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)

A review of the perioperative morbidity and mortality and long-term survival in elderly and high-risk patients with colorectal neoplasia was undertaken. Elderly high-risk patients with localized disease were compared with those with advanced disease. Over a five-year period, 82 high-risk (at least one major organ system disease), or elderly (age > or = 70 years) patients underwent an operation for colorectal neoplasia. Overall, 43 of 82 (52 percent) had advanced disease (obstruction, perforation, hemorrhage, or metastatic disease), while 39 of 82 (48 percent) had localized disease. The mean age of all patients was 78.2 years. Preoperative comorbid diseases included: coronary atherosclerosis, 59 (72 percent); previous myocardial infarction, 17 (21 percent); previous arrhythmia, 10 (12 percent); emphysema, 32 (39 percent); renal failure, 6 (7 percent); and cirrhosis, 3 (4 percent). At the time of surgery, 26 patients (32 percent) had metastatic disease. Six patients (7 percent) died in the perioperative period. The presence of advanced neoplasia did not significantly affect 30-day mortality. There was no difference in major morbidity between patients operated on for localized and for advanced disease. The mean actuarial 18-month survival was less for patients with advanced disease (P < 0.05). Sixty-eight patients (83 percent) are alive at a follow-up of 17.7 +/- 29 months postoperatively. The morbidity and mortality associated with resection of colorectal neoplasia in high-risk elderly patients are acceptable even in the presence of advanced disease. In select patients, resection offers the best palliation and may improve the quality of remaining life.
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PMID:Advanced colorectal neoplasia in the high-risk elderly patient: is surgical resection justified? 842 20

Apolipoprotein A-I, a protein produced mainly by hepatocytes, is of major importance in prevention of atherosclerosis. Its serum level varies according to the degree of liver fibrosis and the mechanism of this regulation is unknown. The aim of this study was to investigate the role of extracellular matrix in the regulation of apolipoprotein A-I by the liver. Primary mouse hepatocytes were cultured on different extracellular matrix components. The apolipoprotein A-I mRNA level was quantified in these different culture conditions by a sensitive quantitative RT-PCR procedure and compared according to the extracellular matrix component used as substrate. A significant decrease in the apolipoprotein A-I mRNA level was observed when cells were plated on fibronectin by comparison with cells cultured on all other components. Potential binding of apolipoprotein A-I to the different matrix components was also studied in vitro. We demonstrated that apolipoprotein A-I significantly bound to fibronectin in a concentration-dependent, saturable and specific manner. Thus, fibronectin, a major liver extracellular matrix component, can interact with apolipoprotein A-I both by downregulating its mRNA level in liver cells and by binding this molecule after its secretion in the extracellular space. Since fibronectin is the first matrix component to be produced in excess and deposited in liver fibrosis, it could be involved in the decrease in serum apolipoprotein A-I in alcoholic patients with liver fibrosis and cirrhosis.
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PMID:Role of liver extracellular matrix in transcriptional and post-transcriptional regulation of apolipoprotein A-I by hepatocytes. 882 8

This article summarizes the results of a recent study of atomic bomb radiation and non-cancer diseases in the AHS (Adult Health Study) population by the RERF (Radiation Effects Research Foundation) along with a general discussion of previous studies. The association of atomic bomb radiation and CVD was examined by incidence studies and prevalence studies of various endpoints of atherosclerosis, such as MI, stroke, aortic arch calcification, isolated systolic hypertension, and pulse wave velocity, and, although the excess was small, all endpoints indicated an increase of CVD in the heavily exposed group. Because of the consistency of the results, it is almost certain that CVD is higher among atomic bomb survivors. However, all CVD risk factors associated with lifestyle had not necessarily been adjusted for in studies to date, and it is difficult at present to conclude that the increase in CVD among survivors was a direct effect of radiation. Recent studies have demonstrated almost certainly that uterine myoma is more frequent among atomic bomb survivors. It cannot, at present, be concluded that uterine myoma is caused by radiation, because there are no reported studies of other exposed populations. Further analyses including the role of confounding factors as well as molecular approaches are needed to verify this radiation effect. The relationship between atomic bomb radiation exposure and hyperparathyroidism can now be said to have been established in view of the strong dose response, the agreement with results of studies of other populations, the high risk in the younger survivors, and the biological plausibility. Future studies by molecular approaches, etc., are needed to determine the pathogenic mechanism. Among other benign tumours, a dose response has been demonstrated for tumours of the thyroid, stomach and ovary. Although fewer studies have been conducted than for cancer, a clear association between radiation and various benign tumours is emerging. Concerning the association between atomic bomb radiation exposure and chronic liver diseases, the recent incidence study of members of the AHS population demonstrated a significant dose response. Both chronic hepatitis and cirrhosis were suggested as being associated with exposure. The possibility that the increased occurrence of chronic liver diseases among the survivors may be due to hepatitis virus infection cannot be excluded, and the results of the ongoing hepatitis C virus antibody titre studies are awaited.
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PMID:Profiles of non-cancer diseases in atomic bomb survivors. 889 51

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.
Atherosclerosis 1997 May
PMID:Plasma lipoprotein composition, apolipoprotein(a) concentration and isoforms in beta-thalassemia. 918 Feb 53

The article presents summarized results of treatment and examinations of 216 patients with gastro-intestinal bleedings due to acute errosive hemorrhagic gastritis and gastroduodenitis, cancer and polyposis of the stomach, liver cirrhosis and portal hypertension, hemorrhage against the background of atherosclerosis and arterial hypertension by administration of hemostatic medicine into the lymphatic system for activation and reinforcement of the reserve monocyte-macrophage mechanism of hemocoagulation. The results obtained confirm the expedience of this method of influencing the monocyte-macrophage hemostasis, having no complications and giving better medical effects.
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PMID:[Hemostatic therapy of gastroduodenal hemorrhage of non-ulcer genesis by the use of reserve mechanisms of hemostasis]. 961 18

Many epidemiological studies have shown that moderate alcohol intake, from 10 to 30 g of ethanol a day, decreases cardiovascular mortality from atherosclerotic ischaemic heart disease and ischaemic stroke as compared to non-drinkers. This beneficial effect outweighs the risks of alcohol consumption in subgroups of people with a higher risk of atherosclerosis: the elderly, people with coronary risk factors and patients with previous coronary events. It has not been demonstrated that alcohol intake, even in moderate amounts, is beneficial for the general population, in particular, men under the age of 40 and women under 50, because it raises mortality due to other causes, especially injury, cirrhosis of the liver and some types of cancer, thereby outweighing the benefits for coronary artery disease. Thus, alcohol consumption should not be recommended as a prophylaxis for the general population. Guidelines on alcohol drinking habits--whether to continue, to start, to modify or to stop--must be given on an individual basis, taking into account the relative risks and benefits for each patient. The benefits of moderate alcohol consumption on the cardiovascular system seem to be exerted fundamentally through its effects on plasma lipoproteins, principally by raising high density lipoprotein (HDL) cholesterol and to a lesser degree, by decreasing low density lipoprotein (LDL) cholesterol. It appears to exert additional beneficial effects on the heart by decreasing platelet aggregability and by bringing about changes in the clotting-fibrinolysis system. Although there has been some debate about the relative superiority of different types of alcoholic beverages (wine, beer or hard liquor), and to a greater extent, about different types of wine, there is no current evidence of any kind of beneficial effect from other components of the beverage besides ethanol. Thus, it does not seem appropriate to recommend any particular type of alcoholic drink, except for sociocultural reasons. The added benefits from some components of different types of wine with a high antioxidant activity on plasma lipoproteins remain only an interesting hypothesis. Meanwhile, encouraging a healthy diet, flavonoid rich and with a predominance of natural ingredients (fruit, legumes, cereals and seeds), in the general population should stop the current tendency of Southern European countries from abandoning the Mediterranean diet. Because of the multifactorial nature of coronary heart disease, it is necessary to remember that atherosclerotic risk reduction is achieved by behavior modification of multiple risk factors present in individual patients and in the general population. Therefore, guidelines regarding alcohol intake should always be linked to pertinent recommendations about other atherosclerotic risk factors.
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PMID:[Wine and heart]. 1021 74

We report the case of a patient with alcoholic liver cirrhosis and generalized atherosclerosis who rapidly developed erythrocytosis. Concomitantly we documented a significative and progressive increase of serum Erythropoietin (Epo) and a small focus of hepatocellular carcinoma (HCC) never diagnosed before. Even in absence of immunohistochemical and/or biomolecular evidence of Epo production in the neoplastic tissue we think the hypothesis of the paraneoplastic syndrome may be the most likely both for the strict temporal relationship between the observation of the neoplastic lesion and the appearance of polycythemia and for the absence of all other known causes of erythrocytosis. Objection to this hypothesis: 1) ectopic production of Epo during HCC has been usually described in large neoplastic lesions 2) liver cirrhosis by itself may be accompanied by increased Epo levels 3) an intratumoral hypoxia with compensatory production of Epo may have occurred 4) generalized vasculopathy could have determined renal hypoxia with greater local production of Epo.
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PMID:[Erythrocytosis in patients with hepatocarcinoma in alcoholic cirrhosis: ectopic production of erythropoietin?]. 967 32

Alcohol taken in moderation may prevent atherosclerosis, whereas heavy drinking has the opposite effect, in part by promoting oxidation of low density lipoproteins (LDL), a pathogenetic factor in atherogenesis. We assess here: 1 ) whether similar alterations can be reproduced in baboons fed 50% of energy as ethanol (the average intake of alcoholics) for 7- 8 years, and 2 ) whether such alterations are affected by supplementation with polyenylphosphatidylcholine (PPC), a mixture of polyunsaturated phosphatidylcholines, shown to prevent alcoholic fatty liver, fibrosis, and cirrhosis. Ten animals were given the ethanol-containing diet and ten were pair-fed isocaloric control diets. In half of the pairs, the diets were supplemented with 2.8 g of polyenylphosphatidylcholine/1000 kcal. Alcohol feeding increased LDL-lipoperoxides and made LDL-proteins more negatively charged, changes that were attenuated or prevented by PPC. The oxidizability of LDL was determined in vitro by the formation of conjugated dienes after oxidation with copper. Alcohol shortened the lag time (which measures LDL antioxidant capacity); this effect was normalized by PPC supplementation. By contrast, PPC produced no changes in the controls. Thus polyenylphosphatidylcholine, by markedly attenuating the ethanol-induced increase in LDL oxidation, opposes one of the effects whereby alcohol promotes atherosclerosis.
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PMID:Oxidation of LDL in baboons is increased by alcohol and attenuated by polyenylphosphatidylcholine. 1035 29

The study of the microcirculation by intravital microscopy represents a sophisticated research tool to analyse complex biological interactions and disease mechanisms as well as to develop and test novel prophylactic and therapeutic approaches aimed at the prevention or attenuation of manifestation of disease-associated microvascular disorders and cellular dysfunction. This may include pathogenesis of atherosclerosis and thrombosis, fibrosis and cirrhosis as well as hypertension, diabetes and tumorogenesis. In addition, using the microscopic technique, circulatory and cellular disorders in surgical diseases and procedures, such as shock and resuscitation, ischaemia/reperfusion and transplantation, trauma, sepsis and inflammation, as well as burn injury and wound healing, may be analysed. With the background of the increasing knowledge of molecular and cellular mechanisms of disease evaluated in vitro, the technique of intravital microscopy ideally allows to bridge over from those in vitro observations to test their potential relevance in vivo.
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PMID:Intravital microscopy for the study of the microcirculation in various disease states. 1056 69


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