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

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

Renal excretion, skeletal muscle content and plasma concentration of electrolytes were studied in 108 patients on long-term diuretic therapy for congestive heart failure and/or arterial hypertension. As reference populations served a group of 16 healthy volunteers and a group of 22 patients with liver cirrhosis, but not on diuretic therapy. Diuretic therapy was found to deprive the patients of their ability to conserve potassium and magnesium when there was a simultaneous cellular depletion of these ions. Magnesium excretion was found to be correlated to the skeletal muscle magnesium content. An inverted Na/K ratio in urine and a low magnesium excretion were fair indicators of cellular magnesium depletion.
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PMID:Renal excretion of electrolytes in patients on long-term diuretic therapy for arterial hypertension and/or congestive heart failure. 409 Oct 44

22 nonneoplastic, noninflammatory effusions (cirrhosis and congestive heart failure), 12 non-neoplastic inflammatory effusions (tuberculosis, lupus erythematosus, rheumatoid arthritis, and idiopathic pleuropericarditis), and 58 neoplastic effusions (cancer of lung, breast, ovary, and pancreas, and lymphoma) were analyzed by radial immunodiffusion for orosomucoid concentration. The average concentration +/-SE was 35+/-4, 65+/-17, and 130+/-13 mg/100 ml in the three types of effusion, respectively. By gel filtration and ion exchange chromatography, orosomucoid was isolated from 12 nonmalignant and 14 malignant fluids. The orosomucoid preparations reacted as single components in acrylamide gel electrophoresis at pH 9.0, and in immunodiffusion and immunoelectrophoresis against antisera to human serum and to human plasma orosomucoid. In radial immunodiffusion, the slope of the line relating concentration to the square of the diameter of the precipitate area was identical for orosomucoid isolated from normal human plasma and from nonneoplastic effusions, but was subnormal for orosomucoid isolated from neoplastic fluids. All orosomucoid preparations had normal amino acid composition. Orosomucoid from the nonmalignant effusions had normal carbohydrate content. 11 of 14 samples of orosomucoid isolated from neoplastic fluids had abnormalities in carbohydrate composition, consisting of subnormal content of sialic acid (11 of 14), hexose (10 of 14), and hexosamine (3 of 14), and abnormally high content of hexosamine (4 of 14). Discriminant analysis showed that concentration of orosomucoid distinguished between neoplastic and nonneoplastic noninflammatory effusions more effectively than concentration of total protein, albumin, alpha(1), alpha(2), beta, or gamma-globulin.
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PMID:Orosomucoid content of pleural and peritoneal effusions. 420 34

Ceftizoxime (CZX), a parenteral cephalosporin derivative belonging to the so-called third generation cephalosporin is reported to have a broad antibacterial activity, particularly against Gram-negative aerobic bacilli and some anaerobes, such as Bacteroides fragilis and a good stability to beta-lactamases. Clinical study was performed on a total of 20 cases, 9 females (1 case had urinary tract infection 3 times) and 11 males, aged from 27 to 82 years. All patients had the underlying diseases. They were bronchial asthma in 3 cases, influenza in 1, chronic pulmonary emphysema in 1, pulmonary fibrosis in 1, chronic bronchitis with strongyloidiasis in 1, lung cancer in 3, esophagus cancer in 2, stomach cancer in 1, hepatoma with urolithiasis in 1, liver cirrhosis with diabetes mellitus in 1, alcoholism with strongyloidiasis in 1, cholelithiasis in 1 and congestive heart failure in 1, respectively. Clinical diagnoses for infections were 2-acute bronchitis, 2-exacerbation of chronic bronchitis, 2-broncho-pneumonia, 2-pneumonia including one suspected case, 1-obstructive pneumonia, 2-secondary pulmonary infection, 1-pulmonary infection, 3-urinary tract infection (UTI), 1-UTI with sepsis, 1-sepsis, 1-sepsis with purulent meningitis, 1-biliary tract infection and 1-infected bronchoesophageal fistula. CZX was given by intravenous drip infusion, at a dose of 1 to 2 g, twice daily for 3 to 15 days. Because of severity in infections and underlying diseases, some cases were treated either steroid, gamma-globulin preparations or other antibiotics in combination with CZX. Twelve out of 15 cases assessed clinically responded satisfactorily to the treatment and efficacy rate was 80.0%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effectiveness of ceftizoxime on various infections in patients with underlying diseases]. 609 Jul 23

The fingernails of 512 consecutive hospital inpatients were examined and Terry's nails (by criteria modified slightly from those of Terry) were found in 25.2%. The nail abnormality was associated with the presence of cirrhosis, chronic congestive heart failure, and adult-onset diabetes mellitus, and was also associated with age. In younger patients the nail disorder was associated with an increased risk of systemic disease. Tissue biopsy showed that the nail abnormality was due to distal telangiectasias.
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PMID:Terry's nails: revised definition and new correlations. 614 96

Cytocentrifuged preparations of mononuclear cells in blood and pleural fluid were stained for acid alpha-naphthyl acetate esterase (ANAE) in order to characterize the lymphocytes of pleural effusions histochemically. The cellular samples were obtained from 42 patients with pleural effusions caused by tuberculosis, pneumonia, cancer, malignant lymphoma, sarcoidosis, congestive heart failure, hepatic cirrhosis or nonspecific causes. The mean percentage of ANAE-positive lymphocytes from patients with tuberculous pleural effusion was significantly greater (P less than 0.001) in pleural fluid (85.6%) than in peripheral blood (70.0%). Tuberculous pleural fluid also contained a higher mean percentage of ANAE-positive lymphocytes than did pleural fluid from patients with cancer (75.0%), malignant lymphoma (50.0%), pneumonia, nonspecific disease (74.9%) or transudates (59.3%). The findings show that ANAE staining is useful for demonstrating T lymphocytes in pleural effusions. The pathogenetic role of these T lymphocytes and the diagnostic significance of demonstrating ANAE-positive cells in pleural effusions are discussed.
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PMID:Acid alpha-naphthyl acetate esterase staining of lymphocytes in pleural effusions. 617 49

Tests were performed to study the angiogenic activity in samples of pleural fluid, ascites and cerebrospinal fluid, in patients with solid tumors and non-neoplastic diseases such as cerebrovascular accidents, cirrhosis, and congestive heart failure. The measurement of the angiogenic activity was carried out on chorioallantoid chick embryo membrane. The cerebrospinal fluid showed angiogenic activity in patients with primitive tumors of the central nervous system and also in cases where the tumor had extended into other organs. The cerebrospinal fluid of controls without tumor revealed angiogenic activity in 28% of the cases. There was a direct correlation between positive assays and age. Sixty-two percent of the samples of ascites from cancer patients were positive. Only 25% of the controls were positive. Only 10% of the pleural fluid from cancer patients was negative, and 75% of the control samples were negative.
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PMID:Angiogenic activity in fluid samples from tumoral patients. 619 55

Immunological analysis of ascitic fluids from 49 patients with gastrointestinal cancer was performed and compared to those from 13 patients with hepatic cirrhosis and 3 with congestive heart failure. The analysis of ascitic fluid was performed using natural killer (NK) activity, MLR, PHA-induced lymphoproliferation (LP) and PPD-LP. Immunologic suppression by malignant ascitic fluid was more remarkably observed in PHA-LP, PPD-LP, MLR and NK assay than that by cirrhotic ascites, and it was further proved to be dose dependent. Ascitic fluids from patients with congestive heart failure showed no suppressive effects. There was no correlation between these suppressions and AFP, CEA or immunosuppressive acidic protein (IAP) levels in ascitic fluids. The first fraction of sephadex G 200 Gel filtration, which has a molecular weight of more than 200,000, showed the immunosuppressive activity. It is concluded from these results that this immunosuppressive factor does not involve AFP, CEA and IAP. Thus, it is presumed that the prognosis of the patients with gastrointestinal cancer might correlate with the immunosuppressive factor in their ascitic fluid.
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PMID:[Suppression of immunological response by ascitic fluid from gastrointestinal cancer patients]. 620 9

Portal hypertension is defined as an increase of the portal venous pressure over 20 cm H2O or 7 mm Hg, respectively. It may be induced by different types of portal venous stenosis or obstruction, primarily by cirrhosis and fibrosis of the liver and, less frequent by posthepatic disorders such as the Budd-Chiari-syndrome or congestive heart failure. Portal hypertension is followed by ectasia and phlebosclerosis of the portal vein, by splenomegaly, ascites and by various types of collateral circulation. Among these, oesophageal varices, are most important since they often lead to acute upper gastrointestinal haemorrhage, the major complication of portal hypertension. Bleeding from oesophaeal varices is essentially based on atrophy of the squamous epithelium, caused by ischemia from local hypoxia and venous stasis. Portal hypertension and the frequently compromised blood clotting mechanism due to reduced synthesis of clotting factors in the liver aggravate the bleeding. Atrophy of the esophageal mucosa presents an area of decreased resistance likely to ulcerate with easy erosion of the varices--usually lying very superficially--; with mechanical irritation by food or peptic erosion from gastroesophageal reflux being frequent inducers of hemorrhage.
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PMID:[Pathologic-anatomic reflections on portal hypertension (author's transl)]. 624 21


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