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)

Systemic causes of leg edema include idiopathic cyclic edema, heart failure, cirrhosis, nephrosis and other hypoproteinemic states. Lymphedema may be primary, or secondary to neoplasm, lymphangitis, retroperitoneal fibrosis and, rarely (in the U.S.), filariasis. Thrombophlebitis and chronic venous insufficiency are not uncommon causes. Finally, infection, ischemia, lipedema, vascular anomalies, tumors and trauma can be responsible for the swollen leg.
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PMID:The swollen leg. 18 30

12 g of albumin are synthesized daily by the bound polyribosomes of all human liver cells together, corresponding to 10% of the intravascular albumin mass. The cell is producing a precursor albumin. During secretion albumin is liberated by splitting of a small peptide. Only 40% of the total body albumin is located intravascularly. 12g of albumin are degraded or excreted daily, 30% of it by the liver, the kidneys and the gastrointestinal tract. The main site of albumin catabolism is unknown. Albumin with a half-life of about 20 days is degraded at a constant fractional catabolic rate. The absolute rate of degradation varies depending on the plasma content. This mechanism allows an effective regulation of the serum albumin level. The fractional catabolic rate, however, is not completely fixed. It is slowly reduced if the serum albumin content is markedly reduced as in protein deficiency, the blind loop syndrome, cirrhosis, nephrosis, and diseases of the gastrointestinal tract. Infusion of albumin increases the fractional catabolic rate slowly. This must be taken in consideration substitution albumin in chronic diseases. The shift from the extravascular to the intravascular compartment is a short-term regulatory mechanism. The regulation of synthesis and degradation are independent from each other. The molecular mechanism of regulation of synthesis and degradation are unknown, partially due to inadequate methods.
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PMID:[The regulation of serum albumin in physiological and pathological conditions (author's transl)]. 87 Jul 44

The exact role of serum pseudocholinesterase (PSCE) is not known. Its main role probably consists in the degradation of butyril-choline, an intermediate of lipid metabolism. Decreased values have been described in liver cirrhosis as an index of diminished proteosynthetic function. An increased activity of this enzyme was reported in obesity, diabetes mellitus, nephrosis, hyperthyroidism and in hyperlipemic subjects without obesity. A significant correlation was found between serum cholesterol, triglycerides and PSCE, as an expression of lipid metabolism. In view of assessing the possible change of this enzyme during fattening, the authors investigated PSCE activity during fattening in pigs (the same breed). The results indicate a statistically significant increase of PSCE during fattening, from 30.4 +/- 1.7 to 43.6 +/- 1.7 (p less than 0.001). These results together with those reported in a previous paper concerning blood lipids and cholesterol, show a positive correlation between these parameters and PSCE during fattening in pigs, which might be due to an adaptative increase of the hepatic synthesis of this enzyme in response to the increased lipid metabolism.
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PMID:Serum pseudocholinesterase activity during experimental fattening. 94 98

The renin system plays a critical role in hypertension as well as in the edematous states of heart failure, cirrhosis, and nephrosis. Properly performed measurements of plasma renin, with techniques now widely available, can be used as indicators of risk and of therapeutic strategies. The results of the plasma renin measurements are equally relevant whether they are high or low. The renin profile should be part of the routine workup of the patient with hypertension of any type or of the patient with an edematous disorder. Once the renin component of hypertension is established, management with angiotensin-converting enzyme (ACE) inhibitors, such as perindopril, follows, for ACE inhibitors attack the pathophysiologic source, thus providing adequate perfusion and protection of vital organs. The role of renin's involvement in hypertensive states is elaborated, as well as that of the ACE inhibitors.
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PMID:A decade of angiotensin-converting enzyme (ACE) inhibition. 158 Feb 77

In the period 1973/74-1983 a prospective observation was carried out on 4591 out-patients (2095 males and 2496 females) aged 18-68, with predominantly non-insulin treated diabetes of 1-10 years' duration. During the ten years period over a third of initial cohort died. Age-standardized mortality rate was twice that for the general population of Warsaw for the median year 1978. The risk of death rose with decreasing age, especially in females. The most frequent causes of death were cardiovascular diseases, particularly coronary heart disease, standardized mortality ratios amounting to 2.7 and 2.4 respectively. Among diabetic cohort the risk of death was also higher for nephritis, nephrosis, cirrhosis of the liver and pneumonia. No excess death rate could be found for tuberculosis, malignant neoplasms, and diabetes itself. Diabetic patients were less frequently exposed to accidental deaths than the general population of Warsaw. The mortality diabetic patients in Warsaw was similar to that seen in most of the developed countries with the exception of the higher mortality due to cirrhosis of the liver and smaller due to accident, trauma and poisoning.
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PMID:[Mortality among patients with diabetes mellitus in Warsaw--a 10-year prospective study]. 262 53

The plasma protein binding of disopyramide (D) was determined in seven patients with cirrhosis, six with nephrotic syndrome, and seven healthy subjects. Plasma samples containing concentrations of 0.2 to 12.0 micrograms/ml were ultrafiltered and the free fractions were measured with fluorescence polarization immunoassay. The mean free fractions at D concentrations ranging from 1 to 6 micrograms/ml were significantly (P less than 0.01) greater in patients with cirrhosis than in healthy subjects. No difference was observed between patients with nephrotic syndrome and healthy subjects. The free fraction at D 3 micrograms/ml correlated better with alpha 1-acid glycoprotein (r = -0.77) than with albumin (r = -0.46). Patients with cirrhosis had significantly (P less than 0.01) lower capacity constants as compared with the other two study groups. There was a significant (P less than 0.01) correlation between capacity constant and alpha 1-acid glycoprotein (r = 0.71). Our results suggest that the D therapeutic range measured as the total plasma concentration in cirrhosis, but not in nephrosis, should be approximately 50% lower than previously believed.
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PMID:Protein binding of disopyramide in liver cirrhosis and in nephrotic syndrome. 374 34

Resistance to loop diuretics is often encountered clinically. Studies in healthy subjects have shown that overall response to loop diuretics depends upon the interplay between the total amount of drug reaching the urine, the time course of its entry into urine and the pharmacodynamics of response to diuretic in the urine. The mechanism by which diuretic resistance occurs has been elucidated in several clinical conditions. Treatment with inhibitors of prostaglandin synthesis has no effect on diuretic appearance in urine but blunts response by blocking the increase in renal blood flow produced by loop diuretics. In the elderly and in patients with moderate renal insufficiency, the mechanism of resistance appears to be purely pharmacokinetic, involving altered access of diuretic into the urine. In contrast, patients with nephrotic syndrome and hepatic cirrhosis manifest a purely pharmacodynamic form of resistance: in nephrosis, diuretic may bind to protein in the urine; in cirrhosis the mechanism of resistance is unclear. Lastly, in patients with congestive heart failure, with intravenous administration, resistance represents a pharmacodynamic phenomenon. With oral administration, however, the time course but not the extent of absorption is altered; consequently, in this setting, both pharmacokinetic and pharmacodynamic changes may contribute to the subnormal response. Strategies for overcoming resistance to loop diuretics in patients receiving NSAIDs or those with renal disease, hepatic cirrhosis or congestive heart failure include one or more of: increasing the dose size; administering frequent 'small' (but effective) doses; continuous intravenous infusion of the diuretic; or concomitant administration of another diuretic such as metolazone or hydrochlorothiazide.
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PMID:Resistance to loop diuretics. Why it happens and what to do about it. 390 37

Hypertension develops in about 10% to 50% of patients with nephrosis or cirrhosis and peripheral edema, but the hemodynamic mechanism of the hypertension and its reversal by diuretic therapy has not been elucidated. In eight patients with marked edema and mild hypertension, diuretics (furosemide and spironolactone) decreased mean arterial pressure because of concurrent decrease in cardiac output and total peripheral resistance. Neither total blood volume nor plasma volume were decreased by the diuretics and the decrease in body weight was therefore attributed to the decrease in interstitial fluid volume. This, in turn, resulted in increased venous capacitance (as can be judged from the diuretic-induced decrease in the ratio of cardiopulmonary blood volume/total blood volume).
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PMID:Hemodynamic effects of diuretics in patients with marked peripheral edema and mild hypertension. 706 Mar 19

Lead, cadmium, mercury and arsenic are widely dispersed in the environment. Adults are primarily exposed to these contaminants in the workplace. Children may be exposed to toxic metals from numerous sources, including contaminated air, water, soil and food. The chronic toxic effects of lead include anemia, neuropathy, chronic renal disease and reproductive impairment. Lead is a carcinogen in three animal species. Cadmium causes emphysema, chronic renal disease, cancer of the prostate and possibly of the lung. Inorganic mercury causes gingivitis, stomatitis, neurologic impairment and nephrosis, while organic mercurials cause sensory neuropathy, ataxia, dysarthria and blindness. Arsenic causes dermatitis, skin cancer, sensory neuropathy, cirrhosis, angiosarcoma of the liver, lung cancer and possibly lymphatic cancer.
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PMID:Occupational and community exposures to toxic metals: lead, cadmium, mercury and arsenic. 716 33

Lactic acid (LA) concentrations in the pleural fluid of 75 patients were determined by the Monotest Lactate Kit (MLK). Lactic acid values in 18 cases of bacterial or tuberculous pleural infection were strikingly higher (mean 81 mg%, range 45-200 mg%), than in 42 cases with pleural effusion due to congestive heart failure, hepatic cirrhosis, nephrosis, trauma, and systemic lupus erythematosus (SLE; mean 19 mg%, range 6-47 mg/). High levels of LA were also found in the pleural fluid of 15 patients with malignancy of pleural cavity. Determination of LA can be an additional rapid tool in the differentiation between bacterial pleural inflammation and pleural effusion of various forms except in cases with malignancy of the pleural cavity.
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PMID:Measurement of lactic acid in pleural fluid. 722 Dec 2


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