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)

Transarterial chemoembolization (TACE) is a nonsurgical therapeutic option for the control of hepatocellular carcinoma (HCC) in patients with cirrhosis. Although less invasive than surgical approaches, this procedure can have severe side effects, with both local and extrahepatic complications, mostly related to treatment-induced ischemic damage. Here, we describe the case of a cirrhotic female patient affected by multinodular HCC, who presented with sudden onset dyspnea and chest pain. After a thorough follow-up, her condition was found to be due to iodinized oil pleural effusion following diaphragm rupture by a fistula. This had developed from a sterile abscess formed on the site of a previously performed TACE. We discuss the differential diagnosis and the management of this case, which, to our knowledge, has never been described as a late side effect of TACE.
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PMID:Iodized oil pleural effusion in a patient previously treated with transarterial chemoembolization for hepatocellular carcinoma. 2060 18

Patients suffering from severe chronic liver disease, in particular cirrhosis, are at risk for pulmonary complications. The leading clinical symptom is shortness of breath, which can accompany the actual disease as indirect effect because of anemia, faint muscles or ascites. On the other hand, dyspnea can have multiple additive causes in case of accompanying cardial or pulmonary disease. The hepatopulmonary syndrome (HPS) and the portopulmonary hypertension (PoPH) belong to the most relevant pulmonary complications in liver cirrhosis. HPS appears to be more common than PoPH and the presence of either entity increases morbidity and mortality in patients with liver disease. The two diseases have to be strictly distinguished, as they have opposed histological and pathophysiological origin. While the HPS is a dilatative pulmonary- vascular disease, the PoPH is a constrictive or obliterative pulmonary-vascular disease in the context of a liver disease or a portal hypertension. Therefore, these diseases are separate entities also when it comes to diagnostics and therapy.
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PMID:[Pulmonary affection in advanced liver disease - hepatepulonary syndrome and portopulmonary hypertension]. 2124 May 91

Portopulmonary hypertension is a complication of chronic liver disease, which has significant effects on survival and prognosis. Although the pathogenesis of pulmonary arterial hypertension has been well known, portopulmonary hypertension is often underestimated in patients with chronic liver disease. Every clinician who manages patients with chronic liver disease complaining of dyspnea should consider portopulmonary hypertension because this disorder requires special treatment. Herein, a 40-year-old woman with liver cirrhosis who complained of dyspnea on exercise is presented. She was diagnosed with portopulmonary hypertension by echocardiography and right-heart catheterization. Beraprost was used to reduce the pulmonary arterial pressure and improve the symptoms. Her symptoms were improved after 2 weeks, and improved symptoms and reduced pulmonary arterial pressure were sustained for 18 months.
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PMID:Successful management of portopulmonary hypertension with beraprost. 2138 99

A 66-year-old woman with hepatitis C related liver cirrhosis presented to our hospital for dyspnoea and cyanosis. Tachypnoea, low grade fever, clubbed fingers, palmar erythaema, spider angioma, wheezing and severe hypoxaemia were found. Chronic obstructive pulmonary disease (COPD) with acute exacerbation was diagnosed and she recovered after bronchodilator and antibiotic treatment. However, dyspnoea and hypoxaemia recurred with widened alveolar-arterial gradient, which was unusual in COPD. A pulmonary function test showed moderate obstructive ventilatory defect and chest high resolution CT scan disclosed some dilated vessels over the left lower lung. Interestingly, platypnoea and orthodeoxia were observed, therefore hepatopulmonary syndrome was suspected and was confirmed by contrast echocardiography, lung perfusion scan and 100% oxygen administration. Her dyspnoea improved gradually after oxygen use. She was followed in our clinic for 3 years and her respiratory condition on home oxygen remained stable, as did the liver cirrhosis.
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PMID:Unusual dyspnoea in a patient with liver cirrhosis. 2168 87

Tolvaptan is a new vasopressin antagonist developed for the treatment of hypervolemic or euvolemic hyponatremia. It has greater affinity for the V(2) receptor than native vasopressin or any other vasopressin antagonist. Blockade of the V(2) receptor induces solute-free water excretion without affecting normal electrolyte excretion. The pharmacokinetics and pharmacodynamics of tolvaptan are suitable for once-daily dosing. Throughout all phases of clinical studies, it was shown to be safe for short- and long-term use. Tolvaptan effectively increases serum sodium levels in patients with heart failure, cirrhosis and syndrome of inappropriate secretion of antidiuretic hormone. In patients hospitalized owing to heart failure, tolvaptan decreased bodyweight, increased urine output and improved dyspnea compared with placebo. However, tolvaptan has not proven to be beneficial for the long-term management of heart failure. Currently, tolvaptan is the only oral agent in its class available in the USA and Europe.
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PMID:Tolvaptan: a vasopressin antagonist for the management of euvolemic and hypervolemic hyponatremia. 2211 41

Hepatopulmonary syndrome (HPS) is characterized by an oxygenation defect induced by pulmonary vascular dilatation in the setting of liver cirrhosis or portal hypertension. It is defined by an alveolar-arterial gradient > 15 mm Hg measured at sea level. This syndrome is seen in 15 to 30% of cirrhotic patients and has been associated with worse survival. Most HPS patients are either asymptomatic or develop the insidious onset of dyspnea. The key event in its pathogenesis is the development of intrapulmonary vascular dilatation (IPVD), which has been linked to increased pulmonary levels of nitric oxide. Pulse oximetry is a useful screening test for HPS, which can guide subsequent use of arterial blood gases. Contrast-enhanced transthoracic echocardiography is the most effective test to demonstrate IPVD. Another method for detecting IPVD is the radionuclide lung perfusion scanning, using technetium-labeled macroaggregated albumin particles. Liver transplantation is the only available treatment for HPS, resulting in complete resolution or significant improvement in gas exchange in over 85% of patients.
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PMID:Hepatopulmonary syndrome. 2244 56

Shortness of breath is a common complaint in those with chronic liver disease. The differential diagnosis for this complaint includes primary pulmonary disorders, systemic disorders that affect the liver and lungs, and extrahepatic manifestations of portal hypertension. Orthotopic liver transplant, when appropriate, is the most effective therapy for many patients with dyspnea and chronic liver disease, although therapies to treat the underlying complications of cirrhosis may provide relief. Shortness of breath in patients with cirrhosis often portends a poor prognosis, and these patients should be evaluated for orthotopic liver transplant because this therapy is most likely to provide long-lasting benefit.
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PMID:Shortness of breath in the patient with chronic liver disease. 2254 1

Mycobacterium tuberculosis infection in patients with cystic fibrosis (CF) is rare. We report a 22-year-old CF patient with high fever, dyspnea and weight loss that progressively worsened over 2 weeks before admission. The patient suffered from liver cirrhosis, was colonized with Pseudomonas aeruginosa and had been repeatedly hospitalized for pulmonary infections. The patient was treated initially as for an exacerbation of P. aeruginosa infection, but tuberculosis (TBC) was suspected due to lack of improvement. A CT of the chest revealed enlarged bilateral cavities in the upper and middle lobes. A tuberculin skin test was positive, and M. tuberculosis nucleic acid was isolated from sputum samples. After receiving first-line anti-TBC drugs for 1 month, the patient's condition continued to worsen so molecular drug susceptibility testing was performed. Multidrug-resistant TBC was discovered, leading to a change in regimen. The patient was treated with ethionamide, moxifloxacin, linezolid, amikacin, imipenem/cilastatin and rifabutin and showed a remarkable clinical improvement. Although nontuberculous mycobacteria are more common in CF, the possibility of TBC should not be ignored. In that setting, early suspicion of infection due to resistant M. tuberculosis can be life saving.
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PMID:Multidrug-resistant tuberculosis in an adult with cystic fibrosis. 2286 52

We report a successful treatment result in a rare case of hepatitis C virus-related cirrhosis, who had sustained hydrothorax after blunt thoracoabdominal trauma. This was a female patient with liver cirrhosis, Child-Turcotte-Pugh class A, without ascites before injury. She sustained blunt thoracoabdominal trauma with a left clavicle fracture dislocation and right rib fractures. There was no hemopneumothorax at initial presentation. However, dyspnea and right pleural effusion developed gradually. We inserted a chest tube to relieve the patient's symptoms, and the daily drainage amount remained consistent. Hepatic hydrothorax was confirmed by the intraperitoneal injection of radioisotope 99mTc-sulfur colloid that demonstrated one-way transdiaphragmatic flow of fluid from the peritoneal cavity to pleural cavities. Finally, the hydrothorax was treated successfully by minocycline-induced pleural symphysis. To the best of our knowledge, this is the first case of hepatic hydrothorax developed after thoracoabdominal trauma.
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PMID:Hepatic hydrothorax after blunt chest trauma. 2290 27

Hepatopulmonary syndrome (HPS) is an important cause of dyspnea and hypoxia in the setting of liver disease, occurring in 10-30% of patients with cirrhosis. It is due to vasodilation and angiogenesis in the pulmonary vascular bed, which leads to ventilation-perfusion mismatching, diffusion limitation to oxygen exchange, and arteriovenous shunting. There is evidence, primarily from animal studies, that vasodilation is mediated by a number of endogenous vasoactive molecules, including endothelin-1 and nitric oxide (NO). In experimental HPS, liver injury stimulates release of endothelin-1 and results in increased expression of ET(B) receptors on pulmonary endothelial cells, leading to upregulation of endothelial NO synthase (eNOS) and subsequent increased production of NO, which causes vasodilation. In addition, increased phagocytosis of bacterial endotoxin in the lung not only promotes stimulation of inducible NO synthase, which increases NO production, but also contributes to intrapulmonary accumulation of monocytes, which may stimulate angiogenesis via vascular endothelial growth factor pathway. Despite these insights into the pathogenesis of experimental HPS, there is no established medical therapy, and liver transplantation remains the main treatment for symptomatic HPS, although selected patients may benefit from other surgical or radiological interventions. In this review, we focus on recent advances in our understanding of the pathophysiology of HPS, and discuss current approaches to the investigation and treatment of this condition.
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PMID:Hepatopulmonary syndrome: update on recent advances in pathophysiology, investigation, and treatment. 2319 Feb 1


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