylitis patient
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Sukki Park, Ji Hyun Lee, Joon Sul Choi, Hyun Woo Kim, Beom Jin Shim, Won Kyu Choi, Sang Hyun Kim
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Yeungnam Univ J Med. 2018;35(1):89-93. Published online June 30, 2018
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DOI: https://doi.org/10.12701/yujm.2018.35.1.89
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Abstract
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- Idiopathic non-cirrhotic portal hypertension (INCPH) is a disease with an uncertain etiology consisting of non-cirrhotic portal hypertension and portal pressure increase in the absence of liver cirrhosis. In INCPH, patients exhibit normal liver functions and structures. The factors associated with INCPH include the following: Umbilical/portal pyremia, bacterial diseases, prothrombic states, chronic exposure to arsenic, vinyl chloride monomers, genetic disorders, and autoimmune diseases. Approximately 70% of patients present a history of major variceal bleeding, and treatment relies on the prevention of complications related to portal hypertension. Autoimmune disorders associated with INCPH are mainly systemic sclerosis, systemic lupus erythematosus and rheumatoid arthritis. To the best of our knowledge, a case of ankylosing spondylitis (AS) associated with INCPH has not been reported thus far. Therfore, we report our experience of a patient with AS accompanied by INCPH, who showed perisplenic varices with patent spleno-portal axis and hepatic veins along with no evidence of cirrhosis on liver biopsy, and provide a brief literature review.
Original Article
- The Effects of Nitric Oxide Inhibitor on Hyperdynamic Circulation in Portal Hypertensive Rats.
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Pill Young Kim, Byeong Ik Jang, Tae Nyeun Kim, Moon Kwan Chung
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Yeungnam Univ J Med. 1999;16(2):181-192. Published online December 31, 1999
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DOI: https://doi.org/10.12701/yujm.1999.16.2.181
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Abstract
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- BACKGROUND
Nitric oxide, a vasodilator synthesized from L-arginine by vascular endothelial cells. accounts for the biological activity of endothelium derived relaxing factor. Previous studies demonstrated that nitric oxide inhibitor. N'-Nitro-L-Arginine(NNA)diminished the hyperdynamic splanchnic and systemic circulation in portal hypertensive rats. The present study was done to determine the role of nitric oxide in the development of hyperdynamic circulations in the prehepatic portal hypertensive rat model produced by partial portal vein ligation. METHODS: The portal hypertensive rats were divided into water ingestion group and NNA ingestion group. After partial portal vein ligation. NNA ingestion group and water ingestion group received NNA, 1mg/kg/day and plain water through the mouth for 14 days, respectively. Cardiac output, mean arterial pressure, organ blood flow and porto-systemic shunting were measured by radioisotope microsphere methods. Vascular resistances were calculated by standard equation. RESULTS: There were significant decreases in mean arterial pressure, increases in cardiac output and cardiac index, and decreases in total systemic and splanchnic vascular resistance in portal hypertensive rats compared to normal control froup(p<0.01). Compared to the water ingestion group, significantly increased mean arterial pressure wit decreased cardiac output and cardiac index were dexeloped in the NNA ingestion group. Total systemic and splanchnic vascular resistance were significantly increased in the NNA ingestion group compared to water ingestion group(p<0.05). But, there was no significant difference in portal pressure between the two groups. CONCLUSION: The hemodynamic results of this study indicate that hyperdynamic circulation in prehepatic portal hypertensive rat model was attenuated by ingestion of NNA. Nitric oxide may play an important role in the development of hyperdynamic circulation with splanchnic vaodilation in chronic portal hypertension.
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