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)

Fitzgerald factor (high molecular weight kininogen) is an agent in normal human plasma that corrects the impaired in vitro surface-mediated plasma reactions of blood coagulation, fibrinolysis, and kinin generation observed in Fitzgerald trait plasma. To assess the possible pathophysiologic role of Fitzgerald factor, its titer was measured by a functional clot-promoting assay. Mean +/- SD in 42 normal adults was 0.99+/-0.25 units/ml, one unit being the activity in 1 ml of normal pooled plasma. No difference in titer was noted between normal men and women, during pregnancy, or after physical exercise. Fitzgerald factor activity was significantly reduced in the plasmas of eight patients with advanced hepatic cirrhosis (0.40+/-0.09 units/ml) and of ten patients with disseminated intravascular coagulation (0.60+/-0.30 units/ml), but was normal in plasmas of patients with other congenital clotting factor deficiencies, nephrotic syndrome, rheumatoid arthritis, systemic lupus erythematosus, or sarcoidosis, or under treatment with warfarin. The plasmas of 21 mammalian species tested appeared to contain Fitzgerald factor activity, but those of two avian, two repitilian, and one amphibian species did not correct the coagulant defect in Fitzgerald trait plasmas.
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PMID:Fitzgerald factor (high molecular weight kininogen) clotting activity in human plasma in health and disease in various animal plasmas. 100 85

Accumulating evidence suggests that extracellular volume (ECV) may be governed in part by a natriuretic hormone. To study its possible role in oedema formation plasma fractions IV from patients with the nephrotic syndrome, with cirrhosis of the liver, and with idiopathic oedema were studied for their effects on frog skin Na-transport and on rat renal Na-excretion. Plasma fractions IV from ECV-expanded healthy subjects and patients with aldosteronoma significantly inhibited PD and SCC and in the rat increased urinary flow, CH29, and UNaV. Neither antinatriferic nor natriuretic activities were observed in patients with the nephrotic syndrome or liver cirrhosis. In patients with idiopathic oedema recurrent episodes of fluid retention up to 9 percent of b.wt. followed by spontaneous natriuresis were well correlated with antinatriferic plasma activity. The results suggest that ECV in healthy subjects may be governed in part by a natriuretic hormone which is absent in ECV-expansion due to oedema. However, this mechanism may operate appropriately, though at an elevated threshold, in patients with idiopathic oedema.
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PMID:Plasma natriuretic activity in oedematous states. 108 25

The factors involved in renin release have been extensively evaluated. The primary determinants are the transmural pressure at the afferent arteriole, sodium delivery to the macula densa, and the activity of the adrenergic nervous system. Other possible factors include circulating catecholamines, the serum and cerebrospinal fluid sodium concentration, serum potassium concentration, angiotensin II concentration, and antidiuretic hormone release. There is no convincing evidence that the renin-angiotensin system mediates renal autoregulation. Plasma renin activity is altered in a number of clinical settings. This parameter is elevated in most patients with cirrhosis and the nephrotic syndrome as well as in individuals with severe congestive heart failure. Despite inappropriately large weight gains, plasma renin suppresses normally with increased salt intake in edematous patients who have a normal glomerular filtration rate. The mechanisms of the alteration in the renin-angiotensin system in Bartter's syndrome is still not clear.
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PMID:Renin and the kidney. 110 Oct 89

Bumetanide2 is a new diuretic with a rapid onset and short duration of action. It is advocated for the treatment of oedema of cardiac origin; that associated with cirrhosis of the liver and renal diseases, including the nephrotic syndrome oedema of pregnancy and in pulmonary oedema. Bumetanide produces a pattern of water and electrolyte excretion closely resembling that of frusemide although it differs structurally from frusemide and other diuretics. 1 mg of bumetanide produces a diuretic effect similar to that evoked by 40 to 60 mg of frusemide. Short-and long-term studies in oedema of varying aetiology have shown bumetanide to be an effective diuretic. Because it is chemically different from existing diuretics, bumetanide may be helpful in oedema resistant to other drugs. It is well tolerated, but like other natriuretics it causes hypericaemia and may cause hypokalaemia during long-term administration.
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PMID:Bumetanide: A preliminary report of its pharmacological properties and therapeutic efficacy in oedema. 112 4

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 15,645 consecutive ultrasound examinations of the abdomen (1986 to 1988), free fluid in the peritoneal cavity was found in 247 patients by internal trial during 397 sessions (= 2.5%). Most frequent basic diagnosis for the reason of this symptom were tumorous diseases (99 patients corresponding to 40.1%), cirrhosis of the liver (52 patients corresp. to 22.1%) and heart failure (31 patients corresp. to 12.6%, among these complex gayprooft myocardial insufficiency 24, right heart failure 7). Ovarian cysts or cystomas (7), acute/chronic-recurrent pancreatitis (6), Crohn's disease (3), infections (3), rheumatoid disorders (3), nephrotic syndrome (2), and extra-uterine pregnancy (2) were more rarely represented. In 23 patients (corresp. to 9.3%) the cause of an ascites remained obscure. Among these, a high prevalence of the female sex in the premenopausal age was remarkable with a score of 20:3 (statistically significant difference in terms of the other patients of our group). This observation suggests that an ovarian factor plays a role in the development of ascites in the absence of other evident causes. The literature implies that endometriosis is rather prominent, followed by oligosymptomatic infections or inflammatory diseases.
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PMID:[Cryptogenetic ascites. Attempts at original pathophysiologic explanation of a monomorphic sonographic image pattern]. 150 31

Acquired antithrombin III (AT III) deficiency is based on either decreased activity or synthesis, increased loss or increased consumption. The activity of AT III is decreased in metabolic acidosis, hyperlipoproteinemias and by lipid peroxides. Chronic liver diseases especially liver cirrhosis are associated with very low levels of AT III due to insufficient hepatic synthesis, reduced transcapillary flux ratios, diffuse intravascular coagulation and loss in the ascites. Gastrointestinal loss of AT III may occur in patients with active inflammatory bowel diseases. AT III deficiency is observed in nephrotic syndrome when urinary loss of protein exceeds 5 g/d. During hemodialysis we have not found low AT III levels. Disseminated intravascular coagulation is characterized by activation of the coagulation system and increased consumption of AT III. AT III complexes with activated coagulation factors are subsequently cleared by the reticuloendothelial system.
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PMID:[Acquired antithrombin III deficiency]. 158 93

We have investigated the influence of variation of the concentrations of serum albumin and immunoglobulins on serum fructosamine concentration in 33 patients with nephrotic syndrome, and 18 patients with cirrhosis of the liver. Protein alterations were evident in these patients and they were compared with 109 normal subjects, 43 patients with type II diabetes mellitus and nine diabetic patients with nephrotic syndrome. The mean serum fructosamine concentration in diabetic patients (2.76 +/- 0.53 mmol/L) was significantly increased (P less than 0.001) by comparison with normal subjects (1.93 +/- 0.20 mmol/L) and the other patients studied. Patients with diabetic nephropathy had higher (P less than 0.01) serum fructosamine concentrations (2.23 +/- 0.54 mmol/L) than non-diabetic patients with the nephrotic syndrome (1.57 +/- 0.37 mmol/L) but remained with the normal range. Positive correlations were observed between fructosamine and immunoglobulins G and M in nephrotic and cirrhotic patients. Serum immunoglobulin A was also directly correlated with serum fructosamine in patients with cirrhosis of the liver. An inverse correlation between albumin and fructosamine in serum of patients with cirrhosis of the liver was also noted. We conclude that the fructosamine assay is not useful in the assessment of glycemic control in patients with cirrhosis of the liver, nephrotic syndrome or in any other clinical situation in which protein metabolism is altered.
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PMID:Serum fructosamine concentration in patients with nephrotic syndrome and with cirrhosis of the liver: the influence of hypoalbuminaemia and hypergammaglobulinaemia. 164 52

The study includes 30 patients: 21 patients with various cardiac diseases which had led to chronic cardiac failure with well expressed edemas, 7 patients with liver cirrhosis and ascites, 2 patients with chronic glomerulonephritis and nephrotic syndrome. For 7 consecutive days the patients received fupyram or furanthril. In the morning, before breakfast, they received either 1 capsule fupyram (which is composed of amyloride hydrochloride 0.005 g and furezemide 0.04 g) or 1 tablet furanthril. In case of insufficient diuresis the daily dose was increased to 2 capsules fupyram (or 2 tablets furanthril respectively). In the patients with satisfactory diuretic effect the dose was reduced to 1 capsule (tablet) every other day or 2 capsules 2 times weekly after the second week. At the end of the 4-th week the general condition of the patients improved considerably. The diuresis increased, the body mass and the arterial pressure decreased. The potassium serum level increased from 4.4 +/- 0.3 mmol/l at the beginning of the treatment to 5.3 +/- 0.7 mmol/l. In 11 patients the potassium level reached values about 5.5 mmol/l. The drug fupyram exerts a pronounced diuretic efficacy. In the patients with preserved renal function fupyram does not change significantly the potassium serum level, but in patients with impaired renal function it can lead to hyperkalemia even after an unprolonged treatment.
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PMID:[A clinico-therapeutic study of the Bulgarian preparation fupiram]. 177 60

Renal glomerular changes are a well recognised complication of cirrhosis and are frequently characterised by mesangial IgA deposition. We report a patient with non-cirrhotic portal hypertension who developed IgA nephropathy and a nephrotic syndrome with renal histological changes classically associated with cirrhosis. Splenectomy with resection of a splenic artery aneurysm resulted in remission of the nephrotic syndrome. This case illustrates the factors which contribute to the pathogenesis of IgA nephropathy in liver disease.
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PMID:IgA nephropathy in non-cirrhotic portal hypertension. 186 47


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