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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Macro- and microvascular diseases are the main chronic complications of diabetes mellitus (DM). 2. It has been shown that DM patients have more severe nailfold microcirculatory disturbances than patients with liver cirrhosis or systemic lupus erythematosus (SLE). 3. It has been shown that the glomerular basement membrane of diabetic rats is significantly thickened compared with that of normal rats (295.5 +/- 45.1 vs 184.8 +/- 33.2 nm). 4. Gastric mucosal blood flow (GMBF) in 41 patients with non-insulin-dependent diabetes mellitus (NIDDM) was determined with a laser Doppler flowmeter. The results showed that average GMBF values at 14 sites in the gastric mucosa were significantly lower in NIDDM patients than in control subjects. 5. The percentage of painless acute myocardial infarction (AMI) among 50 patients with DM was 22.0% and the mortality of AMI was 22.0% (11 cases). Both these values were higher than the corresponding values in patients without DM (9.9 and 11.4%, respectively; P < 0.05). 6. Cerebrovascular disease is more prevalent in diabetic patients than in non-diabetics and the mortality of stroke in DM patients is two-fold higher than that of non-diabetic patients. 7. Diabetes can result in widespread macrovascular atherosclerosis and microcirculatory disorders of multiple organs.
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PMID:Vascular complications of diabetes mellitus. 1062 65

This study was carried out to investigate the relationship between lipoprotein (a) levels and the development of atherosclerosis in chronic renal failure (CRF) patients with the possible role of the liver. Serum Lp (a) levels were measured in samples from 20 CRF patients on hemodialysis (HD), 20 liver cirrhosis (LC) patients, 20 patients having both CRF and LC and undergoing HD, and 20 normal control subjects. Renal function (blood urea nitrogen (BUN) and creatinine), hepatic function (transaminases (ALT and AST), alkaline phosphatase (ALP) and total bilirubin) investigations and serum cholesterol were carried out for all the subjects enrolled in this study. Serum Lp (a) concentration in CRF patients without LC was 87.25 +/- 6.17 mg/dl, which was significantly higher than all the investigated groups (P < 0.001). Lp (a) concentration in patients with both CRF and LC was 24.65 +/- 1.98 mg/dl, which was not significantly different from the controls, but was significantly higher than that in the subjects with LC only (P < 0.001) where the latter group had significantly low Lp (a) values (11.1 +/- 0.99) relative to all the other groups (P < 0.001). Lp (a) correlated positively with cholesterol in all groups except the LC subjects, but did not correlate with age, or renal function in both CRF groups.
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PMID:Serum lipoprotein (a) levels in chronic renal failure and liver cirrhosis patients. Relationship with atherosclerosis. 1068 47

The significance of the pronounced durable systemic arterial hypotension (SAH) in the origin of an acute postoperative ischemic hepatitis (APIH) was established, basing on the analysis of 40 clinical observations. Its occurrence is promoted by hemorrhage with 30% and more the circulating blood volume (CBV) deficiency, chronic cardiovascular system and pulmonary diseases, liver cirrhosis, shock, massive infusions of the blood and its components, the abdominal aorta atherosclerosis with stenosis of tr. coeliacus, a. hepatica. Forgoing SAH, the presence of promoting factors, jaundice, the transpherase activity raising in 3-5 times, the level of blood coagulating factors reduction, stable intestinal paresis were diagnostically significant symptoms. Experimental model of an APIH was elaborated in dogs, which occurs due to hypotension, caused by CBV reduction by 40% during two hours. The refractoriness of a. hepatica propria to the blood reinfusion was established. In the APIH occurrence threat the perftoran application in the 20 ml/kg dosage is the prophylaxis method as well as the method of the curative tactics choice.
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PMID:[Acute postop ischemic hepatitis and hypotension]. 1085 79

Cardiogenic shock developed in a 72-year-old Japanese woman during combination therapy with verapamil and atenolol for recurrent supraventricular arrhythmia. She had coronary atherosclerosis, liver cirrhosis and bradycardia-tachycardia syndrome. Despite of the high-dose catecholamines and counterpulsation, she progressively deteriorated. Bolus administration of intravenous calcium chloride (CaCl2) immediately resolved her hemodynamic collapse.
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PMID:Cardiogenic shock triggered by verapamil and atenolol: a case report of therapeutic experience with intravenous calcium. 1111 Apr 38

Atherosclerosis is manifested as coronary artery disease (CAD), ischemic stroke and peripheral vascular disease. Moderate alcohol consumption has been associated with reduction of CAD complications. Apparently, red wine offers more benefits than any other kind of drinks, probably due to flavonoids. Alcohol alters lipoproteins and the coagulation system. The flavonoids induce vascular relaxation by mechanisms that are both dependent and independent of nitric oxide, inhibits many of the cellular reactions associated with atherosclerosis and inflammation, such as endothelial expression of vascular adhesion molecules and release of cytokines from polymorphonuclear leukocytes. Hypertension is also influenced by the alcohol intake. Thus, heavy alcohol intake is almost always associated with systemic hypertension, and hence shall be avoided. In individuals that ingest excess alcohol, there is higher risk of coronary occlusion, arrhythmias, hepatic cirrhosis, upper gastrointestinal cancers, fetal alcohol syndrome, murders, sex crimes, traffic and industrial accidents, robberies, and psychosis. Alcohol is no treatment for atherosclerosis; but it doesn't need to be prohibited for everyone. Thus moderate amounts of alcohol (1-2 drinks/day), especially red wine, may be allowed for those at risk for atherosclerosis complications.
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PMID:Alcohol and atherosclerosis. 1124 69

During the last decades efforts regarding dietary iron supply focused mostly on the prevention of deficiencies, especially during growth and pregnancy. Correspondingly, homeostatic mechanisms increase intestinal iron absorption in iron deficiency, but its downregulation at high intake levels seems insufficient to prevent accumulation of high iron stores at high intake. There is no regulated iron excretion in overload. Excess of pharmaceutical iron may cause toxicity and therapeutic doses may cause gastrointestinal side effects. Chronic iron excess, e.g. in primary and secondary hemochromatosis, may lead to hepatic fibrosis, diabetes mellitus and cardiac failure. Chronic intake of 50-100 mg Fe/day of highly bioavailable iron with home-brewed beer in sub-Saharan Africans lead to cirrhosis and diabetes. Applying a safety factor of 2 would lead to an upper safe level of 25-50 mg Fe/day for this endpoint of conventional iron toxicity. However, beyond this kind of damage iron is known to catalyze the generation of hydroxyl radicals from superoxide anions and to increase oxidative stress which, in turn, increases free iron concentration. This self-amplifying process may cause damage to lipid membranes and proteins, which relates radical generation and organ damage after ischemia-reperfusion events to available free iron in clinical and experimental settings. Correspondingly, epidemiological studies as well as observations in heterozygotes for hereditary hemochromatosis suggest that the risk of atherosclerosis and acute myocardial infarction is related to body iron stores, though there is conflicting epidemiological evidence as well. The most recent and best controlled studies, however, support the hypothesis that iron stores are related to cardiovascular risk. Iron-amplified oxidative stress may also increase DNA damage, oxidative activation of precancerogens and support tumor cell growth. This is supported by experimental, clinical and epidemiological observations. Due to these mechanisms high iron stores may present a health hazard. Though this has not been finally proven, available evidence strongly recommends not to increase iron intake beyond physiological requirements. To avoid iron deficiency symptoms, on the other hand, care must be taken to meet recommended daily intake.
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PMID:Safety aspects of iron in food. 1142

Obesity is associated with a number of metabolic and haemodynamic risk factors for cardiovascular disease and type 2 diabetes mellitus. This risk depends on a complex of metabolic and haemodynamic consequences of (visceral) fat accumulation, which probably results from the continuous delivery of fatty acids to the liver via the portal vein. Hypertriglyceridaemia, hyperinsulinaemia, hypertension, insulin resistance and increased hepatic glucose production are all independent risk factors for atherosclerosis. Their combination increases the risk of cardiovascular disease considerably. Triglyceride storage in hepatocytes is another consequence of increased fatty acid supply to the liver. Until recently, hepatic steatosis was considered a harmless condition secondary to obesity or alcoholism. However, it may lead to non-alcoholic hepatic steatosis, which predisposes to liver fibrosis and even cirrhosis.
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PMID:[Abdominal obesity: metabolic complications and consequences for the liver]. 1160 19

Platelet-derived growth factor (PDGF) overactivity has been implicated in atherosclerosis and several fibrotic conditions including lung and kidney fibrosis, liver cirrhosis and myelofibrosis. Low oxygen tension (hypoxia) is a known stimulus for transcriptional induction of PDGF ligand and receptor genes in different tissues. We studied the expression and localization of PDGF-A, PDGF-B, and PDGF receptor (PDGFR)-alpha and -beta subunits in adult rat isolated corpus cavernosum (CC) under generalized transient hypoxia (pO(2) 10%) in comparison with normoxic conditions. Semi-quantitative RT-PCR analysis of mRNA extracted from rat penis showed higher amounts of PDGF-A, PDGF-B and PDGFR-beta mRNA transcripts in hypoxic versus normoxic animals. The immunohistochemical analysis showed that the localization of PDGF subunits and PDGFR-beta was confined to the cytoplasm of the perivascular smooth muscle cells, endothelium and trabecular fibroblasts. Our findings indicate that transient low oxygen tension induces PDGF overexpression in rat CC, which in the long term may lead to an increase of connective tissue production. We suggest that a local impairment of the PDGF/PDGFR system may contribute to CC fibrosis, which is an established cause of erectile dysfunction in man.
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PMID:Platelet-derived growth factor (PDGF) and PDGF receptors in rat corpus cavernosum: changes in expression after transient in vivo hypoxia. 1147 35

The endothelium, a continuous cellular monolayer lining the blood vessels, has an enormous range of important homeostatic roles. It serves and participates in highly active metabolic and regulatory functions including control of primary hemostasis, blood coagulation and fibrinolysis, platelet and leukocyte interactions with the vessel wall, interaction with lipoprotein metabolism, presentation of histocompatibility antigens, regulation of vascular tone and growth and further of blood pressure. Many crucial vasoactive endogenous compounds like prostacyclin, thromboxane, nitric oxide, endothelin, angiotensin, endothelium derived hyperpolarizing factor, free radicals and bradykinin are formed in the endothelial cells to control the functions of vascular smooth muscle cells and of circulating blood cells. These versatile and complex systems and cellular interactions are extremely vulnerable. The balances may be disturbed by numerous endogenous and exogenous factors including psychological and physical stress, disease states characterized by vasospasm, inflammation, leukocyte and platelet adhesion and aggregation, thrombosis, abnormal vascular proliferation, atherosclerosis and hypertension. The endothelial cells are also the site of action of many drugs and exogenous toxic substances (e.g. smoking, alcohol). As markers and assays for endothelial dysfunction, direct measurement of nitric oxide, its metabolites from plasma and urine, functional measurement of vascular nitric oxide dependent responses and assay of different circulating markers have been used. In numerous pathological conditions (e.g. atherosclerosis, hypertension, congestive heart failure, hyperhomocysteinemia, diabetes, renal failure, transplantation, liver cirrhosis) endothelial dysfunction has been described to exist. Some of them, as well as hormonal and nutritional factors and drug treatment will be discussed in this short review.
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PMID:Clinically important factors influencing endothelial function. 1153 60

Thrombomodulin is a glycoprotein that can bind to thrombin and activate protein C, thus mitigating the effects of cytokines produced by inflammatory and immunological processes. The molecule exerts a protective function on endothelial cells. Thrombomodulin is cleaved to its soluble form by neutrophil elastase and by other substances produced during acute and chronic inflammatory responses, immunologic reactions and complement activation. ELISA technique yields normal serum levels of 3.1 +/- 1.3 ng/ml; in males these levels are higher; TM levels also rise during menopause. Other circumstances associated with an increase of serum TM levels are smoking, disseminated intravascular coagulation (DIC), cardiac surgery, atherosclerosis, ARDS, liver cirrhosis, diabetes mellitus, cerebral and myocardial infarction, and multiple sclerosis. Serum levels of TM represent an useful prognostic index, because they are associated with an increase in mortality rate, or however a progression of the underlying pathological condition.
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PMID:Clinical importance of thrombomodulin serum levels. 1155 26


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