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)

Moderate alcohol intakes decreases the risk of gallstones; in contrast, the prevalence of gallstones is increased in patients with alcoholic cirrhosis. The aims of this prospective study were to assess the prevalence of cholelithiasis among drinkers according to the histological severity of liver disease, and to estimate the importance of serum apolipoproteins AI and apolipoprotein AII as risk factors for gallstones. Among the 320 drinkers included, 53 patients had cholelithiasis. The prevalence increased (p < 0.0001) from 5% in patients with normal liver (1 of 22) and 6% in patients with steatosis only (3 of 47) to 13% in patients with fibrosis (7 of 54), reaching 27% among patients with biopsy-proven cirrhosis (28 of 103). Among patients with clinically obvious cirrhosis on whom biopsy was not performed mainly because of the severity of liver disease, the prevalence of cholelithiasis reached a maximum of 46% (6 of 13). Among drinkers with nonsevere liver disease, patients with cholelithiasis were older (59 +/- 9 years, mean +/- SD vs. 45 +/- 11, p = 0.003) with lower apolipoprotein AI (118 +/- 37 vs. 163 +/- 45 mg/dl; p = 0.002) and apolipoprotein AII (30 +/- 12 vs. 53 +/- 20 mg/dl; p = 0.0002) in comparison with patients without cholelithiasis. These differences persisted after considering by multiple logistic regression analysis, sex, and ideal body weight. Alcohol consumption during the last 5 years was lower in patients with cholelithiasis (83 g/day) in comparison with patients without cholelithiasis (142 g/day; p = 0.04).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prevalence of cholelithiasis according to alcoholic liver disease: a possible role of apolipoproteins AI and AII. 777 67

We determine the concentration of proapolipoprotein (proapo) A-I and its ratio with total apolipoprotein (apo) A-I (proapo A-I/total apo A-I) in plasma of patients with liver disease; we used a noncompetitive sandwich method, an enzyme-linked immunosorbent assay. The mean (SD) proapo A-I concentrations in patients with decompensated or compensated liver cirrhosis were higher than in normal subjects: 88 (25), 105 (36), and 69 (25) mg/L, respectively. The mean (SD) ratio (expressed as %) for each of these types of liver cirrhosis was also higher than in normal subjects: 10.0 (3.5), 10.2 (3.9), and 4.6 (1.6), respectively. In the patients, the proapo A-I concentration was positively correlated with the concentration of high-density lipoprotein subtype 2 cholesterol (HDL2-C) (r = 0.736), and the proapo A-I/total apo A-I ratio was correlated inversely with the HDL3-C concentration (r = -0.609). The activity of proapo A-I converting enzyme in patients with liver cirrhosis (62 +/- 30 nmol/h per liter) was significantly (P < 0.01) lower than that in normal subjects (172 +/- 55 nmol/h per liter). The increases of the plasma proapo A-I concentration and ratio in patients with liver cirrhosis may be caused by a decreased production of the converting enzyme in the liver. The increase of plasma proapo A-I may thus also affect the circulating HDL subtypes.
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PMID:Increase of plasma proapolipoprotein A-I in patients with liver cirrhosis and its relationship to circulating high-density lipoproteins 2 and 3. 841 59

A case of type III hyperlipoproteinemia (HLP) (dysbetalipoproteinemia) acquired by liver transplantation is reported. The 50-year-old female patient was referred to the Frankfurt University Hospital for orthotopic liver transplantation. She had suffered from ethylic liver cirrhosis. The donor liver showed discrete signs of steatosis. The postoperative course of the patient was satisfactory. Enzyme levels and blood coagulation tests returned to normal within thirty days. However, both cholesterol and triglycerides gradually increased from approximately 2.00 g/L to values ranging from 2.50 to 3.50 g/L within 200 days after transplantation. Cutaneous xanthomas did not develop. The patient's lipoprotein pattern met the criteria of type III HLP: the cholesterol to triglyceride ratio in very low-density lipoproteins (VLDL) was 0.64. Intermediate-density lipoprotein(IDL) cholesterol was 0.48 g/L. Lipoprotein electrophoresis showed a broad beta-band, and beta-migrating particles were present in VLDL. Immunoblotting of apolipoprotein (apo) E from the patient's plasma revealed an E2/2 phenotype. However, restriction isotyping of an in vitro amplified apoE gene fragment showed the genotype of the patient to be epsilon 3/epsilon 4. These data suggest that the development of type III HLP in this patient was due to a change in the apoE phenotype from E3/4 to E2/2 after liver transplantation.
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PMID:Type III hyperlipoproteinemia acquired by liver transplantation. 843 77

The liver plays a major role in lipid metabolism, and quantitative and or qualitative changes in serum lipoproteins and apolipoproteins have been observed in various liver diseases. We investigated changes in hepatic mRNA expression of apolipoproteins A-I, C-III, and E and LDL receptor in human liver diseases, rat D-galactosamine, CCl4 induced liver failure and regenerating liver. The apolipoprotein mRNA expression were significantly decreased in liver and severe acute hepatitis as compared with controls and were correlated with serum albumin levels. LDL receptor mRNA expression were decreased in liver cirrhosis and rat liver failure. These findings indicated that liver biosynthesis of these apolipoproteins and LDL receptor are suppressed in liver disease. On the other hand, LDL receptor mRNA expression increased in regenerating liver, and this shows that serum cholesterol was needed for membrane biosynthesis.
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PMID:[Apolipoprotein A-I, E, C-III and LDL-receptor mRNA expression in liver diseases]. 846 55

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

Deficiency of apolipoprotein can be of genetic origin or due to diseases like advanced chronic liver disease. Deficiency of apolipoprotein A causes Tangier disease without any major hepatic involvement being reported. Deficiency of apolipoprotein B causes abetalipoproteinemia or familial hypobetalipoproteinemia; with hepatic involvement in the form of raised transaminases, fatty liver and cirrhosis. Advanced chronic liver disease itself can cause reduction of apolipoprotein A and apolipoprotein B levels and acanthocytosis. In patients with chronic liver disease of undetermined etiology, lipid profile and apolipoprotein levels should be obtained routinely. If it suggests apolipoprotein B deficiency, then liver biopsy can be avoided, as the etiology of chronic liver disease is established. Isolated deficiency of either apolipoprotein A or apolipoprotein B suggests etiology of chronic liver disease, while deficiency of both apolipoprotein A and apolipoprotein B is a manifestation of advanced chronic liver disease.
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PMID:Apolipoprotein deficiency and chronic liver disease. 1122 45

Because (i) changes in plasma and liver mRNA of apolipoprotein (apo) AI have been observed in patients with alcoholic liver disease, (ii) apo AI mRNA can be induced in non-hepatic tissues, and (iii) apolipoproteins expression is influenced by plasma colloid osmotic pressure (P(CO)) and viscosity (eta), we analyzed the Apo AI mRNA expression in the peripheral white blood cells (PWBC), P(CO), and eta in control volunteers (C), patients with liver cirrhosis (LC), and cirrhotic patients with superimposed alcoholic hepatitis (LC+AH). We found that apo AI mRNA is expressed in the PWBC in 20% of C and it is induced 1.5 fold in 66.6% of LC and 1.95 fold in 85% of LC+AH. A significant decrease of P(CO) in LC and LC + AH (14.8 +/- 2.4 and 16.2 +/- 2.4 mm Hg, respectively) compared to C (27.9 +/- 2 mm Hg) was observed. By contrast, eta was mildly increased from 1.7389 +/- 0.07 in C to 1.8022 +/- 0.154 in LC and 1.9030 +/- 0.177 in LC+AH. No significant correlation was found between P(CO) and eta with apo AI mRNA but with lipid profile. In conclusion, apo AI mRNA expression in PWBC is associated to liver disease severity and could be an indirect indicator of alcoholic liver damage.
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PMID:Expression of apolipoprotein AI mRNA in peripheral white blood cells of patients with alcoholic liver disease. 1594 2

We previously found that transplantation with bone marrow cells (BMCs) improves liver function and liver fibrosis in cirrhotic mice. In the presence of liver damage induced by carbon tetrachloride (CCl4), transplanted BMC migrated into the peri-portal region and trans-differentiated into hepatocytes that produce albumin. Thus under these conditions, BMC transplantation induces liver regeneration. Detecting serum marker proteins is important to monitor the recovery of liver function of cirrhotic mice after BMC transplantation. We therefore initially resolved proteins extracted from serum samples at 48 h after BMC transplantation by 2-DE and compared spot intensity between control and BMC groups of mice. Six protein spots increased in the BMC group compared with the control group. MS revealed that these spots comprised apolipoprotein A1 (apoA1), apolipoprotein C3 (apoC3), vitamin D-binding protein, alpha-1-antitrypsin and proteasome subunit alpha type 1. We subsequently confirmed the levels of apoA1 in serum and liver samples by immunoblotting. ApoA1 increased at early stage (48 h and 1 wk) after BMC transplantation in this mouse model of liver cirrhosis. The early elevation of apoA1 might be useful to predict liver regeneration in cirrhotic mice after BMC transplantation.
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PMID:Proteomic analysis of serum marker proteins in recipient mice with liver cirrhosis after bone marrow cell transplantation. 1654 57

The aim of the present study was to determine the apolipoprotein A (APO-A) an the high density lipoprotein (HDL) plasma concentrations in 25 patients with alcoholic liver cirrhosis. To evaluate the severity of liver disease serum albumin, bilirubin and total bile acids were measured. The serum level of APO-A and HDL was significantly lower in patients with alcoholic liver cirrhosis than in normal controls (p < 0.01) and markedly lower in patients with advanced liver cirrhosis. Apolipoprotein A concentrations in plasma correlated positively with serum albumin (p < 0.01) and negatively with serum bilirubin (p < 0.01) and bile acids (p < 0.01). Thus, he apoliprotein A level seems to reflect the severity of liver disease.
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PMID:[Apolipoprotein A in patients with alcoholic liver disease]. 1797 96

The glyco-isoforms of intact apolipoprotein C3 (ApoC3) were used to probe glycomic changes associated with obesity and recovery following bariatric surgery, liver diseases such as chronic hepatitis C (CHC) and alcoholic liver cirrhosis, as well as severe, multiorgan diseases such as sepsis and graft vs host disease (GVHD). ApoC3 glyco-isoform ratios responded to unique stimuli that did not correlate with serum lipids or with other blood components measured in either a control population or a group of extremely obese individuals. However, glyco-isoform ratios correlated with obesity with a 1.8-fold change among subjects eligible for bariatric surgery relative to a nonobese control population. Bariatric surgery resulted in rapid change of isoform distribution to that of nonobese individuals, after which the distribution was stable in each individual. Although multiple simultaneous factors complicated effector attribution, the isoform ratios of very obese individuals were nearly normal for diabetic individuals on metformin therapy. Glyco-isoform ratios were sensitive to liver diseases such as chronic hepatitis C and alcoholic liver cirrhosis. The correlation coefficient with fibrosis was superior to that of current assays of serum enzyme levels. Diseases of pregnancy that can result in liver damage, HELLP syndrome and pre-eclampsia, did not alter ApoC3 glyco-isoform ratios. Early after umbilical cord blood transplantation the isoform ratios changed and returned to normal in long-term survivors. Larger changes were observed in persons who died. GVHD had little effect. Persons with severe sepsis showed altered ratios. Similar cut-points for mortality (3.5-fold difference from controls) were found for UCBT and sepsis. Similar values characterized liver cirrhosis. Overall, while changes of glyco-isoform ratios occurred in many situations, individual stability of isoform distribution was evident and large changes were limited to high-level disease. If ratio changes associated with obesity are found to document a risk factor for long-term outcomes, the information provided by glyco-isoform ratio changes may provide important, novel information for diagnostic, prognostic and therapy response to metabolic conditions.
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PMID:O-glycoside biomarker of apolipoprotein C3: responsiveness to obesity, bariatric surgery, and therapy with metformin, to chronic or severe liver disease and to mortality in severe sepsis and graft vs host disease. 1905 79


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