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)

We previously studied fibrinolysis and fibrinogenolysis by analyzing fragments of fibrin/fibrinogen degradation products (FDP) employing sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblotting. In this report, we characterized the fragments of FDP in three patients with increased serum FDP, that were caused by various diseases. In the patient suffering from tuberculous constrictive pericarditis (case 1), the most part of the FDP fragments were DD and D. In the patient suffering from infection in addition to liver cirrhosis (case 2), the most part of the FDP fragments were high molecular weight (HMW) and D. In case 1 and 2, serum FDP levels were increased in parallel with the elevations of CRP levels. Although DD and HMW fragments were remarkably increased in case 1 and 2 with our immunoblotting analysis, DD levels assayed with LPIA system were much lower than FDP levels. The reason this discrepancy was explained by the observation that affinities of the monoclonal antibody used in LPIA system with DD and HMW fragment were markedly lower than that to DD-E fragment. In the patient suffering from deep vein thrombosis probably caused by steroid therapy of nephrotic syndrome (case 3), the most part of detected FDP fragments were DD and HMW in the period when APTT was shorter than normal, whereas D was mainly observed in the period when APTT was normal. In case 3, FDP and DD levels were increased in parallel with the shortening of APTT. In these non-DIC patients, increased serum FDP levels were induced by the presence of ascites and/or pleural effusion plus infection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Studies on the fragments of FDP in 3 non-DIC patients with increased FDP levels in the sera]. 836 Oct 25

We describe the case of a patient with non A-non B post-transfusional cirrhosis and type-II mixed cryoglobulinemia, who showed in relation with said processes several acute symptoms of vasculitis, polyarthritis, pericarditis and autoimmune hemolytic anemia, finally dying due to an advanced hepatocellular insufficiency. In this patient the determination of antibodies against hepatitis C virus (anti-HCV) was positive, that is why we assume a possible relationship between both processes and the first literature references, after the clonation of the hepatitis C virus (HCV) genome, are reviewed.
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PMID:[Mixed type-II cryoglobulinemia associated with a chronic hepatitis C virus infection]. 838 74

Pleural effusion (PE) has been increasingly diagnosed over the last eight years in the Department of Internal Medicine of the Centre Hospitalier of Kigali, Rwanda. To determine the etiology of PE and to examine its possible association with HIV-1 infection and tuberculosis (TB), the authors performed an etiological work-up, including thoracocentesis and pleural punch biopsy, of all new patients with PE of undetermined etiology referred to the Division of Pulmonary Diseases at the hospital between September 14, 1988, and October 16, 1989. 81 men and 46 women of mean age 34 years were enrolled in the study. Pleural TB was diagnosed in 86% and confirmed histologically and/or bacteriologically in 82%. 82 of the 98 pleural TB patients tested for antibody to HIV-1 were HIV-1-seropositive. Metastatic cancer was responsible for PE in six patients, Kaposi's sarcoma in three, lymphoma in one, anaplastic carcinoma in one, and adenocarcinoma in one. Non-TB pneumonia was documented in five patients and was associated with HIV-1 infection in four. Other causes of PE were congestive heart failure, decompensated cirrhosis, constrictive pericarditis, or undetermined; only one of these latter patients was HIV-seropositive. The authors therefore found TB to be the predominant cause of PE and it is strongly associated with HIV-1 infection. In an African area highly endemic for HIV-1 and Mycobacterium tuberculosis co-infection, PE should therefore be considered a good marker of TB as well as HIV-1 infection.
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PMID:Pleural effusion, tuberculosis and HIV-1 infection in Kigali, Rwanda. 844 20

Fibrosis is an ubiquitous process. Any tissue injury can culminate in fibroblast accumulation and multiplication with collagen synthesis and deposition. A large number of chronic disease states such as rheumatic heart disease, constrictive pericarditis, cirrhosis of the liver, renal interstitial fibrosis, chronic interstitial lung disease are characterized by extensive fibrosis. In many of these patients, when there is no clinical or laboratory evidence of previous injury, it is presumed that the initiating insult/injury had been 'subclinical'. I propose that 1) the fibroblasts can be activated even in the absence of preceding inflammation, 2) it is the type of 'fibroblast clone' in a given individual together with the 'milieu' in a particular tissue/organ which decides the occurrence and severity of subsequent fibrosis. This fibroblast clonal theory adds a new dimension to the pathogenesis of various disease states and may help in identifying those at high-risk and in evolving a unified therapeutic strategy for amelioration of various disorders characterized by extensive fibrosis.
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PMID:Abnormal fibroblast clone--an alternative hypothesis for pathogenesis of rheumatic heart disease. 845 63

The blood flow in the hepatic veins can normally be studied easily by Doppler ultrasound. The pattern of blood flow in normal individuals is described, and its relation to the cardiac cycle and changing pressure in the right atrium. The blood flow shows variations in healthy persons, and may change in cases of heart disease and hepatic disease. Conditions such as atrial fibrillation, tricuspid regurgitation, abnormal relaxation, restrictive cardiomyopathy, constrictive pericarditis and cardiac tamponade are reflected in the hepatic veins, and the pattern of blood flow may help in diagnosis, and in grading the pathology. In cirrhosis and portal hypertension the heart-synchronous variation in velocity is reduced. This is due to increased resistance to blood flow across the liver and the pressure gradient becoming larger than the variations in pressure in the right atrium.
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PMID:[Doppler ultrasound of blood flow in the hepatic veins]. 918 59

The authors report the cases of two patients suffering from ascites attributed for several years to a non pericarditic aetiology. The first patient presented with a diagnosis of right cardiac failure secondary to a right myocardial infarction. Cardiac catheterisation, magnetic resonance imaging and transoesophageal echocardiogram allowed to establish the diagnosis. In the second case, ascites was attributed to cirrhosis. Presence of pericardial calcifications, visible on a chest X-Ray led to suspect constrictive pericarditis. In both cases, ascites contained a high protein level. A pericardectomy allowed a favourable outcome in both cases. Thus, a diagnosis of constrictive pericarditis must be evoked in face of ascites of unclear origin and a normal cardiac size.
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PMID:[Unexpected origin of recurrent ascites: apropos of 2 cases]. 941 20

We report the case of a patient with refractory ascitis due to a constrictive pericarditis who underwent a liver transplantation with the initial diagnosis of cryptogenic cirrhosis. The cardiac origin was suspected 5 months post surgery when a liver biopsy showed lesions in favor of a post sinusoidal shunt. The diagnosis was confirmed by the increased values of the right intra-ventricular pressures. We discuss the causes of the delay of the diagnosis and, in particular, the difficulty to interpret vascular liver lesions. Such vascular lesions were present on the needle biopsy performed prior to transplantation but wrongly interpreted as cirrhosis.
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PMID:[Liver transplantation and constrictive pericarditis]. 1139 79

Chylous ascites and chylothorax are rare clinical entities and usually caused by neoplasms, particularly lymphomas, liver cirrhosis, superior vena cava thrombosis, nephrotic syndrome, and some cardiac events such as dilated cardiomyopathy or right heart failure. Constrictive pericarditis is an extremely rare cause of this clinical state. We report a 41-year-old male patient undergoing haemodialysis who presented with chylous ascites and chylothorax. Echocardiography and heart catheterisation revealed constrictive pericarditis. He underwent pericardiectomy and after the operation the ascites and pleural effusion resolved rapidly. We suggest that constrictive pericarditis should be considered in the differential diagnosis of chylous ascites and chylothorax.
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PMID:Chylous ascites and chylothorax due to constrictive pericarditis in a patient undergoing haemodialysis. 1512 33

Hepatocellular carcinoma (HCC) is one of the most common malignancies. Many factors are considered to be etiology associated with HCC; the important factors are hepatitis B and C viruses and alcohol. Cirrhosis is present in the majority of patients with HCC. It is assumed that all diseases, which lead to liver cirrhosis, may be complicated by the development of HCC. We report a 36-year-old man with HCC which developed from cardiac cirrhosis caused by constrictive pericarditis in whom both hepatitis B virus and hepatitis C viral marker tests were all negative. CT scan of his heart showed pericardial calcification with diastolic dysfunction of right ventricle. Abdominal CT scan revealed mottled mosaic pattern of contrast enhancement of liver parenchyme and two hepatic lesions that were considered to be HCCs. Left lateral segmentectomy of liver was performed. There were two well-circumscribed masses which were confirmed to be HCC and the remaining hepatic parenchyma showed bridging fibrosis between central zonal regions. To our knowledge, this is the first case of HCC complicating cardiac cirrhosis in Korea.
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PMID:[A case of hepatocellular carcinoma complicating cardiac cirrhosis caused by constrictive pericarditis]. 1597 79

A 55-year-old man was admitted with a four-month history of lethargy, dyspnea and ascites. An idiopathic liver cirrhosis was suspected to be responsible for these symptoms and for elevated hepatic enzymes on blood tests. A few months before he had an angioplasty on the left anterior descending artery for an acute coronary syndrome (ACS). The intervention was complicated by coronary perforation which required the implantation of a polytetrafluoroethylene-covered (PTFE) stent to seal the rupture. On admission, pressure measurements during cardiac catheterism revealed a typical right ventricular dip-plateau consistent with the diagnosis of constrictive pericarditis (CP). Magnetic resonance imaging (RMI) showed localized pericardial thickening next to the right ventricle. We suspect hemopericardium, due to coronary perforation, is responsible for constrictive pericarditis. This mid-term complication of coronary rupture has not been reported before and should be suspected in this particular clinical setting.
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PMID:An unusual mid term complication of coronary rupture. 1601 14


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