Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Low levels of alpha-1-antitrypsin can predispose deficient infants to the development of hepatitis and cirrhosis. Heterozygous PiMZ carriers can be affected by a subclinical liver involvement during their first half year of life. One pathogenic hypothesis of liver damage is that the process seems to be mediated by the activity of toxic oxygen waste products. In the present investigation it was found that the antioxidant vitamin E was able to significantly reduce the frequency of liver involvement in PiMZ carriers at two months of age but not at five months. These findings indicate that oxidative free radicals can promote liver damage in inadequately protected young infants, such as in alpha-1-antitrypsin deficiency. The protective role of vitamin E in relation to the developmental expression of other anti-oxidant scavengers is discussed.
 ...
PMID:Oxidative radicals and liver involvement of infants with alpha-1-antitrypsin deficiency. 166 23

A 56 year-old-male liver cirrhosis patient was admitted because of hepatic encephalopathy with hyperammonemia. We measured cerebral blood flow (CBF), cerebral oxygen extraction fraction (OEF) and cerebral metabolic rate for oxygen (CMRO2) by using PET before and after treatment of hyperammonemia. At the time of the first PET, serum ammonia was 152 micrograms/dl and on the second PET it was 88 micrograms/dl. The electroencephalogram and number connection test also improved on the second PET. CBF and CMRO2 were decreased by 25-42% in comparison to normal control and OEF increased 1-24% at first examination. Similar abnormal reduction of both CBF and CMRO2 and increase of OEF were seen at second examination. Reduced CBF and CMRO2 regardless of serum ammonia level suggests that heptic encephalopathy may be, at least in part, associated with pathological changes in brain tissue induced by hepatic metabolic disorder.
 ...
PMID:[Positron emission tomography (PET) before and after treatment of hyperammonemia in a patient with decompensated liver cirrhosis]. 174 67

The paper presents clinical and instrumental evidence on 47 patients with hepatic cirrhosis. The revealed ventilatory disorders and worse bronchial permeability closely correlated with the degree of pulmonary hypertension which in its turn depended on portal hypertension degree. Pulmonary hypertension decreased with a decline in the activity of the pathological process in the liver due to treatment. External respiration insufficiency observed in hepatic cirrhosis contributes to the onset of arterial hypoxemia and hypoxic impairment of the liver activating in it a pathological process. It is recommended that such patients should receive a combined treatment incorporating oxygen therapy, calcium antagonists, antioxidants.
 ...
PMID:[Study of the right heart and external respiratory functions in patients with liver cirrhosis by Doppler echocardiography]. 176 48

We studied the relationships in 29 patients with cirrhosis between pulmonary arterial atrial natriuretic peptide concentrations and the following: systemic and splanchnic hemodynamics, the hematocrit, arterial oxyhemoglobin saturation, oxygen tension and the severity of cirrhosis. Plasma atrial natriuretic peptide concentrations ranged from 21 to 208 pg/ml and averaged 78 +/- 8 pg/ml (mean +/- S.E.M.). Simple regression analysis showed significant correlations between plasma atrial natriuretic peptide concentration and the following: hematocrit, mean pulmonary arterial pressure, wedged hepatic venous pressure, free hepatic venous pressure, pulmonary wedged pressure and serum bilirubin concentrations. No significant correlations were found between plasma atrial natriuretic peptide concentrations and all other hemodynamic values, arterial oxyhemoglobin saturation and oxygen tension. Multiple stepwise regression analysis showed that the hematocrit, mean pulmonary arterial pressure and wedged hepatic venous pressure were significant and independent predictors of pulmonary artery plasma atrial natriuretic peptide concentrations (R2 = 0.69). Partial regression coefficients were -0.74 (p less than 0.001), 0.61 (p less than 0.001) and 0.44 (p less than 0.05) for the hematocrit, the mean pulmonary arterial pressure and the wedged hepatic venous pressure, respectively. In conclusion, in patients with cirrhosis, increased plasma atrial natriuretic peptide concentrations were related to the degree of hemodilution, increased pulmonary arterial pressure and the degree of portal hypertension. Plasma atrial natriuretic peptide concentrations were not influenced by the arterial oxygenation levels.
 ...
PMID:Relationships between plasma atrial natriuretic peptide concentrations and hemodynamics and hematocrit in patients with cirrhosis. 183 8

Interruption of hepatic blood supply for 60 min deteriorated liver mitochondrial respiratory functional indices--that is, respiratory control index (RCI) and the rate of oxygen consumption in state-III respiration (ST III O2). Recovery of ischemia-induced decreases in these functional indices in a saline-administered cirrhotic liver group was retarded compared with that in a normal liver group, and significantly low RCI and ST III O2 persisted 15 min after reperfusion. Prostaglandin E1 (PGE1) did not improve ischemia-induced decreases in RCI and ST III O2 but accelerated the recovery of mitochondrial respiratory function after reperfusion. Adenosine triphosphate (ATP) levels were markedly decreased during ischemia, and retardation of ATP recovery was also observed in rats with cirrhosis. PGE1 improved the recovery of ATP level in rats with cirrhosis. Liver blood flow in the cirrhotic liver was significantly lower than that of the normal liver. PGE1 enhanced liver blood flow. These results indicate that retardation of the recovery of RCI and ST III O2 in the cirrhotic liver might be based on the decrease in tissue blood flow and that agents increasing tissue blood flow might contribute to the acceleration of the recovery of mitochondrial respiratory function.
 ...
PMID:Effects of prostaglandin E1 on the recovery of ischemia-induced liver mitochondrial dysfunction in rats with cirrhosis. 185 49

The aim of this study is to clarify the liver metabolic changes after major hepatic resection. The survival rate after 70% hepatectomy of rats with cirrhosis was significantly depressed compared with that of the control group. Mitochondrial function in the cirrhotic liver was disturbed compared with the control group. Tissue levels of hypoxanthine and xanthine increased both in the cirrhotic group and the control group. The increase in xanthine levels was remarkable and was prolonged in the cirrhotic group compared with the control group. Decreases in adenine nucleotides were observed after resection both in normal and cirrhotic livers. These were remarkable and were prolonged in rats with cirrhosis. Administration of polyoxyethylene-modified superoxide dismutase improved the survival rate and lessened decreases in adenine nucleotide levels. Moreover, it accelerated the recoveries of serum glutamic oxaloacetic and pyruvic transaminase levels after resection in rats with cirrhosis. These results indicate that disturbances in energy metabolism and increases in oxygen free radical formation are more remarkable in the cirrhotic liver than in the normal liver, which contributes to a low survival rate in rats with cirrhosis.
 ...
PMID:Effects of long-acting superoxide dismutase on liver metabolism after major hepatic resection in rats with cirrhosis. 187 57

Altered metabolism has been shown to exist in the settings of surgical stress, cancer, cirrhosis, sepsis, and trauma. Each condition is characterized by varying degrees of alteration in metabolic processes, and within a given patient, these metabolic alterations will change as the patient's status changes. Nutrition support is an integral part of the metabolic management of critically ill patients. Metabolic changes impact nutritional substrate requirements and utilization. As the patient's clinical condition deteriorates, clinical signs and symptoms become less reliable in predicting or assessing the existing physiologic state. Objective measurements are needed to define the metabolic status during these physiologic changes. The purpose of this article is to review selected indices that have been used to identify abnormalities in nutritional substrate metabolism. Although some of these tests are readily available and inexpensive, many have not been used outside of the research setting and, therefore, their clinical utility has yet to be determined. However, their use as research tools for defining metabolism warrants their inclusion in order to assist the clinician in interpreting research studies. The biochemical markers discussed include glucose, lactate, pyruvate, triglycerides, beta-hydroxybutyrate, acetoacetate, urinary nitrogen, acute phase proteins, visceral proteins, 3-methylhistidine, plasma amino acids, oxygen consumption, and resting energy expenditure. Each marker is defined in terms of its biochemical significance, and the literature describing changes that occur in various stress states is cited.
 ...
PMID:Overview of biochemical markers used for nutrition support. 190 7

Severe hypoxemia is an uncommon feature of hepatic cirrhosis. Its major cause are intrapulmonary arteriovenous shunts, both due to direct arteriovenous communications and abnormally dilated pulmonary capillaries. In the present study, a case of cirrhosis associated with severe hypoxemia is reported. Contrast echocardiography showed pulmonary arteriovenous shunts, and low values of mixed venous blood (15% or less were obtained with the method of 100% oxygen breathing). These data suggest that the basic mechanism of hypoxemia, in this case, were capillary dilatations rather than true pulmonary arteriovenous anastomoses. The pathophysiological mechanisms of hypoxemia in cirrhosis are discussed, with emphasis on the present relevance of echocardiography for a full evaluation of these patients, particularly when liver transplantation is contemplated.
 ...
PMID:[Contrast echocardiography in the diagnosis of severe hypoxemia associated with liver cirrhosis]. 190 66

In 17 compensated liver cirrhosis and 8 chronic hepatitis cases (no histories of cardiac or pulmonary disease), wedged hepatic venous pressure (WHVP), hemodynamics, and pulmonary function were measured and their clinical significance and interrelations evaluated. Both diseases were comparatively analyzed. WHVP was determined by wedging a catheter from the right femoral vein into the right hepatic vein. Hemodynamics was measured with a Swan-Ganz catheter. Spirography, flow-volume curve, closing-volume curve and pulmonary diffusion capacity were measured and aortic blood gas analyzed to assess pulmonary function. Esophageal endoscopy was used to diagnose the presence or absence of esophageal varices. The results showed that the group of liver cirrhosis patients featured elevated WHVP and a hyperhemodynamic pattern and a positive correlation between WHVP on the one hand and cardiac index and right left ventricle stroke work indexes on the other; there was a negative correlation between WHVP and the systemic vascular resistance and pulmonary vascular resistance indexes. The results showed an increase in oxygen consumption in the group of patients with esophageal varices. In all chronic hepatitis cases, findings were normal. Pulmonary function was characterized by abnormal %VC, PaO2, and pulmonary diffusion capacity in both groups along with abnormal PaCO2 in the liver cirrhosis group; no significant differences were noted between the two groups. These results indicate that liver cirrhosis elevates intarahepatic pressure, affecting systemic hemodynamics and resulting in a circulatory distribution disorder, leading to right and left ventricle overload and a decline in potential cardiac function. The results also indicated that mild pulmonary function disorder can occur as early in a state of chronic hepatitis.
 ...
PMID:[Studies on wedged hepatic venous pressure, hemodynamics and pulmonary function in patients with chronic liver disease, with reference to the differences between liver cirrhosis with chronic hepatitis]. 191 74

Nuclear tri-iodothyronine (T3) maximal binding capacity (MBC) and thyroxine- and T3-stimulated cellular oxygen consumption and glucose consumption were examined in mononuclear blood cells from six patients with liver cirrhosis (LC), in six patients with alcoholic hepatitis (AH), and in six healthy control subjects. Serum T3 was decreased in patients with LC. The MBC of T3 was increased significantly (P less than 0.05) in cells from patients with LC compared with patients with AH and controls, whereas the equilibrium association constants did not differ. Unstimulated glucose consumption was slightly increased (P less than 0.05) in cells from patients with AH and LC compared with controls. Thyroid hormone-stimulated glucose consumption was significantly (P less than 0.05) increased in cells from patients with LC compared with controls and patients with AH. Unstimulated oxygen consumption did not differ between the groups, but thyroid hormone-stimulated oxygen consumption was depressed in cells from patients with AC (P less than 0.05) compared with patients with LC and with controls. We conclude that both thyroid hormone-stimulated glucose consumption and T3 nuclear receptor binding in cells from patients with LC are increased, and suggest that the observed changes are responsible for maintenance of euthyroidism in the face of reduced circulating T3.
 ...
PMID:Increased nuclear tri-iodothyronine binding and thyroid hormone-stimulated glucose consumption in mononuclear blood cells from patients with liver cirrhosis. 200 22


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>