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)

Since the discovery of the atrial natriuretic factor (ANF) an endocrine function has been attributed to the mammalian heart. This function may include definition of optimal conditions for efficient performance of the heart, e.g. by reduction of afterload in hypertension or of preload and afterload in heart failure. Plasma ANF levels were measured in various cardiovascular disease states and compared with those of controls and of patients with liver cirrhosis. Plasma ANF levels in hypertensive patients were sevenfold higher than in controls, and in patients with heart failure 40-fold higher than normal values. Small differences were detected between controls and patients with cirrhosis of the liver, in spite of the impaired renal sodium handling seen in cirrhotics. Plasma ANF levels were significantly correlated with haemodynamic parameters and were inversely related to the cardiac index. Treatment with an angiotensin converting enzyme inhibitor led to a significant decrease in plasma ANF levels in parallel with the haemodynamic improvement. Preliminary chromatographic analysis suggested differences in the structure of plasma ANF between normotensive and hypertensive subjects.
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PMID:Atrial natriuretic factor in plasma of patients with arterial hypertension, heart failure or cirrhosis of the liver. 294 36

An assay of Kininase II activity in the serum of 92 jaundice patients revealed a significant difference between the group with viral hepatitis (268.48 +/- 70.93 U/ml), that with biliary obstructions (133.05 +/- 37.64 U/ml) and with cirrhosis (173.76 +/- 79.56 U/ml). The increase encountered in patients with medical jaundice correlates well with total bilirubinaemia but not with cytolysis enzymes. This suggests failed demolition of ACE by the hepatocyte during cellular stress.
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PMID:[Variations in serum kininase II activity in acute jaundice]. 301 14

In hepatic cirrhosis neurohumoral vasoconstrictor systems are activated to compensate for circulatory disturbances. To study the renin-angiotensin-aldosterone system in more detail, angiotensin converting enzyme in 15 patients with advanced liver disease was inhibited with captopril after moderate sodium restriction. Captopril caused an increase in plasma renin activity (p less than 0.005) and a decrease in plasma aldosterone (p less than 0.025) from an elevated baseline, and a moderate drop in systolic (p less than 0.025) and diastolic (p less than 0.05) blood pressure. Hyperreninaemia after captopril was inversely related to the prevailing plasma sodium level (r = -0.66, p less than 0.01), and the changes in both systolic and diastolic blood pressure were correlated with baseline plasma renin activity (r = 0.49, p less than 0.05 for systolic and r = 0.71, p less than 0.01 for diastolic blood pressure). No change occurred in heart rate or in stimulated plasma noradrenaline and vasopressin levels. The data suggest that in these cirrhotic patients the reactivity of the renin-angiotensin-aldosterone system was still intact, although it occurred at a higher level. They confirm the importance of the renin-angiotensin-aldosterone system in arterial blood pressure regulation in cirrhosis.
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PMID:Effect of captopril on renin and blood pressure in cirrhosis. 331 47

Plasma angiotensin I-converting enzyme "activity" (CEA) was estimated as its enzymatic effect on the synthetic substrate HHL in normal subjects and patients with untreated sarcoidosis, alcoholic decompensated liver cirrhosis and scleroderma. CEA was above the upper limit of normal in 60% of sarcoidosis cases and 30% of cirrhotics; it was within normal in scleroderma. The assessment of the influence of chloride concentration on CEA showed that maximum was obtained for a concentration of 300 mM. In addition the inhibitory effect of angiotensin I and the converting enzyme inhibitors SQ 14225 and MK 422 was demonstrated together with the action of high concentrations of penicillamine. The inhibitory influence of these substances was similar when added to the plasma of normal or sarcoidosis subjects.
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PMID:[Clinical value of the estimation of plasma converting enzyme activity]. 608 53

Ascites often appears as a complication of several illnesses. The therapy is essentially based on the use of low-sodium diet, plasma or albumin infusion, diuretics and low-dosed ACE-inhibitors. To use the simple paracentesis or special techniques as Rhodiascit or Lee Veen Shunt means not to resolve definitively the problem and sometimes to cause undesirable complications. The authors present a new therapeutic tactics that joins the use of technique of double filtration of ascitic fluid and reinfusion of concentrated proteins (DFAF) with the injection in the peritoneal cavity of beta-interferon and the venous infusion of ATIII. Twenty patients affected by hepatic cirrhosis with the presence of ascitic fluid not treatable with the usual therapy have been subjected to this treatment. All the patients showed an immediate improvement of the clinical situation. After one year of observation, we describe our results. Twelve patients needed a further treatment with the DFAF technique, two patients died for the original pathology and six patients just needed an adjustment of pharmacologic therapy.
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PMID:[Reinfusion ascites therapy: considerations after a year's experience]. 748 Sep 64

Prerenal acute renal failure is defined as a reduction in the glomerular filtration rate due to a primary disturbance in renal hemodynamics in the absence of any structural kidney damage. In case of moderate hypotension or hypovolemia, a number of adaptative systemic and intrarenal responses preserve renal perfusion and filtration rates, particularly by inducing a marked reduction in preglomerular arteriolar resistance and an increase in postglomerular resistance. However, these mechanisms are inherently limited. In the presence of advanced circulatory failure or iatrogenic pharmacologic interventions compromising these renal defense mechanisms, prerenal failure becomes evident. Therefore, prerenal failure may occur during acute hemodynamic disturbances due to hypovolemia or systemic vasodilatation, in severe cardiac failure, in cirrhosis with ascites, and in certain clinical situations following administration of nonsteroidal antiinflammatory agents or angiotensin converting enzyme inhibitors. The treatment depends on the underlying cause.
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PMID:[Functional acute kidney failure]. 756 89

Fosinopril is distinguished from other ACE inhibitors by a pharmacokinetic pecularity in the sense that is can be metabolized either by liver or kidney. This was the rationale of the present research the aim of which was to verify if administered to patients with liver cirrhosis the drug was liable to alter global liver function and ability to metabolize drugs. Eight cirrhotic males, mean age 56 years, also suffering from high blood pressure, were studied. In these patients, liver and kidney function tests (BUN, creatinine blood level, serum and urinary electrolytes, creatinine clearance, calcium and phosphor blood level, transaminases, alkaline phosphatase prothrombin time, cholinesterase, gamma-glutamyl-transpeptidase) were carried out at baseline and after 30 days' fosinopril treatment (1 capsule every morning in the fasting state); in addition total functioning liver mass was assessed by the galactose test, and drug-metabolizing capacity by the antipyrine test. Treatment resulted in a significant improvement of pressure values in all patients (p < 0.01) and did not alter liver and kidney function parameters. Besides, no side effects were registered, especially no case of orthostatic hypotension. The antipyrine test was not influenced by fosinopril treatment. Therefore, short-term treatment with this ACE-inhibitor can be concluded to be effective and not to cause additional alterations of liver function in patients with liver cirrhosis.
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PMID:[Evaluation of the total hepatic function after treatment with fosinopril in hypertensive patients with liver cirrhosis]. 772 Mar 55

A 49-year-old man with liver cirrhosis and hypertension was found to have hyperkalemia out of a degree of renal insufficiency and metabolic acidosis with low to normal anion gap, aggravated by volume contraction with diarrhea and medications (captopril, spironolactone and atenolol) interfering with potassium homeostasis. Plasma renin activity and serum aldosterone levels of this patient on a regular diet after discontinuation of medications were very low compared to those of five other cirrhotic patients with normokalemia as controls. Also, the renin-aldosterone stimulation testing on this patient performed by sodium restricted diet and furosemide, upright position and by angiotensin converting enzyme inhibition (captopril, 50 mg) showed the blunted renin and aldosterone responses to each of these stimuli, almost no changes from baseline renin and aldosterone levels, it was concluded that the underlying defect responsible for hyperkalemia in this case was hyporeninemic hypoaldosteronism and this was aggravated by other factors or drugs affecting potassium homeostasis.
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PMID:Hyperkalemia due to hyporeninemic hypoaldosteronism with liver cirrhosis and hypertension. 817 35

Differential value of ACE activity and acid alpha 1-glycoprotein was evaluated in the selected liver and biliary tract diseases. The study involved 75 patients divided into 4 subgroups, according to the character of their disease: patients with the acute viral hepatitis, chronic viral hepatitis, liver cirrhosis, and cholelithiasis. It was found that ACE activity was significantly increased in all pathologies involving liver parenchyma, and normal in patients with extrahepatic cholestasis. It was also shown that simultaneous assays of ACE and acid < alpha 1-glycoprotein may serve as a sensitive test differentiating jaundice in parenchymal hepatic diseases from that in the course of extrahepatic pathology.
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PMID:[Activity of angiotensin converting enzyme I and levels of acid alpha glycoprotein in selected liver and biliary tract diseases]. 823 40

The authors describe a case of giant benign cystadenoma of the ovary in a 55 year old woman. The patient came to their observation complaining of severe abdominal pain which started right after she was treated with a paracentesis, because of the suspicion of cirrhosis with ascites. The authors briefly outline the two goals of the diagnostic strategy: the diagnosis of the disease and the diagnosis of the nature of the disease. They stress the utmost importance of ultrasound and computerized tomography scans in the diagnosis of disease. For the diagnosis of the nature of the disease the authors counted on Ca 125, CEA, LDH levels and on Ca 19.9 and ACE levels as well. The surgical management of abdominal mass, which is the only possible treatment, led to the removal of a 60 cm in diameter and 30 kg mucinous cystadenoma. After the viscera of the higher abdomen (liver and stomach) had been repositioned, a plastic closure of the enormously expanded anterior abdominal walls was performed.
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PMID:[Benign giant ovarian cystadenoma. Description of a clinical case]. 878 69


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