Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An autopsy case of a 65-year-old male who died of hepatocellular carcinoma superimposed on liver cirrhosis complicated with systemic sarcoidosis is presented. No organ metastasis of hepatocellular carcinoma was found except for a minute tumor embolus in the left upper lobe of the lung. Involved organs by sarcoidosis were the lymph nodes, lungs, heart, liver and spleen, but its presence was not noticed before death. Its cardiac involvement coincide with his clinical symptom of exertional dyspnea and the ECG finding of A-V block.
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PMID:Hepatocellular carcinoma and myocardial sarcoidosis.--An autopsy case. 21 33

To determine the clinical, laboratory and hemodynamic profile in patients with primary pulmonary hypertension and associated portal hypertension, 7 new cases and 71 previously reported cases were analyzed. There was no gender predilection and the average age at diagnosis was 41 years. Liver cirrhosis was the most frequent cause of hypertension (82%) and a surgical portosystemic shunt was present in 29%. Almost invariably, portal hypertension either preceded or was diagnosed concurrently with pulmonary hypertension, favoring the hypothesis that in portal hypertension, the pulmonary vasculature may be exposed to vasoactive substances normally metabolized or produced by the diseased liver, possibly inducing vasoconstriction or direct toxic damage to the pulmonary arteries. Clinically, exertional dyspnea was the most frequent presenting symptom (81%); other symptoms, such as syncope, chest pain and fatigue, were present in less than 33%. An accentuated pulmonary component of the second heart sound (82%) and a systolic murmur (69%) were the most common physical findings. At least 75% of these patients had evidence of pulmonary hypertension on electrocardiography (right ventricular hypertrophy) or roentgenography (cardiomegaly or dilated main pulmonary arteries, or both). Hemodynamic findings included severe pulmonary hypertension (mean pulmonary artery pressure 59 +/- 19 mm Hg) with normal pulmonary capillary wedge pressure and cardiac output. Treatment was basically palliative and the mean and median survival times were 15 and 6 months, respectively. In brief, on the basis of clinical presentation and laboratory features, patients with combined primary pulmonary hypertension and portal hypertension seldom represent a diagnostic challenge. Further research is needed on treatment, which remains palliative. The survival rate is poor and worse than that seen in isolated primary pulmonary hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Association between primary pulmonary hypertension and portal hypertension: analysis of its pathophysiology and clinical, laboratory and hemodynamic manifestations. 199 8

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 cough, mucous sputa and intermittent fever. The chest X-ray revealed bilateral interstitial shadow particularly localized in lower lung fields. The arteriovenous shunt ratio was shown to be 24% by oxygen method. Perfusion lung scan using 99mTc-labeled MAA revealed perfusion defects in bilateral lung fields and radionuclide uptake was strongly demonstrated in the kidneys. These clinical data suggested that severe hypoxemia was probably due to multiple arteriovenous shunt. With further progression of hypoxemia for 4 months, he died of hepatic failure and pulmonary infection. Autopsy showed Miyake's type B cirrhosis. Multiple pleural and subpleural arteriolar nevi were demonstrated grossly and microscopically. There were no arteriovenous malformations demonstrated after injection of barium-gelatin solution into the pulmonary artery. Histologically, irregularly dilated vessels were found in the lung parenchyma beneath the pleura and filled with blood and injection material. These clinical and pathological findings provided evidence that the mechanism of arterial desaturation was pulmonary arteriovenous shunting due to liver cirrhosis.
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PMID:[Hypoxemia of liver cirrhosis--an autopsy case study]. 229 Feb 37

A 12-year-old boy with Wilson's disease developed exertional dyspnea, cyanosis, and finger clubbing 10 months after diagnosis. The hypoxemia was caused by arteriovenous shunting, demonstrated by radionuclide scanning and pulmonary arteriography. Orthotopic liver transplantation was performed after the development of severe hypoxemia. There was no apparent reversal of the intrapulmonary arteriovenous shunting and he died 10 days posttransplantation of multiple organ failure secondary to hypoxemia. Monitoring arterial oxygen saturation in children with cirrhosis is warranted since the presence of significant arteriovenous shunting may influence prognosis and decisions regarding liver transplantation.
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PMID:Failure of liver transplantation in Wilson's disease with pulmonary arteriovenous shunting. 230 74

A 63-year-old female was admitted with dyspnea on exertion. She had previously suffered from a large amount of epistaxis. Chest X-ray showed the bilateral diffuse granular infiltrates. Arterial blood analysis revealed severe hypoxemia and pulmonary function test showed reduced function of diffusing capacity. Dynamic radionuclide perfusion scintigraphy performed with 99mTc-labeled MAA demonstrated passage of microspheres through the pulmonary vasculature into the systemic circulation, indicating a right-to-left shunt. Although selective pulmonary wedge angiography did not directly demonstrate pulmonary arteriovenous fistulae, the histopathological findings of TBLB specimens revealed multiple dilated alveolar vessels that microspheres could pass through. In addition, chronic hepatitis, dilatation of splenic vein and spleno-renal anastomosis had been present. This type of pulmonary arteriovenous fistula is said to be a rare dispersed telangiectasic type, associated with a part of Rendu-Osler-Weber syndrome and a cause of hypoxemia in liver cirrhosis. We consider that in this case, the chronic hepatitis may have played an important role of developing multiple small pulmonary arteriovenous fistulas.
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PMID:[A case of multiple small pulmonary arteriovenous fistulas with chronic hepatitis and abdominal vessel abnormalities]. 262 13

A 52-year-old woman suffered from exertional dyspnea, 5 years after she was diagnosed with cirrhosis of the liver. Hypoxemia was suspected because of persistent exertional dyspnea and was confirmed by contiguous arterial blood gas tests. After excluding other cardiopulmonary factors, a series of studies including lung perfusion scan, echocardiography and cardiopulmonary cineangiography revealed the cause of hypoxemia to be the patient's liver disease. Hepatopulmonary syndrome was diagnosed. Despite supplemental oxygen therapy and oral garlic powder for 6 months, the patient still had exertional dyspnea and platypnea, and arterial blood gas results did not improve. We report this case to call attention to arterial oxygen desaturation in cases of cirrhosis of the liver, and to emphasize that deteriorating oxygenation in patients with chronic liver disease may be an indication for liver transplantation, as such functional microvascular abnormalities could be reversed by liver transplantation.
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PMID:Hepatopulmonary syndrome in liver cirrhosis: report of a case. 760 81

A 80-year-old man was admitted to our hospital complaining of appetite loss, dry cough, and dyspnea on exertion. Chest X-ray film showed massive right pleural effusion. On physical examination, the right thorax was dull to percussion, and breath sounds of the right lung field were diminished. Examination of the cardiovascular system was unremarkable. Hepatosplenomegaly and ascites were not evident. The character of the pleural fluid was transudative. Cytological findings were negative and culture of the pleural fluid was normal. First, the pleural fluid was diminished by thoracic drainage. But, after the cessation of drainage, the pleural fluid soon reaccumulated. Abdominal ultrasonography showed typical liver cirrhosis pattern without ascites. An intraperitoneal injection of 99mTc-sulfur colloid was followed by positive uptake of radioactivity in the right pleural cavity from 1 hour after the injection, demonstrating the existence of a direct perito-pleural communication. Thus, the diagnosis of liver cirrhosis presenting with right pleural fluid, without ascites was made. This case indicates that the absence of ascites cannot exclude cirrhosis as the etiologic cause of pleural effusion.
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PMID:[A case of liver cirrhosis presenting with right pleural fluid without ascites]. 780 61

A 62-year-old man with liver cirrhosis and hypoxemia was admitted to evaluate the etiology of hypoxemia. The patient had noticed exertional dyspnea for three years. Physical examination, laboratory tests, ultrasonography and liver scintigraphy revealed liver cirrhosis. The arterial blood gas test showed hypoxemia (PO2 46.3 mmHg). Chest roentgenogram showed old pulmonary tuberculosis and the pulmonary function test demonstrated decreased FEV 1.0% and %DLco, which did not account for the marked hypoxemia. Contrast echocardiography was performed by injecting hand-agitated saline into the antecubital vein. Three seconds after the right ventricle was opacified, the contrast echoes appeared in the left atrium and then the left ventricle. Pulmonary arteriography revealed no pulmonary arteriovenous fistula. Hemodynamic data showed low pulmonary vascular resistance. Contrast echocardiography by injecting hand-agitated saline from the catheter tip was performed at both pulmonary arteries and the left atrium was opacified by each injection. The hypoxemia was mainly attributed to a intrapulmonary arteriovenous shunt. Although the etiology of hypoxemia in liver cirrhosis seems to be multifactorial, the intrapulmonary arteriovenous shunt is the most important factor. Contrast echocardiography was useful for detecting this shunt.
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PMID:[Contrast echocardiographic detection of pulmonary arteriovenous shunt in a hypoxemic patient with liver cirrhosis]. 816 48

Effects of inhibitors of arachidonic acid (AA) metabolism on the development of fatty liver, cirrhosis, glutathione-S-transferase placental form (GST-P)-positive nodules and the generation of 8-hydroxydeoxyguanosine (8-OHdG) and thiobarbituric acid-reactive substances (TBARS), caused by a choline-deficient, L-amino acid-defined (CDAA) diet, were examined in male Fischer 344 rats by feeding CDAA diets supplemented with the inhibitors for 12 and 30 weeks. Acetylsalicylic acid (ASA) (at doses of 0.1 and 0.2%) and p-bromophenacylbromide (BPB) (0.1 and 0.2%) were used as inhibitors of, respectively, cyclo-oxygenase and phospholipase A2, and quercetin (QU) (0.75 and 1.5%) and nordihydroguaiaretic acid (NDGA) (0.1 and 0.2%) as inhibitors of lipoxygenase. None of the inhibitors affected the development of fatty liver caused by the CDAA diet. ASA at a doe of 0.2% almost completely prevented the appearance of cirrhosis, GST-P-positive nodules, 8-OHdG and TBARS in seven out of 11 (63.7%) rats. BPB at a dose of 0.2% also exerted inhibitory effects on all of these lesions but to a lesser extent than ASA. QU and NDGA exerted inhibitory effects limited to the GST-P-positive nodule case. The results indicate that a perturbed AA metabolism, particularly of the cyclo-oxygenase pathway, derived secondarily from depletion of labile methyl groups or phosphatidylcholine, might play key roles in the cirrhosis, hepatocarcinogenesis and oxidative stress caused by a CDAA diet. The results also indicated a possible involvement of the lipoxygenase pathway in hepatocarcinogenic processes.
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PMID:Inhibition by acetylsalicylic acid, a cyclo-oxygenase inhibitor, and p-bromophenacylbromide, a phospholipase A2 inhibitor, of both cirrhosis and enzyme-altered nodules caused by a choline-deficient, L-amino acid-defined diet in rats. 863 Nov 32

A 65-year-old man with cryptogenic cirrhosis initially underwent transjugular intrahepatic portosystemic shunt (TIPS) creation for variceal bleeding. For the following 16 months, variceal bleeding and intractable ascites persisted despite TIPS revision with variceal embolization. A surgical distal splenorenal shunt was then created, but, although there was initial improvement, intractable ascites recurred. At presentation at a different hospital, the patient gave a history of dyspnea on exertion and orthopnea. Physical examination demonstrated a distended abdomen, consistent with severe ascites, a large right pleural effusion, and bilateral peripheral edema.
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PMID:SCVIR annual meeting film panel session: diagnosis and discussion of case 2: Left hepatic arterioportal fistula. 1128 46


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