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)

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

When compared to age-matched normal weight normolipidemic control subjects, plasma factor XIII, plasma fibronectin and serum cholinesterase levels were found to be markedly decreased in patients with decompensated cirrhosis of the liver, not significantly changed in hyperlipoproteinemia type IIa (heterozygous subjects) and increased in hypertriglyceridemic subjects (type IIb and IV) as well as in hyperlipidemic nephrotic patients. A possible accelerated hepatic synthesis of certain plasma proteins including factor XIII and fibronectin in patients with the nephrotic syndrome as well as in endogenous hypertriglyceridemia is envisaged. It is also considered that mural thrombi, richer in factor XIII and fibronectin, would be more resistant to fibrinolysis and more readily attached to subendothelial structures.
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PMID:Clinical studies on plasma fibronectin and factor XIII; with special reference to hyperlipoproteinemia. 392 52

Gastroduodenoscopy was performed in 25 patients with various disorders, such as liver cirrhosis, nephrotic syndrome, and ulcerative colitis, to assess the effects of corticosteroids on the stomach and duodenum. The main criterion for entry into the trial was the absence of open ulcer, healed ulcer, erosion, or bleeding from the stomach or duodenum on pretreatment endoscopy performed within 48 hours before administration of corticosteroids. Endoscopy repeated at 2 to 4 weeks disclosed gastroduodenal lesions in 11 cases (44%)and no lesion in 14 cases (56%). The gastroduodenal lesions observed in 11 cases are as follows: one gastric ulcer (4.0%), six gastric erosions (24.0%), two gastroduodenal erosions (8.0%), and two duodenal erosions (8.0%). A lack of correlation between the patients' subjective complaints and endoscopic findings indicates the unreliability of patients' complaints and the importance of endoscopy in assessing gastroduodenal lesions. There were no differences in the total and average daily doses of corticosteroid between a group with gastric and/ or duodenal lesions and a group without such lesions. Corticosteroids may produce gastroduodenal lesions, regardless of the dose.
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PMID:Adrenocorticosteroid therapy and gastroduodenal lesions. 400 36

Peritoneal serositis is not a widely recognised aspect of systemic lupus erythematosus (SLE). Indeed, ascites in SLE is said to occur only when complicated by the nephrotic syndrome, congestive cardiac failure, or hepatic cirrhosis. We describe two patients who developed ascites that could be attributed to none of these complications.
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PMID:Ascites in systemic lupus erythematosus. 406 90

Patients with edema not caused by a primary renal inability to excrete sodium show elevated aldosterone levels but to a very variable degree. The low levels can be explained by the absence of hypovolemia resulting from compensatory volume restoration, as in some patients with heart failure, or a concomitant renal excretory impairment as in many patients with nephrotic syndrome and possibly some early phases of liver cirrhosis. When aldosterone is high it is never the sole factor involved. Ironically, some patients with idiopathic edema seem to be the best examples of volume induced sodium retention in which (inappropriate) aldosterone stimulation is a crucial factor.
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PMID:[Role of aldosterone in the development of edema]. 408 71

Measurements of total body potassium (T.B.K.) were made by whole-body counting in four groups of patients receiving oral frusemide for one year. Patients in group 1 had essential hypertension and normal renal function and received 40 mg frusemide daily without potassium supplements. Patients in group 2 were similar but received oral potassium supplements for the first four months of treatment. Patients in group 3 had hypertension associated with renal disease and received 120 mg frusemide daily without potassium supplements. Patients in group 4 also had hypertension and renal impairment and in addition to 120 mg frusemide daily they received oral potassium supplements for four months. No evidence of depletion of T.B.K. was found in any of the groups after continuous treatment with frusemide for one year. It is questioned whether potassium supplementation in long term diuretic therapy with frusemide is necessary unless there is evidence of pre-existing potassium depletion or of some other factor such as cardiac failure, cirrhosis of the liver, or the nephrotic syndrome.
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PMID:Total body potassium in long-term frusemide therapy: is potassium supplementation necessary? 421 34

A method for the simultaneous measurement of gastrointestinal protein loss and total albumin turnover entailing the use of a combination of (125)iodine- and (51)chromium-labeled albumin is described. Albumin turnover was calculated by the measurement of albumin-(125)I plasma decay and cumulative urinary excretion, and the results obtained agreed closely with previous studies utilizing albumin-(131)I. Gastrointestinal catabolism was calculated from the rate of fecal excretion of (51)Cr and the specific activity of plasma albumin-(51)Cr, and these data were related to the calculated albumin turnover results. During the period of 6-14 days after administration, the ratio of specific activties of albumin-(125)I and -(51)Cr in plasma and in extravascular spaces or gastric and biliary secretions remained almost identical. Fecal excretion of (51)Cr was also quite stable at this time. In six normal subjects gastrointestinal catabolism accounted for less than 10% of total albumin catabolism. Excessive gastrointestinal protein losses did not contribute to the low serum albumin in three patients with cirrhosis or in two adults with the nephrotic syndrome. Multiple mechanisms leading to hypoalbuminemia were demonstrated in other subjects with a variety of gastrointestinal disorders.
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PMID:Use of 125-I- and 51-Cr-labeled albumin for the measurement of gastrointestinal and total albumin catabolism. 563 Apr 19

The association of glomerulonephritis and persistent HBs antigenemia is reported in 4 adults with nephrotic syndrome: 2 cases of membranous glomerulonephritis associated with chronic persistent hepatitis and 2 cases of membrano-proliferative glomerulonephritis associated with active cirrhosis. In 3 patients, all positive for HBsAg, anti-HBc and HBeAg by radioimmunoassay, indirect immunofluorescent study was performed on kidney and liver biopsies. Glomerular deposit of HBcAg was detected in two cases. HBsAg and HBcAg were not found in the liver. The pathogenesis of such glomerulonephritis remains uncertain and the role of HBs antigen-antibody circulating immune complexes is not clearly proved. Two patients were treated with vidarabine intravenously. Vidarabine produced a transitory decrease of HBsAg concentration in 2 cases and a transitory loss of DNA-polymerase activity associated with a decrease of HBeAg concentration in one case. Neither seroconversion nor improvement of the glomerular disease were ascertained.
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PMID:[Glomerular nephropathies and B virus: apropos of 4 cases in adults, with an immunofluorescence study and review of the literature]. 634 98

At laparotomy, many surgeons routinely instill crystalloid solutions into the peritoneal cavity, presumably to dilute out necrotic debris, bacteria, and adjuvant substances which foster bacterial growth. We examined the effect on mortality, bacterial growth, clearance, and phagocytosis of various volumes of saline instilled into the peritoneal cavity of rats during Escherichia coli peritonitis. Minimal intraperitoneal bacterial growth was seen after the introduction of a nonlethal inoculum of viable E. coli in 1 ml of saline, while administration of an identical inoculum in 30 ml of saline intraperitoneally (i.p.) led to increased 48-hour mortality (p less than 0.01), and associated rapid bacterial proliferation (p less than 0.01). Clearance of nonviable radiolabelled E. coli from the peritoneal cavity was delayed, bacterial association with host peritoneal leukocytes was decreased, and blood uptake of radiolabelled bacteria was diminished in animals receiving 30 ml of saline i.p., compared to controls which received the identical inoculum in 1 ml of saline i.p. The clinical relevance of these studies is manifold: (1) they provide a possible explanation why patients with ascites due to cirrhosis or the nephrotic syndrome, or those patients undergoing peritoneal dialysis are more susceptible to primary and secondary bacterial peritonitis, possibly on the basis of impaired peritoneal clearance or diminished phagocytosis and, (2) although irrigation of the peritoneal cavity with crystalloid solution would seem prudent during laparotomy, these solutions must be removed prior to closure to prevent interference with normal peritoneal host defense mechanisms.
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PMID:The adjuvant effect of peritoneal fluid in experimental peritonitis. Mechanism and clinical implications. 636 82

Piretanide is a high-ceiling, loop-active diuretic that has been developed for treatment of congestive heart failure, hypertension and edematous states caused by renal and hepatic diseases. Piretanide is structurally related to furosemide and bumetanide; when administered orally, 6 mg of piretanide is as effective as 40 mg of furosemide, and when administered intravenously, 12 mg of piretanide is as effective as 40 mg of furosemide. Piretanide enhances water and sodium excretion in patients with congestive heart failure, with nephrotic syndrome and with cirrhosis and ascites. Adverse effects reported to date are limited to those attributable to excess loss of fluid and electrolytes. Under some conditions, piretanide appears to be less potassium wasting than thiazide diuretics or other loop-active diuretics.
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PMID:Piretanide: a loop-active diuretic. Pharmacology, therapeutic efficacy and adverse effects. 638 44


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