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)

A clinicopathologic study of congenital hepatic fibrosis in 21 patients confirms a strong association with autosomal recessive renal polycystic disease. The liver specimens were subclassified into two groups according to the severity of fibrosis, showing typical hepatic abnormalities in young infants (mean age 0.3 years) and increased hepatic fibrosis in older patients (mean age 19.6 yr) (p less than 0.02). Apparent progression to perilobular fibrosis with parenchymal nodularity occasionally resembled cirrhosis when the nodules had a regenerative appearance because of rounded contours and inapparent central veins. Progression of fibrosis was observed in second biopsy specimens from 2 cases, but not in that of a 3rd, suggesting that factors other than the heritable disorder itself may be responsible for evolving morphology. Identifiable factors that may have contributed to increased fibrosis included localized intrahepatic biliary obstruction and biliary sepsis with suppuration. A factor possibly contributing to the pathogenesis of biliary sepsis was intrahepatic biliary ectasia, i.e., Caroli's disease, which appears to be one morphologic expression of CHF. This study shows that the hepatic abnormality evolves over time and that it may be altered by secondary complications.
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PMID:Congenital hepatic fibrosis: evolving morphology. 322 22

The pharmacodynamics of torasemide (1-isopropyl-3- ([4-(3-methyl-phenylamino)pyridine]-3-sulfonyl)urea), a new potent loop diuretic, were compared to those of furosemide in a double-blind controlled study in 18 patients with oedema of various origin. Torasemide behaved like furosemide in exerting a potent diuretic effect which culminated during the first 4 h after its administration. Nevertheless, torasemide was about 8 times more potent, exerted a longer lasting diuretic effect and was more potassium sparing than furosemide. Torasemide did not accumulate during repeated administration (5 days). It was well tolerated and efficient in the treatment of oedema due to congestive heart failure and hepatic cirrhosis. The long duration of action and the potassium sparing effect of torasemide compared to furosemide are promising features of this new potent loop diuretic.
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PMID:Comparative pharmacodynamics of torasemide and furosemide in patients with oedema. 328 31

Theophylline plasma levels and FEV1 were measured in patients affected by chronic obstructive pulmonary disease and a concomitant disease state (congestive heart failure, chronic cor pulmonale, obesity, peptic disease, hepatic cirrhosis, chronic renal failure) and treated with a sustained release theophylline preparation. Our results indicate that, only in patients affected by congestive heart failure and chronic cor pulmonale, is there a decreased plasma clearance of the drug. Low levels of plasma theophylline were measured in obese patients probably because they received an inadequate posology.
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PMID:Effect of various disease states on theophylline plasma levels and on pulmonary function in patients with chronic airway obstruction treated with a sustained release theophylline preparation. 330 82

To define the role of the renal nerves in renal sodium-retaining edema-forming states, experiments were conducted in conscious chronically instrumented rats with congestive heart failure (myocardial infarction), nephrotic syndrome (adriamycin injection), and hepatic cirrhosis (common bile duct ligation). In each experimental model, renal excretion, as water or sodium, of an acutely administered oral or intravenous isotonic saline load was significantly less than that in control rats. Bilateral renal denervation of the experimental rats restored their renal excretory response to that of the control rats. In addition, in response to the acute administration of a standard intravenous isotonic saline load, the decrease in efferent renal sympathetic nerve activity was significantly less in all three experimental models compared with that of control rats. These results suggest that the impaired ability to excrete an acute isotonic saline load in these experimental models is partially dependent on an increase in basal efferent renal sympathetic nerve activity that fails to suppress normally in response to the isotonic saline load.
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PMID:Neural control of renal function in edema-forming states. 338 7

Non-steroidal anti-inflammatory drugs (NSAIDs) may produce acute renal failure, papillary necrosis and interstitial nephritis. These adverse drug reactions are rare but have been reported in patients with congestive heart failure, cirrhosis, renal parenchymal disease, lupus nephritis and hypertension. All these conditions may be associated with hypovolaemia and an activated renin-angiotensin system, when renal blood flow and glomerular filtration depend on local renal prostaglandin biosynthesis. A severe impairment of renal function may occur when this synthesis is inhibited by NSAID treatment. It is possible that 1 in 100 of elderly patients have renal parenchymal disease, 1 in 100 arteriolar nephrosclerosis, 1 in 200 unilateral or bilateral renal artery stenosis and an unknown number suffer from atheroembolic renal disease. Fortunately, only a small proportion of 'at risk' patients given NSAIDs appear to develop renal failure. Perhaps bilateral renal disease or salt depletion are necessary factors? Whatever the explanation, NSAIDs should be used with caution in the elderly.
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PMID:Pharmaco-epidemiological considerations in patients with arthritis and vascular disease of the kidney. 349 36

Sixty six patients with ascites of different etiologies were studied. Both serum and peritoneal fluids were examined through proteic electrophoresis, being the haemopexin determined in the peritoneal fluids. Immunoglobulins usually show high values in neoplastic effusions, especially igG (x +/- ES = 928.57 +/- 86.87 mg/dl) and IgA (x +/- ES = 157 +/- 17.84 mg/dl). However, the highest determinations were found in those of the congestive heart failures. The quotients obtained from the ascites immunoglobulin/serum immunoglobulin ratio are useful from a statistics point of view, though their practical value is limited. No plasma/ascites correlation was observed either in cirrhotic or in neoplastic patients. Quantification of haemope in proved to be conclusive in differential diagnosis. The 100% of benign ascites (cirrhosis, congestive heart failure and kidney failure) showed lower values than 170 mg/dl while 90.5% of neoplastic patients showed higher figures than said value. The average was 30.79 +/- 5.31 mg/dl for cirrhotic patients and 205.19 +/- 9.62 mg/dl for neoplastic patients with a statistically significative different for both groups (p less than 0.001). There is a high probability that its determination could show the etiology of the process. It was useful not only in cases of both neoplastic and cirrhotic ascites but also in those which had a cardiac origin, in which it showed intermediate values (mean +/- ES = 83.75 +/- 15.77 mg/dl). We feel that its incorporation to the routine followed when studying peritoneal effusions will afford a quick etiologic orientation.
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PMID:[Hemopexin and immunoglobulins in benign and malignant ascites. Experience in 66 patients]. 357 23

A 17-year-old female with clinically diagnosed Uhl's anomaly died of intractable congestive heart failure, liver cirrhosis, and protein losing gastroenteropathy. Cardiac catheterization, echocardiography and nuclear angiography proved to be valuable in making the diagnosis. At autopsy, there was widespread myocardial disarray and extensive fibrosis of both ventricles which led to, in particular, almost total absence of the myocardium of the right ventricle. The present case implicated that certain case of Uhl's anomaly might be related to widespread myocardial disarray and extensive fibrosis, which is known as idiopathic cardiomyopathy.
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PMID:Uhl's anomaly as a result of progression to ventricular dilation from hypertrophic cardiomyopathy. 368 29

Recent reports in the literature have promulgated nonresective treatment of abdominal aortic aneurysm as a safer procedure than conventional aneurysmectomy with graft replacement in high-risk patients. This review of 106 high-risk patients who underwent conventional aneurysm repair between 1980 and 1985 was undertaken to compare the relative risks, perioperative morbidity, and operative mortality of these patients to that reported for patients treated by nonresective therapy. Excluded were those patients who had rupture initially or underwent a concomitant renovascular procedure. Patients were considered to be at high risk if they met one or more of the following criteria: age equal to or greater than 85 years; receiving oxygen at home, PO2 less than 50 torr, or forced midexpiratory flow less than 25% of predicted; serum creatinine equal to or greater than 3 mg/dl; biopsy-proven cirrhosis with ascites; retroperitoneal fibrosis; or New York Heart Association functional class III-IV angina, left ventricular ejection fraction less than 30%, recent congestive heart failure, complex ventricular ectopy, large left ventricular aneurysm, severe valvular disease, recurrent congestive heart failure or angina after coronary artery bypass grafting, or severe unreconstructed coronary artery disease confirmed by angiography. The mortality rate for conventional aneurysm repair in high-risk patients was 5.7%, compared with a reported 7% mortality rate for nonresective therapy. In those patients with severe cardiac dysfunction, intraoperative pharmacologic manipulation and the selective use of intra-aortic balloon counterpulsation appeared helpful in achieving survival.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Conventional repair of abdominal aortic aneurysm in the high-risk patient: a plea for abandonment of nonresective treatment. 370 38

Cytologic examination of 3H-thymidine-labeled mesothelial cells in the pleural fluid revealed that single and small-sized cells with slight basophilic cytoplasm scarcely stainable by PAS and colloidal iron are in the DNA-synthetic phase and that these are exfoliating cells from the pleural surface. While abnormal labeling in a few arranged and binuclear cells suggesting accelerated or disturbed mesothelial mobilization was frequently found in congestive cardiac failure, liver cirrhosis, and uremia, it never occurred in single and large-sized activated cells possessing rich PAS-positive granules, cells in large clusters or sheet-like arrangements, or multinuclear giant cells. Transmission electron microscopical observation of these labeled cells proved that a smooth cellular surface and scant intracytoplasmic organelles, by which undifferentiated cells are generally characterized, are essential for DNA-synthesizing mesothelial cells. Probably as a result of some pleural irritation, surface lining cells immediately enter the cell cycle and at once revert to an undifferentiated form capable of DNA synthesis, after which they may be released as a single form, and differentiate and transform into mature, activated cells with a bleb-like surface structure or microvilli, and finally may proliferate in the fluid.
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PMID:Cytological and ultrastructural characteristics of DNA synthesizing mesothelial cells in pleural effusion. 378 59

A transudative pleural effusion develops when the systemic factors influencing the formation or absorption of the pleural fluid are altered. The pleural surfaces are not involved by the primary pathologic process. The diagnosis of transudative effusion is simple to establish by examining the characteristics of the pleural fluid. Transudates have all of the following three characteristics: The ratio of the pleural fluid to the serum protein is less than 0.5. The ratio of the pleural fluid to the serum LDH is less than 0.6. The pleural fluid LDH is less than two thirds the upper limit of normal for the serum LDH. Among the conditions that produce transudative pleural effusion, congestive heart failure is by far the most common. Pulmonary embolism, cirrhosis of the liver with ascites, and the nephrotic syndrome are the other common causes. Management of transudative pleural effusions involves managing the primary disease. Refractory, massive effusions can be controlled by tetracycline pleurodesis.
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PMID:Transudative pleural effusions. 384 1


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