liver cirrhosis/نقص الأكسجة

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Hypoxia-inducible Factor may Induce the Development of Liver Fibrosis in Budd-Chiari Syndrome by Regulating CD248/endosialin Expression: A Hypothesis.

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Budd-Chiari syndrome (BCS) leads to the development of liver fibrosis in most of the cases. However, the mechanism of BCS-related liver fibrosis is unclear, and it may be largely different from that induced by chronic viral hepatitis. Hepatic stellate cell (HSC) and its specific marker

[Hypoxemia of liver cirrhosis--an autopsy case study].

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41 year-old male with liver cirrhosis accompanying severe hypoxemia was presented. Shortly after the diagnosis of liver cirrhosis, he suffered from exertional dyspnea and cyanosis. Though home oxygen therapy had been prescribed for 2 years, hypoxemia gradually progressed accompanied by persistent

Platypnea and hypoxemia in Laennec's cirrhosis of the liver.

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A patient with Laennec's cirrhosis of the liver presented with platypnea (dyspnea in the upright position relieved by a recumbent one), severe hypoxemia, and a hyperdynamic cardiovascular state. Diagnostic studies suggest that generalized vasodilatation and shunting account for these findings.

[Adaptation to hypoxia in liver cirrhosis: the role of 2,3-DPG (author's transl)].

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By observing a group of 20 patients with liver cirrhosis, we have clarified some features concerning the tissue hypoxia, which is often present in such a disease. By determining the levels of the haemoglobin and of the intraerythrocytic 2,3-DPG, and by evaluating the acid-base state of such

[Clinical significance of circulating hypoxia inducible factor-1α and hemeoxygenase-1 in patients with liver cirrhosis].

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OBJECTIVE To explore the levels of circulating hypoxia inducible factor-1α (HIF-1α) and hemeoxygenase-1 (HO-1) in liver cirrhosis and to explore their diagnostic values as noninvasive methods. METHODS The levels of circulating HIF-1α and HO-1 were quantitatively detected in 34 patients with liver

Pulmonary and extrapulmonary contributors to hypoxemia in liver cirrhosis.

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To determine and to quantify the pulmonary and extrapulmonary contributors to hypoxemia in liver cirrhosis, we measured in 10 cirrhotics blood gases, P50, hemodynamics, ventilation, and the distribution of ventilation-perfusion ratios (VA/Q) using the multiple inert gas elimination technique. Seven

Liver cirrhosis with severe hypoxemia and paradoxic pulmonary vascular response to graded inspiratory oxygen tension.

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We present the findings in a patient with liver cirrhosis who showed oppositional pulmonary vascular responses to various alveolar oxygen tensions. In this case the pulmonary artery constricted on exposure to hyperoxia and then gradually dilated during progressive hypoxic inhalation. Such a

Arterial hypoxemia in patients with hepatic cirrhosis.

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Pulmonary function tests were studied in 105 patients with cirrhosis of the liver who had no clinical or radiographical evidence of cardiopulmonary disease. Spirometric data such as VC, FRC, RV, TLC, RV/TLC and FEV1.0% were within normal limits in all subjects. However, flow-volume curve and closing

Refractory hypoxemia during liver cirrhosis. Hepatopulmonary syndrome or "primary" pulmonary hypertension?

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We report an uncommon mechanism of severe hypoxemia in two cirrhotic patients under long-term beta-blocker therapy. Our patients presented with profound hypoxemia refractory to oxygen therapy, normal lung radiography and pulmonary function tests, and evidence of right-to-left anatomic shunt.

[Contrast echocardiography in the diagnosis of severe hypoxemia associated with liver cirrhosis].

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Severe hypoxemia is an uncommon feature of hepatic cirrhosis. Its major cause are intrapulmonary arteriovenous shunts, both due to direct arteriovenous communications and abnormally dilated pulmonary capillaries. In the present study, a case of cirrhosis associated with severe hypoxemia is reported.

[Effects of hypoxia on the production of angiotensin converting enzyme in decompensated liver cirrhosis].

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The high angiotensin-converting activity, in 13 of the 17 patients afflicted with hepatic cirrhosis, has been put in relation to the hypoxia influence. The insufficient cession of O2 seems to stimulate the enzyme activity, especially for the patients who simultaneously present low values of blood

Role of Hypoxia-Inducible Factors in the Development of Liver Fibrosis.

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Liver fibrosis remains a significant clinical problem in the United States and throughout the world. Although important advances in the understanding of this disease have been made, no effective pharmacologic agents have been developed that directly prevent or reverse the fibrotic process. Many of

Hepatocyte Hypoxia Inducible Factor-1 Mediates the Development of Liver Fibrosis in a Mouse Model of Nonalcoholic Fatty Liver Disease.

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BACKGROUND Obstructive sleep apnea (OSA) is associated with the progression of non-alcoholic fatty liver disease (NAFLD) to steatohepatitis and fibrosis. This progression correlates with the severity of OSA-associated hypoxia. In mice with diet induced obesity, hepatic steatosis leads to liver

Reduced liver fibrosis in hypoxia-inducible factor-1alpha-deficient mice.

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Liver fibrosis is characterized by excessive deposition of extracellular matrix in the liver during chronic injury. During early stages of this disease, cells begin to synthesize and secrete profibrotic proteins that stimulate matrix production and inhibit matrix degradation. Although it is clear

Hypoxia-inducible factor activation in myeloid cells contributes to the development of liver fibrosis in cholestatic mice.

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Macrophages play an integral role in the development of liver fibrosis by releasing mediators, such as platelet-derived growth factor-B (PDGF-B) and transforming growth factor-β1, which stimulate hepatic stellate cell proliferation, chemotaxis, and collagen production. However, the mechanism by

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