The Hepatopulmonary Syndrome

Lange, P; Stoller, James K.

doi:10.7326/0003-4819-122-7-199504010-00008

Cited by 344 publications

(198 citation statements)

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“…1,2 Hepatopulmonary syndrome with intrapulmonary shunts and hypoxia in patients with portal hypertension also is well described, but less well understood. 3 These stand as just two examples of how otherwise healthy organs remote from the liver can be adversely affected in the face of cirrhosis and portal hypertension. Another example, although much less known, is postshunt myelopathy, or hepatic myelopathy, as it also is known.…”

Section: Commentsmentioning

confidence: 99%

Hepatorenal syndrome, hepatopulmonary syndrome, and now, hepatospinal syndrome?

Bain

2003

Liver Transpl

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Background & Aims: Hepatic myelopathy is a rare complication of chronic liver disease, causing progressive spastic paraparesis. Today, no therapy of this disorder has been established. Commonly used therapeutic strategies for hepatic encephalopathy aiming at the reduction of plasma ammonia levels such as protein restriction, oral neomycin, lactulose, or ornithine aspartate fail to improve the symptoms of hepatic myelopathy. The aim of this study was to find out whether orthotopic liver transplantation (OLT) may improve hepatic myelopathy. Methods:

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Section: Commentsmentioning

confidence: 99%

Hepatorenal syndrome, hepatopulmonary syndrome, and now, hepatospinal syndrome?

Bain

2003

Liver Transpl

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“…This imbalance between vasodilator and vasoconstrictor substances, is also involved in the pathophysiology of others vascular abnormalities observed in cirrhosis, such as the clubbing, palmar erythema and SA (21,22) .…”

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confidence: 99%

Are the Spider Angiomas Skin Markers of Hepatopulmonary Syndrome?

Silvério

Guimarães

Elias

et al. 2013

Arq. Gastroenterol.

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Context Hepatopathies can significantly influence both veins and arteries, these changes may cause some cutaneous stigmas, such as spider angioma (SA) and some systemic vascular changes, such as those observed in hepatopulmonary syndrome (HPS). Based on this common pathophysiological root we can assume that the SA can be skin markers of HPS. Objective The objective of this study is to assess whether there is a relationship between the presence of SA and HPS. Methods Records of 40 patients with liver cirrhosis who underwent contrast echocardiography were evaluated, in which we researched the description of SA, physical examination, and other clinical and laboratory data. For diagnosis of HPS we use these signs of the disease: presence of liver disease (cirrhosis in the case), abnormalities in gas exchange by arterial blood gases, and evidence of pulmonary vasodilations by the contrast echocardiography. Results The SA were found in 21/40 (52.5%) patients and hepatopulmonary syndrome in 9/40 (22.5%). The HPS was observed in 8/21 (38.1%) of patients with SA and 1/19 (5.3%) patients were without this sign (P<0.01). We found no statistically significant difference between the SA and the presence of HPS with sex or age. Patients with SA had a higher hypoxemia [PaO2 84.8 ± 11.5 mmHg and 19.8 ± 14.7 mmHg alveolar-arterial gradient of oxygen (AAG)] than those without SA (PaO2 90.8 ± 10.7 mmHg and 10.9 ± 11.7 AAG mmHg) (P<0.05). Conclusion Our findings show a correlation between the presence of SA and HPS, suggesting that the SA may be cutaneous markers of HPS.

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“…Most cases are congenital, frequently related to hereditary hemorrhagic telangiectasia (HHT), an autosomal dominant disorder. Abnormal communications between blood vessels of the lung may also be found in a variety of acquired conditions such as hepatic cirrhosis, schistosomiasis, mitral stenosis, trauma, actinomycosis, Fanconi's syndrome and metastatic thyroid carcinoma [4,5]. Fifty-three to seventy percent of PAVMs are found in lower lobes, 75% of patients have unilateral disease, 36% have multiple lesions, and half of those with multiple lesions have bilateral disease [6].…”

Section: Discussionmentioning

confidence: 99%