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)

Atrial natriuretic factor (ANF) is a humoral agent isolated in recent years from cardiac atrial tissue, and produced by atrial cardiocytes as a peptide precursor containing 152 amino acids. In secretory atrial granules, it is stored in reserve form as a prohormone and released into circulation as a 28-amino acid peptide from the C-terminal portion of the peptide precursor representing the active circulating hormone. ANF possesses potent natriuretic, myorelaxant, vasodilatory and blood pressure-lowering properties. Besides, it inhibits renin, aldosterone and vasopressin secretion. It is present also in the CNS and its function is closely related to the sympathetics nerves. By its direct renal and vascular effect, renin-angiotensin-aldosterone system and vasopressin inhibition and, by its neuromodulatory action on the central and sympathetic nerves, ANF plays an important role in electrolyte, volume and pressure homeostasis. The development of a radioimmunoassay for ANF determination in the plasma of rats and man enabled us to follow up its changes under various experimental conditions (water deprivation, increased or decreased salt intake, effect of anaesthetics, ontogenetic changes in ANF concentration during development of hypertension in the spontaneously hypertensive rat) and in clinical studies (effect of ECV expansion in controls, arterial hypertension, liver cirrhosis as well as ANF changes in congestive heart failure or chronic renal failure). These findings of ours have supported the concept that ANF represents an important adaptive and corrective mechanism mobilized during intravascular volume and blood pressure changes in an effort to normalize these. ANF is expected to find use also in the treatment of oedema, arterial hypertension and acute renal failure.
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PMID:Atrial natriuretic factor and its role in the regulation of electrolyte, volume and pressure homeostasis. 252 70

Low frequencies of renal sympathetic nerve stimulation increase renal tubular sodium reabsorption without causing renal hemodynamic changes. We tested the hypothesis that the natriuretic responses to synthetic atrial peptides (atriopeptin III [APIII], 24 amino acids) are modulated by the renal tubular actions of the renal nerves. Responses to intravenous infusions of APIII (0.5 and 2.0 micrograms/kg/min) were examined in three groups of chloralose-anesthetized rats. Bilateral renal function studies were done in all three groups in which the right kidney was denervated and the left kidney was either left innervated (group I, n = 10) or the distal portion of the transected left renal nerves was stimulated at 15 V, 1 msec, and 0.5 Hz (group II, n = 8) or 1.0 Hz (group III, n = 8). In groups I, II, and III, diuretic and natriuretic responses to APIII were significantly (p less than 0.05) less in the kidneys with intact innervation or low-frequency (0.5 and 1.0 Hz) renal nerve stimulation than in the denervated kidneys. In conclusion, renal excretory responses to APIII are substantially modulated by the renal tubular actions resulting from low-frequency renal nerve stimulation. We speculate that the decrease in renal excretory responses to atrial peptides in pathophysiologic states such as congestive heart failure, nephrotic syndrome, and cirrhosis may result in part from an increase in the prevailing level of renal sympathetic nerve activity.
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PMID:Renal sympathetic nerves attenuate the natriuretic effects of atrial peptide. 253 Feb 94

The value of ascitic fluid adenosine deaminase activity in distinguishing tuberculosis from other causes of ascites was examined in a retrospective study of 41 patients with bacteriologically confirmed tuberculous peritonitis and 41 control patients, matched for age and sex, with ascites of other causes (12 alcoholic cirrhosis, 5 cryptogenic cirrhosis, 12 malignant disorders, 3 pancreatitis, and 9 miscellaneous causes). The mean ascites adenosine deaminase activity was 99.8 (SD 49.1) in tuberculous patients and 14.8 (8.4) U/l in control patients (p less than 0.0001). A cutoff of 32.3 U/l had a sensitivity of 95% and specificity of 98% in distinguishing between the two groups. In a subsequent prospective study of 64 patients with ascites, 11 were found to have tuberculosis. Of the others, 23 had cirrhosis (18 alcoholic, 5 cryptogenic), 17 malignant disorders, 3 pancreatitis, 5 cor pulmonale, 3 congestive cardiac failure, 1 systemic mastocytosis, and 1 renal failure and hypothyroidism. The mean ascites adenosine deaminase activity was 112.6 (45.0) U/l in the patients with tuberculous ascites and 16.3 (36.7) U/l (p less than 0.0001) in those with ascites of other causes. In this study, adenosine deaminase had a sensitivity of 100% and specificity of 96% in discriminating tuberculosis from other causes of ascites. These findings suggest that the ascitic fluid adenosine deaminase activity may be used to identify patients in whom the diagnosis of abdominal tuberculosis must be pursued.
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PMID:Diagnostic value of ascites adenosine deaminase in tuberculous peritonitis. 256 65

We reviewed 79 patients with a picture of pleural effusion (EP) and ascites, who represented 8% of a total of 982 pleural effusions studied. Liver cirrhosis (CH), 37 cases (47%), disseminated carcinomatosis, 31 cases (39.5%), and congestive heart failure, 6 cases (7%), were the main causes. We made two groups of liver cirrhosis: A) liver cirrhosis with hydropic decompensation, 12 patients (15%), and B) liver cirrhosis with an additional complication added to the above, 25 patients (31.5%), this being infectious in 88% of the cases. In the B group there were cases of left hydrothorax, more features of effusion and a lower survival at 3 months of follow-up than in tha A group. Effusions of neoplastic origin were most frequently seen in tumors of the ovary, digestive system, lymphomas and undetermined origin. In malignant effusions, the cytology was positive in pleura in 60% and in ascites in 55%. Twenty percent of peritoneal fluids and 47% of pleural effusions were serohemorrhagic and 100% and 88%, respectively, were of exudative nature. In liver cirrhosis the ascites was serofibrinous and transudated (100% in group A and 85.5% in B) and the pleural effusion was a serofibrinous transudate except in the cases in which there was an added infection. We confirm the ominous prognosis of the coexistence of pleural effusion and ascites.
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PMID:[Ascites and pleural effusion. Study and follow-up of 79 patients]. 259 69

In healthy subjects intravenous glucagon administration induces a prompt (at 1 h) fall in serum T3 concentration and a later (at 4 h) rise in biologically inactive rT3. Since high levels of plasma glucagon have frequently been found in some patients with severe chronic illnesses, together with an anomalous thyroid condition (low serum T3, high serum rT3), it has been supposed that hyperglucagonemia could play a pathogenetic role in causing selective T3 deficiency. In the present study fasting plasma glucagon concentration was measured in 48 patients with low T3 and severe nonthyroidal illnesses: hepatic cirrhosis in 16 cases, chronic non-A non-B hepatitis in 4 cases, uncontrolled type II diabetes mellitus in 5 cases, renal failure in 12 cases, congestive heart failure in 5 cases, tumor in 16 cases. In comparison with a group of 21 healthy controls fasting plasma glucagon concentration was significantly higher in the patients (198.75 +/- 13.20 pg/ml vs. 127 +/- 6.80 pg/ml; p less than 0.001). However, only 29 patients (60.4%) had elevated plasma glucagon levels, whereas 19 (39.5%) had abnormal plasma glucagon levels. Furthermore, no significant difference was found between the thyroid hormone pattern of the patients with hyperglucagonemia and of the patients with normal glucagonemia. On the other hand, a significant correlation between plasma glucagon concentrations and serum T3 and rT3 concentrations was not found. All these findings indicate that in patients with severe chronic illnesses the fall in circulating T3 cannot be due to hyperglucagonemia only which, therefore, might simply be a contributory factor together with other as yet unidentified disorders.
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PMID:[Role of high blood glucagon in the reduction of serum levels of triiodothyronine in severe non-thyroid diseases]. 263 98

The focus of this review is on the role of the renal nerves in contributing to the sodium retention associated with cirrhosis, congestive heart failure, and nephrotic syndrome. With respect to these three disease state information is presented which indicates that conditions exist which would be predicted to activate the sympathetic nervous system. Consistent with this, indirect indices of increased peripheral and renal sympathetic nerve activity are observed in these diseases. Acute experiments have indicated that the renal nerves are influencing sodium excretion in these sodium-retaining disorders. The renal nerves have the capacity to influence tubular sodium transport, renal hemodynamics, and renal endocrine release, all of which may affect the renal handling of sodium. Experiments are discussed which have implicated all three mechanisms of action in cirrhosis and congestive heart failure. Despite the fact that studies are demonstrating an increasing importance of the renal nerves, experiments have not been conducted to definitively implicate the renal nerves as being responsible for the long-term sodium retention in these disease conditions.
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PMID:Renal nerves in renal sodium-retaining states: cirrhotic ascites, congestive heart failure, nephrotic syndrome. 264 28

Hypertension can be ameliorated by certain concomitant disease states, especially those in which serum globulin is elevated. Blood pressure has been reduced in cases of cirrhosis of the liver, chronic alcoholism, congestive heart failure, arthritis, hypothyroidism, and myeloma. These clinical findings were confirmed experimentally when animals with various models of hypertension became normotensive after the development of a modest degree of liver damage with hyperglobulinemia. Other diseases, not associated with hyperglobulinemia, that can lower blood pressure are stroke, uremia, hyperparathyroidism, and malnutrition. When any of these diseases occur in hypertensive patients, their influence on blood pressure must be considered when determining treatment and prognosis.
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PMID:Disease states in which blood pressure is lowered. 261 Jul 59

Clinical laboratory and endoscopic data were collected prospectively in 268 patients with bleeding gastric ulcer who were admitted between September 1985 and November 1987. There were 22 deaths, giving a hospital mortality rate of 8.2%. Surgery was undertaken in 68 patients (25.4%) with a mortality rate of 17.6% (11.8% at 30 days). There was one fatality in 104 (1.0%) patients less than or equal to 60 years compared with 21 deaths (12.8%) in patients greater than 60 years (P less than 0.001). Cirrhosis (P less than 0.01), malignant disease (P less than 0.03), chronic obstructive airways disease (P less than 0.02), congestive cardiac failure (P less than 0.02) and ischaemic heart disease (P less than 0.08) were each associated with an increased risk of mortality. Outcome in patients greater than 60 years was related to systolic blood pressure at admission (P less than 0.03), haemoglobin (P less than 0.02), serum bilirubin (P less than 0.02), and total transfusion requirements (P less than 0.001). For ulcers less than or equal to 1 cm, 1- less than or equal to 2 cm, greater than 2 cm in size, mortality rates were 1.9%, 11.4% and 18.0%, respectively. Initial endoscopy findings of a visible vessel, fresh blood, or active spurting/oozing haemorrhage were associated with rebleeding rates necessitating emergency surgery of 30.0%, 36.4% and 40.0%, respectively. There was no evidence of rebleeding in 187 patients (79.9%) managed conservatively and only five patients (2.7%) in this group succumbed, whereas rebleeding did occur in 47 patients (20.1%) with 13 subsequent deaths (27.7%; P less than 0.001). In patients greater than 60 years the presence of endoscopic stigmata of recent haemorrhage should lead to early consideration of therapeutic endoscopy and/or early surgery, particularly for ulcers greater than 1 cm in size.
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PMID:Bleeding gastric ulcer: a prospective evaluation of rebleeding and mortality. 275 45

The most frequent causes of pleural effusion are congestive heart failure, advanced cirrhosis and nephrotic syndrome. In some rare cases urine can be found accumulated in the pleural compartment, being this entity denominated urinotorax. This phenomenon is generally considered secondary to an urinary obstruction or to an urinoma on the same side as the effusion through mechanisms not yet clarified. Given that it is a benign condition, easily resolved by clearing the obstruction of the urinary tract and that there is little information about it in the literature, we report a case of a massive pleural effusion secondary to hydronephrosis.
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PMID:[Massive pleural effusion secondary to hydronephrosis]. 277 33

Ascitic fluid from tumour patients (hepatoma, gastric cancer, gallbladder cancer, colorectal cancer, ovarian cancer) and from non-malignant diseases (liver cirrhosis, congestive heart failure) were compared with respect to their content of determinants of the fibrinolytic system, tissue-type plasminogen activator antigen (t-PAag) and activity (t-PAact), urokinase-type plasminogen activator antigen (u-PA) and plasminogen activator inhibitor activity (PAI). Furthermore, SDS-polyacrylamide slab-gel electrophoresis (SDS-PAGE) was performed to evaluate molecular weight distribution of the detectable fibrinolytic parameters. In malignant ascites, PAI activity was three to four times higher, and increased complex formation of PAI with t-PA could be demonstrated, compared with non-malignant ascitic fluid. Tissue-type plasminogen activator antigen and activity showed a similar concentration in ascites of both study groups. Urokinase-type plasminogen activator antigen was detectable neither in ascites of malignant nor in ascites of non-malignant origin. It is concluded that t-PA is the physiological plasminogen activator in ascites and that increased PAI levels followed by increased complex formation between t-PA and PAI might reflect a reaction of the peritoneum.
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PMID:Plasminogen activators and plasminogen activator inhibitor in malignant and non-malignant ascitic fluid. 285 12


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