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)

In a group of 80 patients (50 male and 30 female) aged between 44 and 65, affected by alcoholic liver disease (46 with steatosis and 34 with liver cirrhosis) the Authors examined the relationship between the plasma lipid, in particular of Lp(a), and the incidence of vascular atherosclerotic plaques. The results were compared with those found in the controls (50 subjects of similar age, social and working status to that of the above patients but nondrinkers without liver or other metabolic disease). In the patients with steatosis we found a moderate increase in plasma lipid fractions including total, HDL and LDL cholesterol, but low levels of Lp(a), with an incidence of arterial plaques of 10.86%. In those with liver cirrhosis the findings were characterized by low levels of lipids and in particular of Lp(a), with an incidence of arterial plaques of 8.82%, decidedly less marked than in the controls (16%). In both cases the low incidence of vascular involvement appears to be in some way linked with low levels of Lp(a) and the severity of liver disease and not with the behaviour of HDL cholesterol.
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PMID:Lp(a) levels and reduced risk of vascular atheromatosis in patients with alcoholic liver disease. 748 Sep 70

The plasma Lp(a) concentrations were evaluated in several groups of patients. Groups with liver cirrhosis (n = 20), type-1 diabetes mellitus (n = 148), type-2 diabetes mellitus (n = 65), hypertension (n = 51), lung cancer (n = 48) and deep venous thrombosis (n = 31) were compared with a group of healthy volunteers (n = 69). Significantly higher median values were found in the hypertension (142 mgl-1 vs. 43 mgl-1, p < 0.001) and lung cancer groups (241 mgl-1 vs. 43 mgl-1; p < 0.0001). Significantly lower values were recorded in the group with liver cirrhosis (11 mgl-1 vs. 43 mgl-1; p = 0.02). But in this last group there were significant differences between patients in the Child-Turcotte severity stages A to C.
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PMID:The behaviour of lipoprotein(a) in patients with various diseases. 786 33

Recent research has demonstrated that the major site of apolipoprotein(a) synthesis, the characteristic protein of lipoprotein(a) (Lp(a)), is the liver and that patients affected by liver cirrhosis have low serum concentrations of Lp(a). Nevertheless, it is still not clear whether Lp(a) behaviour in these patients is related to reduced hepatic protein synthesis, or to decreased serum lipid levels or to both these conditions. In order to investigate further the behaviour of Lp(a) and, in particular, its relationship with some indices of blood lipids and coagulation, 30 patients affected by liver cirrhosis have been studied. Significantly low serum values of Lp(a) were observed in patients with more severe hepatic injury included in classes B and C according to the Child-Pugh score. Lipoprotein(a) was directly correlated with prothrombin plasma activity and with apolipoprotein B-100 and albumin concentrations in serum. This study confirms low serum levels of Lp(a) in cirrhotic patients and suggests that its decrease could be partly due to impaired liver protein synthesis.
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PMID:Relationship between lipoprotein(a) levels in serum and some indices of protein synthesis in liver cirrhosis. 800 82

Several observations have suggested that lipoprotein (a) (Lp(a)) is a risk factor for coronary artery disease because of potential interference with fibrinolysis secondary to its activation of plasminogen. However, there are few data on the possible role of Lp(a) in liver cirrhosis. The present study was carried out, to better elucidate its relationship to the fibrinolytic system in liver cirrhosis. We studied the plasma levels of Lp(a) and the fibrinolytic parameters of 95 patients with liver cirrhosis (57 men, 38 women, aged 26-81). Patients in Child-Pugh class C (n = 32) had significantly lower levels of Lp(a) than those in class B (n = 45), and the class B had lower Lp(a) values than class A (n = 18) (1.4 (0.0-3.7) vs 2.9 (0.0-6.1) vs 3.4 (1.8-5.5); the data are log-transformed). Alpha-2-antiplasmin and plasminogen, had patterns similar to those of Lp(a), tissue plasminogen activator (t-PA) was significantly increased only in class C (class A: 7.5 +/- 5.8 ng/ml; class B: 10.8 +/- 7.7 ng/ml; class C: 19.1 +/- 11.3 ng/ml). Patients with systemic hyperfibrinolysis (cross-linked fibrin degradation products, XDP > 200 ng/ml) also had lower levels of Lp(a) than those without 1.6 (0.0-4.4) vs (0.0-6.1); p = 0.0002. There was a significant correlation between Lp(a) and plasminogen (r = 0.43; p = 0.001). Lipoprotein (a) progressively decreases as liver cirrhosis worsens but it appears unlikely to be involved in causing the hyperfibrinolytic state often observed in advanced liver cirrhosis, in which there are marked abnormalities of several other fibrinolytic parameters, also including increased t-PA and decreased inhibitors.
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PMID:Lipoprotein (a) and fibrinolytic system in liver cirrhosis. Coagulation Abnormalities in Liver Cirrhosis (CALC) Study Group. 856 64

Liver disease is accompanied by major qualitative and quantitative disturbances in plasma lipoprotein metabolism, the extent and intensity of which depend on the degree of parenchymal damage, cholestasis, or both. The main objective of this study was to determine the cholesteryl ester transfer CETP activity and its association with the lipoprotein neutral lipid composition in patients with either liver cirrhosis or cholestasis, as compared to normal controls. Lipoproteins were isolated by ultracentrifugation, lipids and apolipoproteins were measured by conventional methods, and the fatty acid composition was established by gas chromatography; CETP activity in lipoprotein-deficient plasma was measured by determining the transfer of [3H]cholesteryl esters from HDL to VLDL. Lipoprotein lipase and hepatic lipase activities were measured in post-heparin plasma by radiochemical methods. In patients with liver cirrhosis, low levels of VLDL, HDL, apo B, and Lp(a) were observed, as well as a change in the composition of HDL particles, with increases in the relative proportion of triglyceride and free cholesterol. Respectively, the last two changes could be attributed in part to the low hepatic lipase activity observed in this study, and to the low lecithin:cholesterol acyltransferase activity previously observed by others. In patients with cholestasis, a moderate hyperlipidemia due to the elevation of LDL was found. In contrast, HDL and apo A-I levels were very low reflecting a low number of HDL particles, which also had altered compositions with increases in the triglyceride and free cholesterol contents relative to apo A-I and esterified cholesterol, respectively. As regards the fatty acid composition of lipoprotein lipids, the two groups of patients showed, in general, a lower proportion of linoleic acid and a compensating higher proportion of oleic acid as compared to the controls, changes that were observed in both cholesteryl esters and triglycerides. In contrast, the proportions of oleic and palmitoleic acids in phospholipids were increased, whereas that of stearic acid was decreased in patients as compared to controls. In patients with liver cirrhosis, as well as in controls, no changes were observed in the fatty acid compositions of cholesteryl ester, triglycerides, or phospholipids among the different lipoproteins, which probably reflects the equilibration reached by the action of CETP. In patients with cholestasis, no differences were observed in fatty acid composition among the lipoprotein phospholipids but, interestingly, cholesteryl esters from VLDL had a significantly lower linoleic acid content than those from HDL, whereas triglycerides from VLDL had significantly higher oleic acid and lower linoleic acid contents than those from HDL. This distinct fatty acid composition of the neutral lipids between lipoproteins was associated with a significant decrease (25%) in the cholesteryl ester transfer activity in patients with cholestasis. We suggest that fat malabsorption due to the biliary defect may induce a decrease in cholesteryl ester transfer protein synthesis or section, which in turn would slow the equilibration of the neutral lipids among plasma lipoproteins.
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PMID:Cholesteryl ester transfer activity in liver disease and cholestasis, and its relation with fatty acid composition of lipoprotein lipids. 874 May 80

Over the last few years, lipoprotein(a) [Lp(a)] levels have been investigated because clinical studies have related it to increased cardiovascular and cerebrovascular risk. Although it is known that serum Lp(a) concentrations are controlled genetically, little is known about its metabolism. We studied changes in the lipid profile and Lp(a) values in 57 patients (34 males and 23 females) affected by cirrhosis of the liver subdivided into Child's classes in order to assess whether this lipoprotein is sensitive to reduced liver protein synthesis. The patients presented with low total cholesterol, normal HDL-cholesterol (HDL-c), LDL-cholesterol (LDL-c), triglycerides, apoprotein A1 (Apo-A1) and apoprotein B100 (Apo-B100) concentrations, while Lp(a) concentrations seemed elevated. Grouping the patients into Child's classes revealed that all the lipid parameters investigated reduced as the disease progressed. Lp(a) reduced significantly between Child's Classes I and II and seems to be correlated with the severity of cirrhosis and the clinical worsening of the patients' conditions. These findings suggest that Lp(a) is not only an index of atherosclerosis risk, but also plays a role in monitoring liver functions.
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PMID:Lipoprotein(a) in cirrhosis. A new index of liver functions? 901 Jun 14

Patients with homozygous beta-thalassemia show an abnormal lipoprotein profile. In asymptomatic heterozygotes the lipid pattern is less markedly affected but interestingly related to a diminished cardiovascular risk. The extent and significance of these findings are still a matter of debate and no data are available on lipoprotein(a) plasma levels. Seventy patients with homozygous beta-thalassemia (HT-P), 70 beta-thalassemia trait carriers (TT-C) and 70 sex and age-matched controls were investigated and their plasma lipoprotein profile and apo(a) phenotypes determined. In a subgroup of these same subjects (12 HT-P, 12 TT-C and 24 controls) and in 12 bone marrow-transplanted homozygous beta-thalassemic patients (BMT-P) plasma lipoprotein composition was assessed. HT-P disclosed significantly lower total-cholesterol, LDL-cholesterol, HDL-cholesterol, apo A-I, apo B plasma levels and higher triglyceride concentration than TT-C (-7, -11, -8, -8, -13 and +11%, respectively) or controls (-39, -50, -46, -32, -30 and + 35%, respectively). All lipoprotein subclasses were triglyceride-enriched, while LDLs were also protein-enriched and HDLs protein-depleted. TT-C disclosed a small but significant reduction in apo A-I and apo B plasma levels but only minor lipoprotein abnormalities with respect to the controls. BMT-P lipoprotein composition was intermediate between HT-P and normal subjects. Apo(a) plasma levels did not differ among the groups. A higher prevalence of 'small' apo(a) isoforms was present in HT-P. Within the same 'isoform group', apo(a) plasma levels were significantly lower in HT-P than in TT-C or controls. Since liver cirrhosis is almost always present in HT-P, it is conceivable that an altered hepatic apo(a) synthesis or catabolism due perhaps to diminished apolipoprotein glycation may be involved. In TT-C a partially improved cardiovascular risk profile was apparent (low hematocrit, low LDL-cholesterol and apo B), thus justifying the claim for a low prevalence of ischemic heart disease, but no Lp(a) plasma level modification could be detected.
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PMID:Plasma lipoprotein composition, apolipoprotein(a) concentration and isoforms in beta-thalassemia. 918 Feb 53

Lipoprotein (a) [Lp(a)] is synthesised by liver cells, and patients with liver cirrhosis (LC) show low serum levels of Lp(a) associated with the degree of liver failure. On the contrary, increased serum levels of Lp(a) have been reported in patients with cancer. In this report, the behaviour of Lp(a) serum levels in patients with hepatocarcinoma (HC), a complication of LC, has been evaluated with the aim to study whether HC cells were able to cause an increase of serum concentrations of this lipoprotein when impaired liver protein synthesis is present. We selected eighteen patients affected by LC + HC, eighteen patients matched for sex, age and degree of liver failure with LC only, and eighteen patients with other cancer types. A significant increase of serum levels of Lp(a) was observed in patients affected by LC + HC or other cancer types compared with healthy subjects. Forty-four percent of LC + HC patients showed Lp(a) values more than 70.4 Units/dl, i.e., the upper limit of values observed in patients with LC only. Lp(a) serum concentrations were significantly associated with serum albumin both in LC and in LC + HC but not in other cancer-type patients. Thus, comparing patients with similar serum albumin concentrations, Lp(a) serum levels were significantly higher in patients with LC + HC than in patients with only LC and quite similar to those observed in patients with other cancer types. In conclusion, HC cells, in vivo, seem able to produce a greater amount of Lp(a) despite the reduced liver protein synthesis typical of LC.
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PMID:Lipoprotein (a) serum levels in patients with hepatocarcinoma. 920 9

There is abundant epidemiological and clinical evidence showing that light-moderate drinking is associated with a reduced risk of coronary heart disease (CHD), total and ischaemic stroke and total mortality in middle-aged and elderly men and women. The epidemiological evidence suggests a J- or U-shaped relationship between alcohol and CHD. However, the apparent benefits of moderate drinking on CHD mortality are offset at higher drinking levels by increasing risk of death from other types of heart diseases (cardiomyopathy, arrhythmia etc.), neurological disorders, cancer, liver cirrhosis, and traffic accidents. The plausible mechanisms for the putative cardioprotective effects include increased levels of high-density lipoprotein cholesterol, decreased levels of low-density lipoprotein cholesterol, prevention of clot formation, reduction in platelet aggregation, and lowering of plasma apolipoprotein(a) concentration. Thus, alcohol reduces the risk of coronary vascular diseases both by inhibiting the formation of atheroma and decreasing the rate of blood coagulation.
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PMID:Cardioprotective effects of light-moderate consumption of alcohol: a review of putative mechanisms. 1221 28

Lipoprotein (a) [LP(a)] is a genetic variant of low density lipoprotein (LDL) and is mainly synthesized in liver. We conducted a study to evaluate the association of serum [Lp(a)] level with hepatitis viral infections. A total of 130 patients including 50 patients with acute viral hepatitis (AVH), 30 with chronic active hepatitis (CAH), 30 with cirrhosis of liver and 20 patients with fulminant hepatic failure (FHF) were analysed for different hepatitis viral markers and Lp(a) level in their serum samples. For comparison, 50 healthy persons were also tested for Lp(a) level. Serum Lp(a) level in patients in all the disease groups was significantly reduced compared to that observed in controls. Lp(a) level could not be detected in 40 per cent cases with AVH, 46.6 per cent with CAH, 70 per cent with cirrhosis and 80 per cent of FHF patients. On correlating Lp(a) level to viral etiology in these patients, it was found that the extent of diminution in Lp(a) level did not follow any trend with some particular viral infection and was recorded nearly same in all the infections. The findings of this study suggested that serum Lp(a) level was significantly (P<0.001) reduced in patients with liver diseases irrespective of the viral etiology.
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PMID:Serum lipoprotein (a) levels in liver diseases caused by hepatitis. 1565 40


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