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)

The plasma levels of atrial natriuretic peptide (ANP) have been determined by direct radioimmunoassay in 36 clinically-healthy subjects, 24 patients with compensated cirrhosis of the liver, and 20 patients with cirrhosis and ascites. When compared with controls, plasma levels of ANP in compensated cirrhosis do not demonstrate a significant difference (p greater than 0.05). Patients with decompensated cirrhosis of the liver show significantly (p less than 0.001) higher levels of ANP with respect to the controls and to compensated patients. In the control group, a significant (p less than 0.001) negative correlation between plasma levels of ANP and plasma renin activity and plasma aldosterone is demonstrated. The patients without ascites do not present any correlation between these variables (p greater than 0.05). The patients with ascites show a significant (p less than 0.01) positive correlation between ANP and plasma renin activity and plasma aldosterone levels. These results and other data suggest that ANP, although appearing to have plasma levels correlated with the disease stage, and with increases in both renin activity and plasma aldosterone levels, does not seem to have a very important role in sodium retention, or in genesis of ascites in cirrhosis of the liver. Activation of the renin-angiotensin-aldosterone system, activation of the sympathetic nervous system, and the circulatory modifications as well as other mechanisms seem to be more important in the formation of ascites in cirrhotic patients.
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PMID:Plasma levels of atrial natriuretic peptide in compensated and decompensated cirrhosis of the liver. Relationship with the renin-aldosterone system. 253 27

Plasma levels of human atrial natriuretic peptide (hANP) were investigated in patients with liver cirrhosis, and the relationships between plasma hANP levels and the following factors were studied: presence of ascites, serum and urine electrolytes, plasma renin activity, angiotensin I and II, aldosterone, catecholamines, prostaglandin derivatives, conventional liver function tests and circulating blood volume. Plasma hANP level was significantly (P less than 0.05) elevated in patients with ascites (mean = 58.6 pg/mL, s.e.m. = 8.8) compared with cases without ascites (mean = 36.6 pg/mL, s.e.m. = 2.6). With the disappearance of ascites, the level fell to normal in most cases. Urine sodium excretion was positively correlated with plasma hANP in patients without ascites, but not in patients with ascites. The plasma hANP level was disproportionately high for the rate of urinary Na excretion in cirrhotics with ascites. The plasma hANP level was not correlated with any of the other factors such as blood volume, renin-angiotensin-aldosterone levels, catecholamines and liver function tests. These results suggest that plasma hANP levels are elevated in cirrhotic patients especially with ascites, but the natriuretic response of the kidney to this raised hANP level can be impaired in patients with liver cirrhosis and ascites.
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PMID:Plasma human atrial natriuretic peptide levels in patients with liver cirrhosis. 253 28

The present study aimed to assess relationships between plasma levels of atrial natriuretic peptide (ANP) and plasma volume, systemic vascular resistances, cardiac output and plasma renin activity in patients with cirrhosis. Thirty patients were included: eight with no history of liver disease were used as controls; 22 patients had biopsy-proven alcoholic cirrhosis without ascites (n = 11) and with ascites (n = 11). Mean ANP plasma level was significantly higher in both groups of cirrhotic patients than in controls (P less than 0.05). In the control group, ANP and plasma renin activity were inversely correlated (P less than 0.05) but no correlation was found in cirrhotic patients. In the group of patients with ascites, ANP plasma levels were inversely correlated to plasma volume (P less than 0.05) and to cardiac output (P less than 0.01) and directly correlated to systemic vascular resistances (P less than 0.01). Using multiple regression analysis, ANP remained correlated only with systemic vascular resistances (P less than 0.05). These results suggest that cirrhotic patients have high plasma levels of ANP whether or not they have ascites. In the light of current knowledge of ANP actions, the relationships between ANP plasma levels and plasma volume, cardiac output, and systemic vascular resistances are paradoxical in cirrhotic patients with ascites. ANP does not seem to play a critical role in the pathogenesis of sodium and water retention observed in these patients.
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PMID:Atrial natriuretic peptide, plasma renin activity, plasma volume, systemic vascular resistance and cardiac output in patients with cirrhosis. 253 41

The pharmacokinetics and pharmacodynamics (blood pressure, heart rate, serum angiotensin-converting enzyme, and plasma renin activity) of enalapril and enalaprilat were studied after oral administration of enalapril maleate (10 mg) to seven biopsy-proven cirrhotic patients and to seven healthy subjects. The mean Cmax, AUC, and urinary excretion of enalapril and enalaprilat were greater and less (p less than 0.01), respectively, and mean oral clearance of enalapril was less (p less than 0.01) in the cirrhotic group than in the healthy group. However, there was no significant difference in the mean total drug (enalapril plus enalaprilat) excretion between the two groups. Blood pressure fell (p less than 0.05) only at 3 or 4 hours postdose, with no change in heart rate in the two groups. Serum angiotensin-convering enzyme (ACE) decreased (p less than 0.001) and plasma renin activity (PRA) increased (p less than 0.05) in the two groups. The magnitude of the percentage of inhibition of ACE activity was comparable between the two groups. Serum enalaprilat concentration correlated (p less than 0.001) with the percentage of inhibition of ACE activity. The results suggest that the bioactivation of enalapril to enalaprilat is considerably impaired in patients with cirrhosis but that the pharmacodynamic effects do not appear to be blunted in those patients. The mechanism and clinical implications remained unclear.
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PMID:Kinetics and dynamics of enalapril in patients with liver cirrhosis. 254 35

1. Perindopril, a new ACE inhibitor, is a prodrug requiring conversion into its active form perindoprilat by hydrolysis in the liver. 2. The pharmacodynamics and pharmacokinetics of perindopril (8 mg oral) and perindoprilat (2 mg intravenously) were studied in a double-blind randomised crossover study in a group of patients with compensated biopsy-proven hepatic cirrhosis. 3. Blood pressure and heart rate responses were similar after the two routes of administration as were plasma renin activity and aldosterone levels following dosing. 4. The AUC of perindoprilat after oral administration of perindopril represented 46 +/- 4% of the total AUC of perindopril and its metabolite when expressed in molar terms. Comparison with the AUC of perindoprilat after its intravenous administration suggested that 30 +/- 6% of the oral dose of perindopril was converted to its active metabolite. 5. The findings are comparable with those in healthy subjects. It appears that the presence of relatively mild hepatic cirrhosis does not significantly alter the pharmacokinetics of perindopril.
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PMID:The pharmacokinetics and pharmacodynamics of perindopril in patients with hepatic cirrhosis. 255 45

The relationship between adrenocorticotropic hormone as well as renin and potassium activity and blood aldosterone secretion was examined in normal subjects and patients with chronic hepatic diseases. It is demonstrated that aldosterone stimulation is controlled by simultaneous renin-angiotensin (RA) and hypothalamo-adenopituitary effects in normal subjects and patients with chronic active hepatitis (CAH), the RA effects prevailing in normal subjects, and hypothalamo-adenopituitary ones, in CAH patients. Cirrhosis of the liver was associated with the greatest deviations in the stimulant-aldosterone relationship. Viral cirrhosis with ascites featured a considerable RA increase, affecting the adrenals, while the contribution of ACTH was reduced considerably. ACTH level was the highest in patients with alcoholic cirrhosis.
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PMID:[Hormonal changes in chronic diffuse diseases of the liver]. 255 Oct 48

Ascites is a frequent complication in patients with liver cirrhosis. The accumulation of fluid in the abdominal cavity is associated with disturbances of systemic and splanchnic haemodynamics and of kidney function, which contribute to the poor prognosis of these patients. Classically, the treatment of ascites in patients with cirrhosis has been based on the combination of a sodium-restricted diet and the administration of diuretics. However, this treatment is not entirely satisfactory, since it is associated with a relatively high incidence of side-effects, and about 20% of patients hospitalized for the treatment of an episode of ascites do not respond to such therapy. In the last two decades, alternative therapies to diuretics have been introduced. PVS is an effective method of treating ascites. The high incidence of complications observed in early studies may be reduced by adequate perioperative management and careful selection of patients. The role of the PVS in the treatment of cirrhotics with ascites, however, still remains to be established. Recently, paracentesis has emerged as an alternative method of treating ascites in patients with cirrhosis. Several studies have shown that therapeutic paracentesis plus i.v. albumin infusion is more effective than conventional diuretic therapy and is associated with a lower incidence of complications. It has also been demonstrated that therapeutic paracentesis without the i.v. administration of albumin is associated with a marked increase in plasma renin activity, suggesting an impairment of effective blood volume, and with the development of hyponatraemia and/or renal failure in 20% of cases. Therefore, the i.v. administration of albumin is an essential measure in preventing the impairment of systemic haemodynamics and renal function that frequently follows the mobilization of ascites by paracentesis.
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PMID:Treatment of ascites and renal failure in cirrhosis. 265 48

Systemic, femoral, and renal hemodynamics were evaluated in 7 control subjects and 20 cirrhotic patients with ascites, 14 of them without (group A) and 6 with (group B) functional renal failure. Hyperdynamic systemic circulation, increased plasma volume, and hyperreninism were present in groups A and B. These changes were more severe in group B, which showed, as compared with group A, lower total vascular resistances and mean arterial pressure together with increased cardiac index and plasma renin activity. Significant differences in regional hemodynamics were also observed between groups. In group A, femoral and renal fractions of cardiac output were respectively increased and reduced as compared with controls. By contrast, in group B, both fractions of cardiac output were reduced when compared either with controls or with group A. In the entire patient group there was a close direct correlation between femoral and renal fractions of cardiac output (r = 0.88; p less than 0.001) and both of them correlated independently with total vascular resistances (r = 0.79; p less than 0.001 in both cases). These results indicate that, in nonazotemic cirrhotics with ascites, vasodilatation in extrasplanchnic areas contributes to the genesis of the hyperdynamic circulation. The presence in group B of a reduced flow to extrasplanchnic territories, in association with an increase of the hyperdynamic circulatory status, suggests that exacerbation of splanchnic vasodilatation is involved in the development of the hepatorenal syndrome. Finally, in cirrhosis, the changes that occur in systemic hemodynamics appear to influence renal function and renal blood flow.
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PMID:Systemic and regional hemodynamics in patients with liver cirrhosis and ascites with and without functional renal failure. 267 83

The pathogenetic role of ADH in determining hyponatremia in patients with liver cirrhosis is still much debated. Osmotic stimuli are not able to inhibit secretion of ADH in refractory ascites and under such conditions the reduction in effective plasma volume has been put forward as the main cause. Twenty patients with liver cirrhosis and refractory ascites were studied before and during extraction-concentration-reinfusion (ECR) of ascitic fluid by means of Rhodiascit. ADH, renin, aldosterone, blood and urine osmolarity, plasma and urinary concentration of sodium, potassium, chlorine, and the clearance of free water were evaluated. All patients presented high renin values (15.4 +/- 11.7 ng/ml), aldosterone (341 +/- 172 ng/ml), ADH (6.3 +/- 5.2 pg/ml). During ECR, a significant drop was observed in renin (p less than 0.001), aldosterone (p less than 0.001) urinary osmolarity (p less than 0.001) and an equality significant increase in diuresis (p less than 0.001), natriuria (p less than 0.005), kaliuria (p less than 0.001) while ADH presented an irregular course: in 11 cases it remained unchanged, in 3 it fell and in 6 it presented a constant increase. To conclude, data suggest that the diminished filtrate reaching the distal tubule constitutes the greatest cause of the inability to dilute urine in many patients with cirrhosis and that ADH is a permissive rather than a primary factor.
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PMID:[Changes in antidiuretic hormone (ADH) in liver cirrhosis with resistant ascites]. 268 81

Fasting plasma caffeine concentrations, plasma levels of catecholamines and plasma renin activity were measured in patients with cirrhosis and control patients without hepatic dysfunction. A careful dietary history showed no significant difference in caffeine consumption (mean +/- S.E.) among 46 cirrhotics (86 +/- 7 mg per day) vs. 34 control patients (91 +/- 8 mg per day). Fasting plasma caffeine concentrations, however, were significantly higher (7.68 +/- 1.42 micrograms per ml) in cirrhotics than in controls (1.01 +/- 0.20 micrograms per ml) (p less than 0.01). Fasting plasma caffeine concentrations in cirrhotics varied significantly with Child's criteria, namely Child's A patients (2.06 +/- 0.38 micrograms per ml); Child's B patients (6.92 +/- 1.86 micrograms per ml), and Child's C patients (17.70 +/- 3.65 micrograms per ml) (p less than 0.001). In 44 cirrhotics, fasting plasma caffeine concentrations were compared with plasma levels of catecholamines and plasma renin activity. Plasma epinephrine concentrations were normal; however, plasma norepinephrine concentrations were increased in six cirrhotics, and plasma renin activities were increased in 28 cirrhotics. After a 3-day caffeine abstinence, plasma caffeine concentration and renin activity were significantly decreased (p less than 0.01), and high plasma norepinephrine levels were also decreased in 12 cirrhotics. Plasma caffeine concentration, renin activity and norepinephrine level did not change in a control group of cirrhotics who continued to receive caffeine for 3 days (n = 6). After abstinence from caffeine, the decrease of fasting plasma caffeine concentration correlated well with the decrease of plasma renin activity (r = +0.746, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fasting plasma caffeine level in cirrhotic patients: relation to plasma levels of catecholamines and renin activity. 268 39


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