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)

The morbidity and mortality burden of heart valve disease is increasing in the developing world, especially among the elderly. Whereas surgery remains the standard of care in fit patients with degenerative aortic stenosis, percutaneous aortic valve replacement could become an effective alternative to surgery in selected higher risk patients. The authors report on two women with aortic stenosis, both at high surgical risk (an 81-year-old female with coronary artery and cerebro-vascular disease, and a 70-year-old female with end-stage cirrhosis), in whom percutaneous valve replacement was effectively performed by means of transfemoral access and retrograde CoreValve Re-valving System implantation. Two major post-procedural complications occurred, both effectively managed, in the second patient: a third degree atrio-ventricular block (requiring permanent pace-maker implantation) and bleeding from the right femoral artery access (requiring implantation of two covered stents and blood transfusion). Despite the increased baseline risk, both patients were discharged asymptomatic, the first twelve days and the other three weeks after admission. In the authors' experience percutaneous aortic valve replacement can be performed with reasonable safety in patient with severe aortic stenosis at high surgical risk.
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PMID:Percutaneous aortic valve replacement in two cases at high surgical risk: procedural details and implications for patient selection. 1920 24

Vaquez and Aubertin advance three theories in explanation of the adrenal hyperplasia; first, that it may not be the cause of hypertension but "an antitoxic hyperplasia" caused by the retained products of metabolism which may be responsible also for the hypertension; second, that it may be the cause of hypertension but secondary to the renal lesion; third, that it may be the cause of hypertension but may antedate the renal lesion or be entirely independent of it. They, as well as other French writers, insist that this hyperplasia is almost constantly associated with chronic nephritis of the interstitial type and it is seldom found with the parenchymatous type of nephritis, or with other lesions. Hyperplasia of the adrenal, as far as my material enables one to judge, does not occur during the first and second decades. In the third decade it is relatively frequent in the absence of chronic arterial and renal disease but reaches the maximum in association with such disease after the fourth decade. It is an almost constant lesion in arteriosclerosis associated with chronic interstitial nephritis and left-sided heart hypertrophy, but occurs with almost equal frequency in arteriosclerosis with chronic nephritis of the parenchymatous type. It is a relatively frequent lesion of arteriosclerosis without chronic nephritis and of the latter without arteriosclerosis also. As the result of this analysis one is led to the view that while hyperplasia of the adrenal is a very frequent concomitant of chronic renal and arterial disease it is not exclusively a feature of either type of nephritis or yet of chronic vascular disease; but it probably represents the effect of some factor operating in that period of life in which chronic renal and arterial affections are most frequent. Worthy of special emphasis is the observation that the characteristic lesion of an adrenal, the seat of local arteriosclerosis, is of the type of the chronic productive inflammation seen in arteriosclerosis of the pancreas and kidney; that is, thickening of the vessels, increase of connective tissue and round cell infiltration. Associated with these changes is a hyperplasia which is very constant, and which may be, in part, of the nature of a compensatory hyperplasia similar to that seen in the liver of cirrhosis and acute yellow atrophy. A hyperplasia of this type, as has been shown, may occur in destructive lesions of the gland. This, however, does not explain hyperplasia in the absence of local vascular changes which fact is, possibly, as suggested by Landau, evidence, not of a correlation between kidney and adrenal, but of a vicarious hypertrophy depending upon lesions of some other organ of the body than the kidney, possibly some other ductless gland, affected by arteriosclerosis or other disease.
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PMID:THE RELATION OF LESIONS OF THE ADRENAL GLAND TO CHRONIC NEPHRITIS AND TO ARTERIOSCLEROSIS; AN ANATOMICAL STUDY. 1986 60

The pathogenesis, incidence, complication rates, response to acid suppression and Helicobacter pylori (H. pylori) eradication therapy in peptic ulcer associated with chronic disease such as liver cirrhosis, chronic renal failure, diabetes mellitus, and critically ill conditions are different from those with general population, so that the management strategies also should be differentiated. The eradication of H. pylori are not so effective for preventing recurrence of peptic ulcer in liver cirrhosis patients as shown in general population, and conservative managements such as preventing deterioration of hepatic function and decrease in portal pressure are mandatory to reduce the risk of ulcer recurrence. The standard triple therapy for H. pylori eradication are as effective in chronic renal failure patients as in normal population, but the frequency of side effects of amoxicillin is higher in the patients not receiving dialysis therapy. Delay in eradication therapy until beginning of dialysis therapy or modification of eradication regimen should be considered in such cases. High prevalence of asymptomatic peptic ulcers and increased mortality in complicated peptic ulcer disease warrant regular endoscopic surveillance in diabetic patients, especially with angiopathy. The prolongation of duration of eradication therapy also should be considered in diabetic patients with angiopathic complication because of lower eradication rate with standard triple regimens as compared to normal population. Prophylactic acid suppressive therapy is highly recommended in critically ill patients with multiple risk factors. Herein, we propose evidence-based treatment guidelines for the management of peptic ulcer disease in special conditions based on literature review and experts opinion.
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PMID:[Guidelines of treatment for peptic ulcer disease in special conditions]. 1993 13

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

Gastric antral vascular ectasia (GAVE) syndrome is an uncommon but well-described cause of recurrent upper gastrointestinal bleeding or iron deficiency anaemia. Atiology is unknown but several associated diseases have been reported like connective tissue or autoimmune disorders or cirrhosis. Cases have been reported in systemic sclerosis, achlorhydia, atrophic gastritis and chronic renal failure. The most common cause is portal hypertension and portal hypertensive gastropathy. This is especially so after eradication of oesophageal varices by sclerotherapy or banding. Diabetic complications are characterised by microvascular diseases especially in the retina, glomerulus and vasa nervorum. It involves apoptosis and remodelling of endothelial cells. Hyperglycaemia is an essential cause of reactive oxygen species (ROS)-mediated oxidative stress in this complication. Angiopathy of gastric mucosa in diabetes mellitus has not been reported so far in the literature. We are presenting an interesting case of diabetes mellitus with gastric vascular ectasia without evidence of any other systemic illness.
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PMID:Gastric antral vascular ectasia (GAVE) in a non-cirrhotic patients with diabetes: case report and possible pathophysiological mechanism. 2273 55

Up to 60 percent of adults report that they have had nocturnal leg cramps. The recurrent, painful tightening usually occurs in the calf muscles and can cause severe insomnia. The exact mechanism is unknown, but the cramps are probably caused by muscle fatigue and nerve dysfunction rather than electrolyte or other abnormalities. Nocturnal leg cramps are associated with vascular disease, lumbar canal stenosis, cirrhosis, hemodialysis, pregnancy, and other medical conditions. Medications that are strongly associated with leg cramps include intravenous iron sucrose, conjugated estrogens, raloxifene, naproxen, and teriparatide. A history and physical examination are usually sufficient to differentiate nocturnal leg cramps from other conditions, such as restless legs syndrome, claudication, myositis, and peripheral neuropathy. Laboratory evaluation and specialized testing usually are unnecessary to confirm the diagnosis. Limited evidence supports treating nocturnal leg cramps with exercise and stretching, or with medications such as magnesium, calcium channel blockers, carisoprodol, or vitamin B(12). Quinine is no longer recommended to treat leg cramps.
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PMID:Nocturnal leg cramps. 2296 30

Portal vein thrombosis (PVT) is one of the most common vascular disorders of the liver with significant morbidity and mortality. Large cohort studies have reported a global prevalence of 1%, but in some risk groups it can be up to 26%. Causes of PVT are cirrhosis, hepatobiliary malignancy, abdominal infectious or inflammatory diseases, and myeloproliferative disorders. Most patients with PVT have a general risk factor. The natural history of PVT results in portal hypertension leading to splenomegaly and the formation of portosystemic collateral blood vessels and esophageal, gastric, duodenal, and jejunal varices. Diagnosis of PVT is made by imaging, mainly Doppler ultrasonography. According to its time of development, localization, pathophysiology, and evolution, PVT should be classified in every patient. Some clinical features such as cirrhosis, hepatocellular carcinoma, and hepatic transplantation are areas of special interest and are discussed in this review. The goal of treatment of acute PVT is to reconstruct the blocked veins. Endoscopic variceal ligation is safe and highly effective in patients with variceal bleeding caused by chronic PVT. In conclusion, PVT is the most common cause of vascular disease of the liver and its prevalence has being increasing, especially among patients with an underlying liver disease. All patients should be investigated for thrombophilic conditions, and in those with cirrhosis, anticoagulation prophylaxis should be considered.
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PMID:Portal vein thrombosis: what is new? 2553 38

Non-alcoholic fatty liver disease (NAFLD) is a major cause of liver disease around the world. It includes a spectrum of conditions from simple steatosis to non-alcoholic steatohepatitis (NASH) and can lead to fibrosis, cirrhosis, liver failure, and/or hepatocellular carcinoma. NAFLD is also associated with other medical conditions such as obesity, diabetes mellitus (DM), metabolic syndrome, hypertension, insulin resistance, hyperlipidemia, and cardiovascular disease (CVD). In diabetes, chronic hyperglycemia contributes to the development of both macro- and microvascular conditions through a variety of metabolic pathways. Thus, it can cause a variety of metabolic and hemodynamic conditions, including upregulated advanced glycation end-products (AGEs) synthesis. In our previous study, the most abundant type of toxic AGEs (TAGE); i.e., glyceraldehyde-derived AGEs, were found to make a significant contribution to the pathogenesis of DM-induced angiopathy. Furthermore, accumulating evidence suggests that the binding of TAGE with their receptor (RAGE) induces oxidative damage, promotes inflammation, and causes changes in intracellular signaling and the expression levels of certain genes in various cell populations including hepatocytes and hepatic stellate cells. All of these effects could facilitate the pathogenesis of hypertension, cancer, diabetic vascular complications, CVD, dementia, and NASH. Thus, inhibiting TAGE synthesis, preventing TAGE from binding to RAGE, and downregulating RAGE expression and/or the expression of associated effector molecules all have potential as therapeutic strategies against NASH. Here, we examine the contributions of RAGE and TAGE to various conditions and novel treatments that target them in order to prevent the development and/or progression of NASH.
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PMID:Involvement of the TAGE-RAGE system in non-alcoholic steatohepatitis: Novel treatment strategies. 2554 75

Nonalcoholic fatty liver disease (NAFLD) ranges from simple steatosis to nonalcoholic steatohepatitis (NASH), leads to fibrosis and potentially cirrhosis, liver failure, and hepatocellular carcinoma, and is one of the most common causes of liver disease worldwide. NAFLD has also been implicated in other medical conditions such as insulin resistance, obesity, metabolic syndrome, hyperlipemia, hypertension, cardiovascular disease, and diabetes. Continuous hyperglycemia has been implicated in the pathogenesis of diabetic micro- and macro-vascular complications via various metabolic pathways, and numerous hyperglycemia-induced metabolic and hemodynamic conditions exist, including the increased generation of various types of advanced glycation end-products (AGEs). We recently demonstrated that glyceraldehyde-derived AGEs (Glycer-AGEs), the predominant components of toxic AGEs (TAGE), played an important role in the pathogenesis of angiopathy in diabetic patients. Moreover, a growing body of evidence suggests that the interaction between TAGE and the receptor for AGEs may alter intracellular signaling, gene expression, and the release of pro-inflammatory molecules and also elicits the generation of oxidative stress in numerous types of cells including hepatocytes and hepatic stellate cells. Serum levels of TAGE were significantly higher in NASH patients than in those with simple steatosis and healthy controls. Moreover, serum levels of TAGE inversely correlated with adiponectin (adiponectin is produced by adipose tissue and is an anti-inflammatory adipokine that can increase insulin sensitivity). Furthermore, immunohistochemical staining of TAGE showed intense staining in the livers of patients with NASH. Serum levels of TAGE may be a useful biomarker for discriminating NASH from simple steatosis. The administration of atorvastatin (10 mg daily) for 12 months significantly improved NASH-related metabolic parameters and significantly decreased serum levels of TAGE. The steatosis grade and NAFLD activity score were also significantly improved. These results demonstrated that atorvastatin decreased the serum levels of TAGE in NASH patients with dyslipidemia and suggest the usefulness of TAGE as a biomarker for the attenuation of NASH. Serum levels of TAGE were significantly higher in non-B or non-C hepatocellular carcinoma (NBNC-HCC) patients than in NASH subjects without HCC or control subjects. TAGE may be involved in the pathogenesis of NBNC-HCC, and could, therefore, be a biomarker that could discriminate NBNC-HCC from NASH. We propose that serum levels of TAGE are promising novel targets for the diagnosis of and therapeutic interventions against NASH.
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PMID:Serum levels of toxic AGEs (TAGE) may be a promising novel biomarker in development and progression of NASH. 2569 14

Vascular disorders of the liver frequently affect women of childbearing age. Pregnancy and the postpartum are prothrombotic states. Pregnancy seems to be a trigger for Budd-Chiari syndrome in patients with an underlying prothrombotic disorder. Whether pregnancy is a risk factor for other vascular liver disorders is unknown. In women with a known vascular liver disorder and a desire for pregnancy, stabilisation of the liver disease, including the use of a portal decompressive procedure when indicated, should be reached prior to conception. The presence of esophageal varices should be screened and adequate prophylaxis of bleeding applied in a manner similar to what is recommended for patients with cirrhosis. Most women likely benefit from anticoagulation during pregnancy and the postpartum. Labor and delivery are best managed by a multidisciplinary team with experience in this situation. Assisted vaginal delivery is the preferred mode of delivery. Although the risk of miscarriage and premature birth is heightened, current management of these diseases makes it very likely to see the birth of a live baby when pregnancy reaches 20 weeks of gestation.
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PMID:Pregnancy and vascular liver disease. 2594 32


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