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)

A 67 year old male with non-resectable hepatocellular carcinoma (HCC) in both lobes and liver cirrhosis was treated with transcatheter arterial embolization and regional chemotherapy. He was doing well for 18 months. He was readmitted for fever, chest pain and multiple pulmonary metastases. During interleukin-2 therapy, he suddenly developed dyspnoea and palpitation, and was in shock. Left-sided haemothorax was confirmed by draining 3 L of fresh blood. In spite of intensive care, he died within 36 h. Autopsy showed that the haemothorax was caused by rupture of one of the metastases in the upper lobe of the left lung, and that the primary HCC was totally necrotic. Survey of the literature failed to find a report of fatal bleeding from a lung metastasis of HCC.
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PMID:A rupture of lung metastasis of hepatocellular carcinoma causing haemothorax. 828 Aug 50

We compared arterial blood gas analysis and 99mTc-MAA lung perfusion scintigraphy before and after endoscopic injection sclerotherapy (EIS) in 17 cases of esophageal varices complicating liver cirrhosis. EIS was performed by the intra-variceal injection method with 5% ethanolamine oleate (EO) as the sclerosant agent. In blood gas analysis, the mean values of partial arterial oxygen tension (PaO2) and oxygen saturation (SaO2) were decreased, and the mean value of alveolar-arterial O2 difference (AaDO2) was increased, compared with before EIS while breathing room air. On lung perfusion scintigram, the pulmonary blood flow was markedly decreased, demonstrating hypoperfusion and/or perfusion defect, compared with before EIS in most the cases. It was suggested that pulmonary embolism and/or pulmonary circulatory disturbance occurred after EIS. It is important to note that pulmonary circulatory disturbances potentially may occur after EIS without any accompanying symptoms such as dyspnea, cough, or hemoptysis.
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PMID:[Pulmonary circulatory disturbance following endoscopic injection sclerotherapy]. 836 22

Hemochromatosis is an autosomal-recessive disease which causes iron-overload of various organs including liver, pancreas and heart. This report analyzes the course of hemochromatosis in two patients (a 28-year-old man and a 57-year-old woman) in whom hemochromatosis was detected because of severe cardiomyopathy. Initial symptoms were edema, anasarca and dyspnea. Further examinations showed pleural effusion, decreased left-ventricular-function, skin pigmentation, diabetes mellitus and liver cirrhosis. Although phlebotomy treatment and iron-chelation therapy with deferoxamine initially resulted in some improvement, both patients died from cardiomyopathy three months after diagnosis. The reports of these two cases underline that hemochromatosis-associated cardiomyopathy is often irreversible if severe congestive heart failure is present. In cardiac decompensation heart transplantation has to be considered as early as possible.
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PMID:-Cardiomyopathy as the cause of death in genetic hemochromatosis-. 865 Sep 71

We describe two cases of pneumonia caused by Sho-saiko-to. Patient 1 was a 61-year-old man with type-C liver cirrhosis. About 50 days after starting to take Sho-saiko-to, he complained of fever and diarrhea, and progressive dyspnea developed. Analysis of arterial blood obtained in the emergency room showed severe hypoxemia:, PaO2 26 Torr. A chest radiograph and a CT scan showed bilateral diffuse fine granular and ground-glass opacities predominantly in the upper lung fields. Despite repeated pulse therapy with methylprednisolone and aggressive medical treatment including mechanical ventilation, the patient remained in respiratory distress, which was later complicated by gastrointestinal bleeding. He died on the 45th hospital day. The bronchoalveolar lavage contained abnormally high fluid percents of lymphocytes and neutrophils. Postmortem examination of the lungs revealed alveolar septal thickening, marked hyperplasia of type 2 pneumocytes, and no hyaline membrane formation. Patient 2 was a 68-year-old man. Eighty days after he began taking Sho-saiko-to, he presented with a 4-day history of shortness of breath accompanied by fewer and progressive coughing. On arrival of the hospital, arterial blood gas analysis showed mild hypoxemia (PaO2, 61 Torr) and a chest radiograph revealed bilateral irregular infiltrates in the lower lung fields. Analysis of bronchoalveolar lavage fluid showed an abnormally high percent of lymphocytes (especially CD8 + lymphocytes), and examination of a biopsy specimen revealed exudates of fibrin and neutrophils in the alveolar spaces and patechy intraluminal organization. The response to prednisolone was good and he was discharged on the 40th hospital day in stable condition. Drug lymphocyte stimulation tests of peripheral blood to Sho-saiko-to were positive in both patients. Patients 2 was though to have a typical case of Sho-saiko-to-induced pneumonia, patient 1 was thought to have fulminating variant of this disease.
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PMID:[Two cases of pneumonia caused by Sho-saiko-to]. 896 2

Pulmonary hypertension (PH) is a classic complication associated with intravenous drug addiction. Various pathogenic mechanisms may be involved but HIV infection now appears to be the main etiologic factor. We report herein 10 case of PH occurred in HIV+ intravenous drug abusers. Each patient had several pathogenic factors: HIV infection, pills crushed and intravenously injected (6 cases), heavy and repeated consumption of amphetamines and cocaine (6 cases), cirrhosis with portal hypertension (2 cases), anticardiolipid antibodies (2 cases). The clinical findings were similar to those reported for PH in HIV seronegative patients; however, in 5 cases, opiates could have alleviated dyspnea, which became perceptible only at the time of drug withdrawal. Because drug addicts usually exhibit a weak support for medical prescriptions, long term therapy needing regular follow-up such as anticoagulation appears to be hazardous and even dangerous. The prognosis remains poor, since the progression of PH led to the death of one third patients within the year following the diagnosis.
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PMID:[Pulmonary artery hypertension in HIV seropositive drug addicts. Apropos of 10 cases]. 955 21

The hepatopulmonary syndrome (HPS) is a reversible pulmonary insufficiency in association with liver disease, most frequently liver cirrhosis. The pathogenesis of HPS is poorly understood. HPS is characterized by arterial hypoxemia caused by intrapulmonary arteriovenous shunts or marked vasodilatation of the pulmonary vessels and ventilation-perfusion mismatch in the absence of intrinsic heart or lung disease. Typical clinical signs are dyspnea in the upright position which improves in supine position (platypnoe) and decrease of arterial pO2 in the upright position (orthodeoxia). The diagnosis of HPS is based on clinical features, arterial blood gas analyses in supine and upright position, contrast echocardiography and lung perfusion scanning. Arteriovenous fistula can be excluded by pulmonary angiography. There is no established medical treatment of HPS. New medical and noninvasive therapies, such as transjugular intrahepatic Stent-shunt (TIPS), lead to improvement of HPS. These treatment modalities need further elucidation. HPS was shown to be reversible after orthotopic liver transplantation (OLTx) in some cases. Severe HPS, therefore, may be an indication rather than a contraindication for OLTx.
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PMID:[Hepatopulmonary syndrome]. 957 9

A 66-year old man was admitted to our hospital because of vomiting, diarrhea and progressive dyspnea. Acute respiratory distress syndrome (ARDS) due to bilateral pneumonia was diagnosed and he was also in septic shock. The patient had a history of partial hepatectomy for hepatoma, and suffered from liver cirrhosis. Emergency bronchoalveolar lavage (BAL) revealed abundant gram-positive cocci and polymorphonuclear leukocytes in the collected sample. Blood culture revealed corynebacterium. Treatment consisted of mechanical ventilation and administration of fluids, effective antibiotics, and high-dose methylprednisolone (MPS). MPS was administered from the onset of ARDS with a starting dose of 1,000 mg, which was gradually reduced to 60 mg over 8 days. Pulmonary infiltrates shown on the chest X-ray film were alleviated, and arterial blood gas data rapidly improved. The patient was successfully extubated on the 10th hospital day, and discharged on the 30th hospital day. Serial BAL and plasma levels of inflammatory cytokines decreased rapidly in parallel with the improvement of the patient's clinical condition. This is a case report of severe bacterial pneumonia that was successfully treated with effective antibiotics and high-dose MPS for several days from the onset of ARDS.
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PMID:[Successfully treated acute respiratory distress syndrome with serial plasma and bronchoalveolar measurement of inflammatory cytokines]. 984 90

The hepatopulmonary syndrome (HPS) is a rare complication of liver cirrhosis and is characterised by the typical triad of liver cirrhosis, arterial hypoxemia, and intrapulmonary vascular dilatation. Except for pleural effusions associated with liver cirrhosis no other disease of the lungs or the heart is detectable. The structural hallmark of HPS is dilatation of pulmonary precapillary vessels which impairs diffusion-perfusion and causes unequal ventilation-perfusion. The diagnosis of HPS is based on PaO2 measurements when breathing room air and 100% oxygen. The increased intrapulmonary vascular diameter allows microbubbles to traverse the lung capillaries when agitated saline is administered intravenously. Only on rare occasions is a patient limited by his pulmonary impairment, the leading morbidity is that of liver disease and its classical complications. Drug therapy is of no proven benefit, oxygen supplementation might improve dyspnea. Vascular embolisation of discrete arteriovenous shunts, if present, or liver transplantation may dramatically improve pulmonary function in selected patients.
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PMID:Hepatopulmonary syndrome. 1040 94

We report the case of a patient with liver cirrhosis who successively developed hepatopulmonary syndrome and portopulmonary hypertension. Initially, the patient presented with severe dyspnea and hypoxemia at rest. Technetium-99 macroaggregated albumin lung perfusion scan demonstrated right-to-left shunt, and hemodynamic study revealed a hyperdynamic state with low pulmonary vascular resistance, thus confirming the diagnosis of hepatopulmonary syndrome. More than 2 years after the onset of pulmonary symptoms, a marked improvement in dyspnea and gas exchange was observed. Lung perfusion scan did not disclose any right-to-left shunt and right-sided heart catheterization showed evidence of severe pulmonary hypertension. We conclude that hepatopulmonary syndrome and portopulmonary hypertension are not mutually exclusive. We hypothesize that, by reversing the phenomenon of intrapulmonary vasodilatation, the development of portopulmonary hypertension interfered with each of the potential causes of hypoxemia in hepatopulmonary syndrome (ventilation-perfusion inequalities, intrapulmonary shunting, oxygen diffusion limitation) and, as a result, led to a correction of hypoxemia.
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PMID:Pulmonary hypertension following hepatopulmonary syndrome in a patient with cirrhosis. 1045 52

This review summarizes current strategies in the treatment of patients with pleural effusion. To determine whether a patient has a transudative or exudative pleural effusion, Light's criteria should be applied to measure the concentrations of protein and lactate dehydrogenase (LDH) in the pleural fluid and serum. If the effusion is transudative, therapy should be directed toward the underlying congestive heart failure, cirrhosis, or nephrosis. Consideration should be given to pleurodesis with a sclerosant if patients with recurrent transudative effusion have severe dyspnea due to their effusion. If the effusion is exudative, attempts should be made to define the etiology. The diagnosis of pleural malignancy is most easily established via pleural fluid cytology. If this is negative and the patient is suspected of having pleural malignancy, thoracoscopy is indicated. The concentrations of adenosine deaminase and gamma-interferon in pleural fluid are useful in the diagnosis of pleural tuberculosis. Patients with pneumonia and pleural effusion should undergo therapeutic thoracentesis; the pleural fluid should be Gram-stained and cultured, and the differential cell count, glucose and LDH concentration, and pH should be determined. Indicators of a poor prognosis include the presence of frank pus, a positive Gram-stain, a pleural glucose concentration of less than 2.2 mmol/L, a pH less than 7.00, the presence of pleural loculations, and an LDH concentration greater than three times the upper limit of normal in serum. If the pleural fluid cannot be completely evacuated because of loculations, intrapleural thrombolytic therapy should be considered. If thrombolytics are ineffective, thoracoscopy or thoracotomy with decortication should be performed. Dyspneic patients with malignant pleural effusions whose dyspnea is relieved with therapeutic thoracentesis should be considered for pleurodesis using a tetracycline derivative. Talc is not recommended because it induces acute respiratory distress syndrome in about 5% of patients, with an overall mortality of 1%.
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PMID:Management of pleural effusions. 1092 61


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