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)

Twenty patients with cirrhosis and ascites were randomly divided in two groups to receive 20 mg/die of the new-loop-diuretic torasemide (T), and 50 mg/die of furosemide (F). All patients also received 200 mg/die of potassium canrenoate. Natriuretic and diuretic effects and consequent loss of weight were significantly better in the torasemide-group (T-group). Otherwise, loss of potassium and sodium/potassium ratio in urine were not significantly higher for T-group. Ammonium lowered with T and remained unchanged with F, but the difference was not statistically significant. No change was observed in blood-pressure, pulse-frequency, electrolyte plasmatic levels, azotemia, creatininemia and serum albumin. A significant increase of diuresis was obtained from the fourth day of treatment onwards by replacing F with T in the F-group. The T-group maintained T for eight days just to evaluate its efficacy and tolerability in the middle term: diuresis kept efficient and no side-effects occurred. This trial showed that T was a good and handy drug for cirrhosis with ascites whether as an alternative to F, or as a sequential treatment.
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PMID:[Comparison between torasemide and furosemide in the treatment of ascites in cirrhotic patients]. 914 26

A 63-year-old woman who had received hemodialysis therapy since she fell acute on chronic renal failure 4 years ago presented with multiple joint pain. Nephrocalcinosis was not detected by abdominal X-ray when hemodialysis therapy was initiated. Laboratory testing showed azotemia, anemia, hypoproteinemia and mild liver dysfunction but no liver cirrhosis. Biopsied bone tissue demonstrated numerous calcium oxalate crystal depositions. Laparoscopy revealed black liver in macroscopic view. Histological studies showed numerous lipofuscin-like dark brown granules were deposited in hepatocytes. The activity of alanine : glyoxylate aminotransferase (AGT) was less than 0.1 U/g in biopsied patient's liver tissue. Generally, clinical symptoms demonstrated by Japanese primary hyperoxaluria type I (PH-I) patients are milder than those of European patients. Some PH-I patients may successfully avoid urinary tract calcification unless they fall into oliguria by some other causes. The lipofuscin granules are most likely the source of the dark color. Massive deposition of the lipofuscin granules indicated that the duration of the liver metabolic abnormality had lasted for long time. Thus, black liver may be related to a mild form of PH-I.
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PMID:A case of late onset primary hyperoxaluria type I (PH-I) presented with black liver. 977 23

Invasive disease due to Group B streptococci has been increasingly recognized as a problem in chronically ill adults. We studied all adults presenting with bacteremia due to Group B streptococci at Hartford Hospital over a period of more than five years. Fifty-nine episodes of septicemia occurred with a mortality rate of 15.3%. Markers for mortality included cirrhosis, azotemia, transaminase elevation, respiratory distress on admission, and ionized hypocalcemia Although commonly thought of as a maternal and pediatric pathogen, nonpregnant, chronically ill adults make up the vast majority of patients with Group B streptococcal sepsis.
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PMID:Group B streptococcal bacteremia in adults at Hartford Hospital 1991-1996. 978 35

Spontaneous bacterial peritonitis (SBP) is the prototypical ascitic fluid infection occurring in patients with advanced liver disease and ascites. The key to successful treatment of SBP is a knowledge of appropriate antibiotic regimens and an understanding of the setting in which infection develops, particularly those individuals at high risk for infection. A high index of suspicion should lead to early diagnostic paracentesis and ascitic fluid analysis. Treatment of SBP involves the use of non-nephrotoxic broad-spectrum antibiotics expected to cover the typical bacterial flora associated with SBP. SBP typically involves infection with a single organism, with Escherichia coli, Klebsiella spp, and Streptococcus spp responsible for nearly three fourths of cases. The treatment of choice is cefotaxime 2 g given intravenously every 8 hours for a total of 5 days. The antibiotic regimen is adjusted based on the results of ascitic fluid cultures. Other antibiotic regimens for SBP are less well studied. Given the significant morbidity and mortality rates associated with SBP, efforts to prevent its development and recurrence with antibiotic prophylaxis are warranted. The most extensively studied form of prophylaxis involves selective intestinal decontamination (SID) with the oral fluoroquinolone norfloxacin. Individuals with low-protein ascites (ascitic fluid total protein < 1g/dL) benefit from SID with norfloxacin 400 mg daily during times of hospitalization. Long-term primary prophylaxis during outpatient management of individuals awaiting liver transplantation with severe ascites and advanced liver failure should also be considered. Patients with cirrhosis and upper gastrointestinal bleeding should receive norfloxacin 400 mg twice daily for 1 week following their bleed. Those individuals surviving an episode of SBP should be treated with norfloxacin 400 mg daily until the risk of SBP is removed by definitive resolution of the ascites or liver transplantation surgery. Although the infection-related mortality associated with SBP has decreased to less than 10%, hospitalization-related mortality remains as high as 30% as a result of the severe underlying liver disease in which the infection arises and the marked generation of cytokines and nitric oxide resulting from the infection. Recently, the simultaneous administration of intravenous albumin and antibiotics for SBP has been shown to result in the decreased development of azotemia and hospitalization-related mortality. Further improvement in the outcomes of SBP will require treatments targeting this cytokine cascade rather than the development of more potent antibiotics.
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PMID:Spontaneous Bacterial Peritonitis. 1240 85

Ascites is the most common complication of cirrhosis and occurs in more than half of all patients with cirrhosis. The development of ascites indicates progression of the underlying cirrhosis and is associated with a 50% 2-year survival rate. Conventional therapies used for the treatment of ascites include sodium restriction (<88 mmol/d), diuretics, and large volume paracentesis (LVP) (>5 L). The most effective diuretic combination is that of a potassium-sparing, distal-acting diuretic (eg, spironolactone) with a loop diuretic (eg, furosemide). LVP provides rapid resolution of symptoms with minimal complications and is well tolerated by most patients. Post-paracentesis circulatory dysfunction (PPCD) may occur after LVP and is characterized by hyponatremia, azotemia, and an increase in plasma renin activity. PPCD is associated with an increased mortality and may be prevented by administration of albumin intravenously (6 to 8 g/L of ascites removed) along with LVP. The development of either diuretic-resistant or diuretic-intractable ascites occurs in approximately 5% to 10 % of all cases of ascites. This is a poor prognostic sign, as 50% of such patients die within 6 months of its development. The only definitive therapy for refractory ascites with cirrhosis is orthotopic liver transplantation. The other options that are available include LVP, peritoneovenous shunts, and transjugular intrahepatic portosystemic shunts (TIPS). The TIPS procedure has not been shown to have any influence on survival in patients with cirrhosis and refractory ascites, and TIPS is contraindicated in patients who have advanced liver failure because it can hasten death in such individuals. Peritoneovenous shunts are associated with a high incidence of complications and frequent occlusion. They are, therefore, rarely used for refractory ascites. Spontaneous bacterial peritonitis (SBP) is a common complication of cirrhotic ascites. It may precipitate hepatorenal syndrome. The overall mortality rate from an episode of SBP is approximately 20%. Following an episode of SBP, the 1-year mortality rate approaches 70%. Hospitalized patients should be treated with intravenous third-generation cephalosporins (eg, cefotaxime), and patients at risk should receive prophylaxis with either orally administered quinolones (eg, norfloxacin) or cotrimoxazole.
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PMID:Treatment of Ascites. 1458 37

Renal failure in cirrhosis has multiple etiologies and numerous aggravating factors with evidence of worsening of prognosis. Our study was performed on 130 cirrhotic patients hospitalized in HDF between January 1st, 1994, and December 31st, 1999. We have evaluated the causes of renal failure and the relation of different aggravating factors with the onset of renal failure. Causes of renal failure included drug-induced renal failure, organic nephropathy, pre-renal azotemia, acute tubular necrosis and hepato-renal syndrome. Among the aggravating factors, lactulose was found to alter renal function (p = 0.0175). We studied the survival with respect to the serum creatinine levels and to the severity of liver disease. Three-year survival was respectively 59% and 42% in case of Child A and Child B patients with creatinine lower than 90 micromol/L. No three-year survivors were noted in these subsets of patients when creatinine level was higher than 90 micromol/L (p = 0.0247 and p = 0.0121 respectively). No difference in survival was noted in Child C cirrhosis. The occurrence of renal failure is a factor of bad prognosis in cirrhotic patients irrespective of Child's classification. In patients with Child A and Child B cirrhosis, a serum creatinine level higher than 90 micromol/L is a bad prognostic factor with a significantly decreased survival rate. This factor does not affect survival in Child C cirrhosis because of mortality related to cirrhosis complications.
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PMID:[Cirrhosis and renal failure: the influence of creatinine value on prognosis]. 1518 56

Ascites that does not respond or recurs after high-dose diuresis and sodium restriction should be considered refractory ascites. As cirrhosis advances, the escaping fluid overwhelms the lymphatic return. Decrease in renal plasma flow leads to increased sodium reabsorption at the proximal tubule leading to decreased responsiveness to loop diuretics and mineralocorticoid antagonists, which work distally. These complex hemodynamic alterations lead to refractory ascites. In refractory ascites, high-dose diuresis (400 mg of spironolactone and 160 mg of furosemide) and sodium restriction (<90 mmol/d) result in inadequate weight loss and sub optimal sodium excretion (<78 mmol/d). Further use of diuretics is limited by complications such as encephalopathy, azotemia, renal insufficiency, hyponatremia, and hyperkalemia. Therapy for refractory ascites is limited. The available therapies are repeated large volume paracentesis (LVP), transjugular intrahepatic portosystemic shunts, peritoneovenous shunts, investigational medical therapies, and liver transplantation. LVP with concomitant volume expanders is the initial treatment of choice. Transjugular intrahepatic portosystemic seems to be superior to LVP in reducing the need for repeated paracentesis and improves the quality of life. Several treatments that act at different steps in the pathogenesis of ascites are investigational, and some show promising results. Splanchnic and peripheral vasoconstrictors (Octreotide, Midodrine, and Terlipressin) increase effective arterial volume and decrease activation of the renin-angiotensin system with resultant increase in renal sodium excretion. Clonidine when given with spironolactone has been shown to cause rapid mobilization of ascites by significantly decreasing the sympathetic activity and renin-aldosterone levels. Natural aquaretics and synthetic V2 receptor antagonists (satavaptan) are being evaluated for mobilization of ascites by increasing the excretion of solute-free water. Liver transplantation remains the only definitive therapy for refractory ascites. Because refractory ascites is a poor prognostic sign, liver transplantation should be considered and incorporated early in the treatment plan.
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PMID:Management of refractory ascites. 2119 46

Renal dysfunction in patients with chronic liver disease encompasses a clinical spectrum of hyponatremia, ascites, and hepatorenal syndrome. Clinical observation has suggested that patients with cirrhosis have hyperdynamic circulation, and recent studies strongly suggest that peripheral arterial vasodilatation and subsequent development of hyperdynamic circulation are responsible for disturbances in renal function. Arterial vasodilatation predominantly occurs in the splanchnic vascular bed, and seems to precede an increase in blood flow in the splanchnic circulation. Nitric oxide plays a central role in progressive vasodilatation, as evidenced by in vivo and in vitro studies. Renal dysfunction negatively affects the prognosis of patients with cirrhosis, as hyponatremia, ascites, and azotemia are associated with increased rate of complications and mortality. Recent advances in understanding the pathophysiology of renal dysfunction have enabled clinicians to develop new diagnostic criteria and therapeutic recommendations. Hepatorenal syndrome is regarded as a potentially reversible disorder, as systemic vasoconstrictors with concomitant albumin administration are emerging as a promising management option, especially in terms of providing bridging therapy for patients awaiting liver transplantation.
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PMID:Renal dysfunction in patients with chronic liver disease. 2146 85

Hepatorenal syndrome (HRS) is a pre-renal azotemia-like acute renal failure occurring in patients with end-stage cirrhosis. HRS results from arteriolar vasodilatation, arteriolar underfilling, and intense renal vasoconstriction. By definition, it is not responsive to volume expansion, and the prognosis is especially poor even with the use of terlipressin or albumin dialysis or both. It may be difficult, on the basis of the current criteria, to clearly differentiate HRS from other causes of acute renal failure in cirrhosis. In addition, patients with HRS frequently have underlying chronic kidney changes that may not be reversible after transplantation. In the previous issue of Critical Care, a group of experts proposed a new classification of acute, acute-on-chronic, or chronic renal impairment in cirrhosis on the basis of the RIFLE (Risk, Injury, Failure, Loss, and End-stage kidney disease) criteria. The group proposed the term 'hepatorenal disorder' to define patients with advanced cirrhosis and kidney dysfunction at an earlier stage, regardless of the mechanisms. As stated by the authors, more data are needed to clearly identify, by non-invasive means, those with a potential for improvement with liver transplantation and those who can undergo a combined liver and kidney transplantation.
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PMID:A new look at renal dysfunction in the cirrhotic patient. 2232 77

Acute kidney injury (AKI), defined as an abrupt increase in the serum creatinine level by at least 0.3 mg/dL, occurs in about 20% of patients hospitalized for decompensating liver cirrhosis. Patients with cirrhosis are susceptible to developing AKI because of the progressive vasodilatory state, reduced effective blood volume and stimulation of vasoconstrictor hormones. The most common causes of AKI in cirrhosis are pre-renal azotemia, hepatorenal syndrome and acute tubular necrosis. Differential diagnosis is based on analysis of circumstances of AKI development, natriuresis, urine osmolality, response to withdrawal of diuretics and volume repletion, and rarely on renal biopsy. Chronic glomerulonephritis and obstructive uropathy are rare causes of azotemia in cirrhotic patients. AKI is one of the last events in the natural history of chronic liver disease, therefore, such patients should have an expedited referral for liver transplantation. Hepatorenal syndrome (HRS) is initiated by progressive portal hypertension, and may be prematurely triggered by bacterial infections, nonbacterial systemic inflammatory reactions, excessive diuresis, gastrointestinal hemorrhage, diarrhea or nephrotoxic agents. Each type of renal disease has a specific treatment approach ranging from repletion of the vascular system to renal replacement therapy. The treatment of choice in type 1 hepatorenal syndrome is a combination of vasoconstrictor with albumin infusion, which is effective in about 50% of patients. The second-line treatment of HRS involves a transjugular intrahepatic portosystemic shunt, renal vasoprotection or systems of artificial liver support.
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PMID:Kidneys in chronic liver diseases. 2279 39


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