Localizing intrapulmonary shunt in hepatopulmonary syndrome by transesophageal echocardiography.
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Transesophageal echocardiography combining with peripheral injection of agitated saline solution is a useful diagnostic tool to detect the intrapulmonary shunt. We performed transesophageal contrast echocardiography in a case of hepatopulmonary syndrome with normal pulmonary angiography to define the intrapulmonary right-to-left shunt bilaterally. (+info)
Hypoxaemia--think of the liver! Every internist should be aware of the hepatopulmonary syndrome.
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Hepatopulmonary syndrome is characterised by arterial hypoxaemia, liver disease, and intrapulmonary vascular dilatation. A case is reported in which severe hypoxaemia, detected by chance, led to the diagnosis of liver disease and hepatopulmonary syndrome. (+info)
Endothelin-1 stimulation of endothelial nitric oxide synthase in the pathogenesis of hepatopulmonary syndrome.
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Biliary cirrhosis in the rat triggers intrapulmonary vasodilatation and gas exchange abnormalities that characterize the hepatopulmonary syndrome. This vasodilatation correlates with increased levels of pulmonary microcirculatory endothelial nitric oxide synthase (eNOS) and hepatic and plasma endothelin-1 (ET-1). Prehepatic portal hypertension induced by portal vein ligation (PVL) does not cause similar changes, suggesting that ET-1 in cirrhosis may modulate pulmonary eNOS and vascular tone. We assessed whether ET-1 altered eNOS expression and nitric oxide production in bovine pulmonary artery endothelial cells (BPAECs) and if a 2-wk low-level intravenous ET-1 infusion in PVL animals modulated pulmonary eNOS levels, microcirculatory tone, and gas exchange. ET-1 caused a 2.5-fold increase in eNOS protein in BPAECs, inhibitable with an endothelin B receptor antagonist, and an increase in eNOS mRNA and nitrite production. ET-1 infusion in PVL animals caused increased pulmonary eNOS levels, intrapulmonary vasodilatation, and gas exchange abnormalities without increasing pulmonary arterial pressure. ET-1 produced during hepatic injury may contribute to the hepatopulmonary syndrome by modulating eNOS and inducing pulmonary microcicrulatory vasodilatation. (+info)
Interleukin-10 inhibits pulmonary NF-kappaB activation and lung injury induced by hepatic ischemia-reperfusion.
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Hepatic ischemia and reperfusion cause local and remote organ injury. This injury culminates from an integrated cascade of proinflammatory cytokines, chemokines, and adhesion molecules, many of which are regulated by the transcription factor nuclear factor-kappaB (NF-kappaB). The anti-inflammatory cytokine interleukin-10 (IL-10) has been shown to have inhibitory effects on NF-kappaB. The objective of the current study was to determine whether IL-10 could suppress pulmonary NF-kappaB activation and ensuing lung injury induced by hepatic ischemia-reperfusion. C57BL/6 mice underwent partial hepatic ischemia with or without intravenous administration of IL-10. Hepatic ischemia-reperfusion resulted in pulmonary NF-kappaB activation, increased mRNA expression of tumor necrosis factor-alpha (TNF-alpha), and macrophage inflammatory protein-2 (MIP-2), as well as increased pulmonary neutrophil accumulation and lung edema. Administration of IL-10 suppressed lung NF-kappaB activation, reduced TNF-alpha and MIP-2 mRNA expression, and decreased pulmonary neutrophil recruitment and lung injury. The data suggest that IL-10 protects against hepatic ischemia and reperfusion-induced lung injury by inhibiting lung NF-kappaB activation and the resulting pulmonary production of proinflammatory mediators. (+info)
Hepatopulmonary syndrome after allogeneic bone marrow transplantation.
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A 10-year-old girl with aplastic anemia received an allogeneic bone marrow transplantation (BMT). Three years after an uneventful course apart from chronic graft-versus-host disease (GVHD) she presented with chronic hypoxemia, reduced diffusion capacity of the lungs, normal spirometric lung function and increased bilirubin and liver enzymes. Intrapulmonary vascular dilatations were demonstrated. Pulmonary complications after BMT may include a hepatopulmonary syndrome (liver disease, hypoxemia, intrapulmonary vascular dilatations). (+info)
Use of transjugular intrahepatic portosystemic shunt as a bridge to liver transplantation in a patient with severe hepatopulmonary syndrome.
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Hepatopulmonary syndrome (HPS) is defined by the presence of the triad of liver disease, arterial hypoxemia, and intrapulmonary vascular dilatation. The clinical implication of this disorder is impairment of gas exchange. Numerous reports in the literature show that this condition is reversible with orthotopic liver transplantation (OLT). However, patients with HPS often present with PaO(2) levels that are quite low. OLT with a preoperative PaO(2) less than 50 mm Hg is associated with unacceptably high mortality and morbidity. We report a case of severe HPS in which a transjugular intrahepatic portosystemic shunt was successfully used to improve oxygenation, thus allowing a successful elective OLT. (+info)
Novel presentation and approach to management of hepatopulmonary syndrome with use of antimicrobial agents.
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A 44-year-old man with hepatitis C-associated liver cirrhosis, cyanosis, digital clubbing, and platypnea presented with left-side hemiplegia found to be due to a brain abscess. Hepatopulmonary syndrome was diagnosed after demonstration of the presence of a massive intrapulmonary shunt. Although the anomalous vascular channel never was defined anatomically, follow-up studies confirmed the presence of a functional shunt. Culture of a sample from the abscess yielded Streptococcus intermedius. It was hypothesized that the patient's pulmonary vascular pathology was due, in large part, to chronic elevated levels of nitric oxide (a potent vasodilator thought to be generated by endotoxin absorbed from the gut). Treatment with oral norfloxacin was initiated on the basis of data that this antibiotic reduces endotoxemia and concomitant nitric oxide production in patients with cirrhosis. Four months after initiation of treatment, the patient's hypoxia had resolved. (+info)
Hepatopulmonary syndrome in poorly compensated postnecrotic liver cirrhosis by hepatitis B virus in Korea.
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BACKGROUND: Hepatopulmonary syndrome (HPS) refers to the association of hypoxemia, intrapulmonary shunting and chronic liver disease. But there is no clear data about the prevalence of HPS in postnecrotic liver cirrhosis by hepatitis B virus (HBV), the most common cause of liver disease in Korea. The aim of this study was to investigate the prevalence of HPS in poorly compensated postnecrotic liver cirrhosis by HBV, and the correlation of the hepatopulmonary syndrome with clinical aspects of postnecrotic liver cirrhosis by HBV. METHODS: Thirty-five patients underwent pulmonary function test, arterial blood gas analysis and contrast-enhanced echocardiography. All patients were diagnosed as HBV-induced Child class C liver cirrhosis and had no evidence of intrinsic cardiopulmonary disease. RESULTS: Intrapulmonary shunt was detected in 6/35 (17.1%) by contrast-enhanced echocardiography. Two of six patients with intrahepatic shunts had significant hypoxemia (PaO2 < 70 mmHg) and four showed increased alveolar-arterial oxygen gradient over 20 mmHg. Only cyanosis could reliably distinguish between shunt positive and negative patients. CONCLUSIONS: The prevalence of intrapulmonary shunt in poorly compensated postnecrotic liver cirrhosis by HBV was 17.1% and the frequency of hepatopulmonary syndrome was relatively low (5.7%). 'Subclinical' hepatopulmonary syndrome (echocardiographically positive intrapulmonary shunt but without profound hypoxemia) exists in 11.4% of cases with poorly compensated postnecrotic liver cirrhosis by HBV. Cyanosis is the only reliable clinical indicator of HPS of HBV-induced poorly compensated liver cirrhosis. Further studies are required to determine if the prevalence and clinical manifestations of HPS varies with etiology or with geographical and racial differences. (+info)