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)

Serum rubella, measles and cytomegalovirus antibodies were measured in patients with various forms of chronic liver disease and compared with those in age-matched controls. In CAH all three antibodies were found in significantly greater titre than in controls,and in cryptogenic cirrhosis titres to rubella were significantly increased. In alcoholic cirrhosis none was increased. There was no correlation between antibody titres and either the presence of portal-systemic shunts or the use of steroids. In patients with CAH measles titres were significantly related to the presence of ANF and SMA.
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PMID:Viral antibodies and chronic liver disease. 18 61

The "Peripheral Arterial Vasodilation" hypothesis most completely explains the clinical spectrum of cirrhosis ranging from compensated to decompensated to the hepatorenal syndrome (Figure 15-1). As the systemic peripheral vasodilation increases, the neurohumoral responses to arterial underfilling are stimulated with resultant renal vasoconstriction, sodium and water retention. Hypoalbuminemia and portal hypertension, as well as local effects of vasodilation at the capillary level, also contribute to ascites formation and peripheral edema. The suppressed plasma renin activity and aldosterone concentrations and exaggerated natriuresis, which are observed in some patients with early cirrhosis during HWI and the supine position, probably indicate greater central translocation of splanchnic fluid in these volume expanded cirrhotic patients when compared with normal subjects. This interpretation is supported by the greater increases in ANF during HWI in these patients when compared with controls. The neurohumoral responses to arterial vasodilation in cirrhosis combine to decrease distal sodium and water delivery, an event which impairs escape from the sodium retaining effects of aldosterone and causes resistance to the distal tubular effect of ANF (Figure 15-3). As discussed, the peripheral arterial vasodilation of cirrhosis is no doubt multifactorial in nature and the resultant arterial underfilling may be worsened by events that could impair the cardiac response to afterload reduction, including bile salt accumulation, alcoholic cardiomyopathy, and tense ascites decreasing cardiac preload. This pathogenetic schema of cirrhosis is compatible with the unifying body fluid volume hypothesis (Figure 15-3), which we have recently proposed.
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PMID:Pathogenesis of sodium and water retention in liver disease. 129 35

The first human studies using relatively high-doses of ANF revealed similar effects as observed in the preceding animal reports, including effects on systemic vasculature (blood pressure fall, decrease in intravascular volume), renal vasculature (rise in GFR, fall in renal blood flow), renal electrolyte excretion (rises in many electrolytes), and changes in release of a number of different hormones. Whether all these changes are the result of direct ANF effects or secondary to a (single) primary event of the hormone remains to be determined. Certainly, it has been proven that more physiological doses of ANF fail to induce short-term changes in many of these parameters leaving only a rise in hematocrit, natriuresis and an inhibition of the RAAS as important detectable ANF effects in humans. This leads us to hypothesize that ANF is a "natriuretic" hormone with physiological significance. The primary function in humans is to regulate sodium homeostasis in response to changes in intravascular volume (cardiac atrial stretch). Induction of excess renal sodium excretion and extracellular volume shift appear to be the effector mechanisms. The exact mechanism of the natriuresis in humans still needs to be resolved. It appears however, that possibly a small rise in GFR, a reduction in proximal and distal tubular sodium reabsorption, as well as an ensuing medullary washout, are of importance. The pathophysiological role of ANF in human disease is unclear. One may find elevated plasma irANF levels and/or decreased responses to exogenous ANF in some disease states. Whether these findings are secondary to the disease state rather than the cause of the disease remains to be resolved. Therapeutic applications for ANF, or drugs that intervene in its production or receptor-binding, seem to be multiple. Most important could be the antihypertensive effect, although areas such as congestive heart failure, renal failure, liver cirrhosis and the nephrotic syndrome cannot be excluded. Although the data that have been gathered to date allowed us to draw some careful conclusions as to the (patho)physiological role of ANF, the exact place of ANF in sodium homeostatic control must still be better defined. To achieve this, we will need more carefully designed low-dose ANF infusion, as well as ANF-breakdown inhibitor studies. Even more promising, however, is the potential area of studies open to us when ANF-receptor (ant)agonists become available for human use.
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PMID:Atrial natriuretic factor: its (patho)physiological significance in humans. 131 17

In 12 patients with cirrhosis of the liver (six with ascites) and six controls the authors made catheterizations of the hepatic veins and portal circulation, assessing concurrently the in cardiac output by thermodilution. The patients with ascitic cirrhosis had, as compared with controls, a significantly higher portohepatic gradient, central venous pressure, mean pressure in the pulmonary artery and also pulmonary capillary wedged pressure and a significantly lower mean arterial pressure and systemic vascular resistance. These patients had also, as compared with controls, a significantly higher concentration of ANF (atrial natriuretic factor) in the pulmonary artery (15.89 +/- 2.26 vs. 8.04 +/- 0.97, p less than 0.01) and in the hepatic vein (7.44 +/- 0.44 vs. 3.91 +/- 0.63, p less than 0.01); the difference between ANF concentrations in the peripheral blood stream was not significant (9.52 +/- 2.46 vs. 5.71 +/- 1.24 n. s.). Patients with ascitic cirrhosis of the liver had a significantly higher calculated cardiac production of ANF than controls (24.36 +/- 3.44 vs. 8.12 +/- 2.9, p less than 0.01); the difference in the splanchnic extraction of ANF between patients with ascitic cirrhosis of the liver (0.46 +/- 0.1) and controls (0.51 +/- 0.06) was not significant. The ANF concentration in the pulmonary artery in patients with cirrhosis of the liver correlated significantly with the central venous pressure (r = 0.677, p = 0.02) and the pressure in the pulmonary artery in a wedged position (r = 0.639, p = 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Atrial natriuretic factor in liver cirrhosis. Relation to hemodynamic parameters]. 213 92

Thirty-seven patients with volume-retaining disorders (liver cirrhosis with ascites, n = 8; heart failure NYHA III-IV, n = 12; endstage renal failure, n = 17) and twelve healthy age-matched controls were given a small dose (33 micrograms) of hANF (human atrial natriuretic factor). We tested the resulting hemodynamic and renal effects as well as the effect on plasma cyclic GMP levels and compared them with the properties of platelet ANF receptors. The ANF injection evoked an increase in cyclic GMP plasma levels of 19.3 +/- 2.2 nM in healthy controls. This increase tended to be smaller in the cirrhosis group (15.5 +/- 3.3 nM) and in the heart failure group (16.8 +/- 2.3 nM) than in the dialysis group (20.5 +/- 2.5 nM). The invasion rates of cyclic GMP were comparable in all groups, but the evasion rates increased more in the heart failure and endstage renal failure groups (27.9 +/- 7.7 min and 26.1 +/- 3.4 min, respectively) than in the cirrhosis and control groups (14.9 +/- 1.9 min and 14.2 +/- 1.9 min, respectively). Patients with endstage renal failure and congestive heart failure showed a smaller decrease in diastolic blood pressure than controls and patients with liver cirrhosis. Renal actions of ANF were diminished in cirrhosis and heart failure patients. Binding capacities of platelet ANF receptors were higher in the control group (12.2 +/- 1.5 receptors/cell) than in the patient groups (cirrhosis, 7.8 +/- 1.2; endstage renal failure, 8.0 +/- 0.9; heart insufficiency, 8.0 +/- 1.0 receptors/cell), with no differences among the patient groups. Binding affinities were not significantly different. Correlation analysis showed that the relationship between the actions of ANF and the increases in plasma cyclic GMP levels is loose and cannot predict the hemodynamic or renal effects of exogenous ANF in a given patient. Although the behavior of plasma cyclic GMP levels fails to predict the responsiveness of the body to ANF in a given patient, it does reflect the differences between the patient groups and the control group. In contrast, we found no correlation between the properties of platelet ANF receptors and ANF action.
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PMID:Effects of a small bolus dose of ANF in healthy volunteers and in patients with volume retaining disorders. 216 5

Plasma immunoreactive atrial natriuretic factor (irANF) levels and the effects of alpha-human ANF (alpha-hANF) infusion were investigated in 7 patients with liver cirrhosis and ascites. Under basal conditions, supine blood pressure (BP) averaged 136/76 +/- 9/4 mm Hg (mean +/- SEM). Plasma irANF concentrations (124 +/- 33 pg/ml) were higher (p less than 0.01) than those in age-matched normal subjects (47 +/- 5 pg/ml). Plasma renin activity (PRA 5.9 +/- 2.2 ng/ml/h), aldosterone (18 +/- 7 ng/dl) and norepinephrine (NE, 66 +/- 5 ng/dl) levels were also elevated compared to the age-related normal range. Alpha-hANF infusion for 60 min at 0.036 micrograms/kg/min decreased the mean BP (-14%; p less than 0.05), increased PRA (+179%; p less than 0.05) and plasma NE (+24%; p less than 0.05). Glomerular filtration rate (GFR), effective renal plasma flow (ERPF), diuresis and natriuresis were not modified. A subsequent 60-min infusion of alpha-hANF at 0.067 micrograms/kg/min produced a marked fall in mean BP (-26%; p less than 0.001), hemoconcentration (hematocrit +6%; p less than 0.001) despite stable body fluid balance and a further increase in PRA (+350%, p less than 0.005). GFR and ERPF were severely reduced (-55 and -56%, respectively; p less than 0.001), while diuresis and natriuresis were not modified. Plasma aldosterone was unaltered during, but rose (+72%; p less than 0.01) after the cessation of alpha-hANF infusion. Variations in natriuresis during alpha-hANF infusion correlated positively with BP (r = 0.47; p less than 0.01), ERPF (r = 0.53; p less than 0.01) or GFR (r = 0.51; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypotension and renal impairment during infusion of atrial natriuretic factor in liver cirrhosis with ascites. 253 Sep 3

Plasma levels of atrial natriuretic factor (ANP) were examined in 12 patients with liver cirrhosis (6 with ascites) and 6 controls before and after the administration of the infusion of 2000 ml of saline solution per 70 kg of body weight during 2 hours. Basal concentration of ANF tended to be slightly, but nonsignificantly higher in patients with ascitic liver cirrhosis (5.5 +/- 1.3 fmol/ml) than in controls (3.0 +/- 1.0 fmol/ml) and in patients with non-ascitic liver cirrhosis (4.6 +/- 1.3 fmol/ml). Saline administration led to the comparable increase of plasma ANF in ascitic (14.2 +/- 4.0 fmol/ml) and non-ascitic cirrhotics (15.7 +/- 3.7 fmol/ml) and in controls (12.4 +/- 4.3 fmol/ml). The increase of plasma ANF was accompanied by the suppression of plasma renin activity (PRA) and plasma aldosterone (PA) in all groups; in ascitic patients, however, PRA and PA remained above the normal range. While in controls and non-ascitic cirrhotics saline administration led to the increase of urine flow rate /from 0.74 +/- 0.13 to 2.04 +/- 0.44 ml/min, P less than 0.01, in controls; from 0.83 +/- 0.05 to 1.28 +/- 0.07 ml/min, P less than 0.01, in non-ascitic cirrhotics) and urinary sodium excretion (from 110.7 +/- 21.3 to 364.8 +/- 74.4 umol/min, P less than 0.01, in controls; from 125.0 +/- 16.7 to 218.7 +/- 24.3 umol/min, P less than 0.01 in non-ascitic cirrhotics), in patients with ascitic liver cirrhosis neither urine flow rate (from 0.66 +/- 0.1 to 0.72 +/- 0.15 ml/min, n.s.), nor urinary sodium excretion (from 16.7 +/- 9.9 to 54.2 +/- 40.3 umol/min, n.s.) changed significantly.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial natriuretic factor in liver cirrhosis--the influence of volume expansion. 253 Nov 15

Defects of the ANF system in cirrhosis have not been demonstrated in terms of absolute deficiency of plasma levels or by evidence of major abnormalities of processing in patients with cirrhosis. In the present study, the responsiveness of the ANF system to acute volume stimulation by water immersion and the diuretic and natriuretic effects of ANF infusion were examined. Stimulation of ANF release by 1-h immersion was significantly blunted in ten cirrhotic patients with ascites (increase of plasma ANF by 46 +/- 18%), whereas 11 cirrhotics without ascites showed a 104 +/- 16% increase, similar to the 117 +/- 29% stimulation in 25 healthy controls. Immersion increased urinary volume by 3.6 +/- 0.6/2.0 +/- 0.8/0.7 +/- 0.4 ml/min and urinary sodium excretion by 146 +/- 38/75 +/- 43/43 +/- 19 mumol/min in controls/cirrhotics without/cirrhotics with ascites. Infusion of ANF for 30 min prompted an increase in diuresis and natriuresis in seven cirrhotic patients, which was less marked in patients with ascites, as compared to patients without ascites. Thus, the stimulus response coupling for ANF may be impaired in patients with cirrhosis and ascites.
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PMID:[Pathophysiologic and clinical relevance of atrial natriuretic factor in patients with cirrhosis of the liver]. 297 Jan 81

1. Evidence from numerous experiments incorporating central blood volume expansion and changes in sodium status supports atrial stretch as the prime determinant of ANF release. 2. Plasma ANF levels are the result of both secretion and clearance of the peptide. Clearance is altered by a number of factors, including changes in posture in normal man and is probably impaired in disease states with diminished renal and hepatic blood flow. 3. In normal subjects an inverse relationship exists between plasma ANF values and renin-angiotensin-aldosterone system activity. This relationship is lost and replaced by a positive association in heart failure, presumably reflecting the abnormal concurrence of increased atrial stretch and diminished renal perfusion in this condition. Plasma ANF values rise with increasing severity of heart failure and fall with effective treatment. 4. Plasma ANF values are elevated in hypertension and cardiac tachyarrhythmias possibly reflecting raised central venous and atrial pressures. 5. A variety of other disorders may be associated with abnormal plasma ANF values including cirrhosis and the syndrome of inappropriate ADH secretion. 6. Evidence from low-dose infusions of ANF in normal volunteers suggests that the variations in plasma ANF seen in health and disease are sufficient to exert biological effects. 7. The advent of a specific antagonist is needed to provide further insight into the physiological and pathophysiological roles of ANF.
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PMID:Atrial natriuretic factor in human pathophysiology. 297 38

Serum concentrations of ANF, Renin and Aldosterone were measured in animals with experimental cirrhosis and volume overload. We studied 75 Wistar rats divided in five groups. Group I: rats with hepatic cirrhosis induced by CCl4; Group II: Control rats; Group III: rats with hepatic cirrhosis and continuous infusion of saline serum; Group IV: control rats with continuous infusion and Group V: cirrhotic rats and bolus infusion of saline. There were no statistical differences in serum concentrations of ANF (232 +/- 75 vs 195 +/- 42 pg/ml) and Renin concentration (182 +/- 24 vs 171 +/- 34 ng/ml/hour) between controls and rats with cirrhosis. However, Aldosterone levels were elevated in cirrhotic rats in basal conditions as compared to controls (1197 +/- 287 vs 475 +/- 88 pg/ml; p < 0.001). The volume overload caused a paradoxical decrease of ANF in cirrhotic rats (124 +/- 15 and 122 +/- 17; p < 0.001). On the other hand, no changes were observed in Renin and Aldosterone after volume expansion. These results suggest the existence of a hemodynamic response to compensate the volume overload. Other studies are necessary to confirm this hypothesis.
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PMID:[Effects of blood volume expansion on atrial natriuretic factor and the renin-aldosterone axis in experimental cirrhosis]. 803 15


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