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)

Plasma and 24-hour urinary cyclic AMP and cyclic GMP levels were determined by saturation analysis in specimens from normal subjects and from 101 patients with tumours of the gastrointestinal tract, breast, lung, bladder or prostate, or with cirrhosis of the liver. Relative to 46 control subjects, plasma cyclic GMP concentrations were significantly elevated in seven patients with gastric tumours, 20 patients with cancer of the breast, six patients with lung cancer, and 12 patients with cirrhosis of the liver. Urinary cyclic GMP/creatinine ratios were significantly increased in cirrhotic patients and in the lung and oesophageal cancer groups. In no cancer group were increases in plasma or urine cyclic GMP levels sufficiently consistent to be of value in the diagnosis of human malignant disease. Changes in extracellular fluid cyclic nucleotide levels in the cirrhotic group were very similar to those that have been reported for primary hepatoma patients.
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PMID:Plasma and urine cyclic nucleotide levels in malignant disease and cirrhosis of the liver. 23 Feb 5

Three patients with cirrhosis, ascites, and dilutional hyponatremia were treated with demeclocycline in an attempt to correct the abnormal water retention. Demeclocycline administration (600 to 900 mg/day for 8 to 9 days) resulted in [a] increased blood urea nitrogen and plasma creatinine concentrations; [b] reduction of the inulin clearance by between 63% to 78% and of paraaminophippurate clearance by 36% to 77%; and [c] an impairment of the renal concentrating ability. Urine osmolality decreased to hypotonic levels, but polyuria did not appear, probably because it was prevented by the reduction of the glomerular filtration rate. Renal failure was reversible on withdrawal of demeclocycline. No other causes than demeclocycline administration could be found to explain the reduction of the glomerular filtration rate and the estimated renal plasma flow.
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PMID:Renal failure associated with demeclocycline in cirrhosis. 40 25

Renal function is known to be abnormal in patients with cirrhosis. Diminished cortical blood flow due to active renal vasoconstriction is present. Renal prostaglandins, potent vasodilators, could be released by the kidney in an attempt to maintain renal blood flow. This possibility was investigated by measuring the effect of indomethacin, an inhibitor of prostaglandin synthetase, in patients with alcoholic liver disease. Administration of indomethacin reduced the effective renal plasma flow (ERPF) and creatinine clearance by 23% and 19%, respectively (P less than 0.001), and increased serum creatinine by 29% (P less than 0.001). The response to indomethacin was variable (fall in ERPF (+)7.8% to (-)67%), but was greatest in patients with ascites. Eighty percent of ascitic patients had a greater than 15% fall in ERPF after administration of indomethacin compared with 20% of nonascitic patients (P less than 0.025). An infusion of prostaglandin A1 in 13 patients corrected the decrease in ERPF and creatinine clearance that had followed the administration of indomethacin. The administration of indomethacin caused a significant fall in plasma renin activity, 8.2 +/- 2.5 to 3.6 +/- 1.4 ng/ml/hr (P less than 0.025). The fall in plasma renin activity occurred when ERPF was depressed maximally, suggesting that endogenous prostaglandins exert more control over renin release than does ERPF. Prostaglandins appear to be an important factor in maintaining renal blood flow in patients with cirrhosis and sodium retention.
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PMID:Effect of indomethacin and prostaglandin A1 on renal function and plasma renin activity in alcoholic liver disease. 44 34

Twenty-four patients with biguanide-induced lactic acidosis were reported to the Adverse Drug Reaction Register of the Finnish National Board of Health from 1974-1977. Of them, 23 had been treated with phenformin and one with metformin. The mean age of the patients was 71 years, and all but one were more than 65 years of age. The mortality rate was 63%. One patient had cirrhosis of the liver and one was already known tohave had impaired renal function. Fourteen of the patients had a normal serum creatinine concentration either before or after the development of lactic acidosis. Thus, in most patients it had not been possible to prevent development of lactic acidosis by observing the contraindications to biguanide therapy. Most patients had some form of co-existing cardiovascular disease. Tetracycline therapy was a probable precipitating factor in three cases. Based on the statistics of biguanide consumption in Finland, the annual incidence of biguanide-induced lactic acidosis in 1976 and 1977 was between 1/2000 and 1/3000 and that of fatal lactic acidosis was 1/4000.
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PMID:Biguanide-induced lactic acidosis in Finland. 49 89

Measurements of urinary lysozyme were used to evaluate renal tubular integrity in 34 patients with cirrhosis or fulminant hepatic failure who had developed renal impairment. In 18 of the patients the lysozyme values were normal but in the remaining 16 were increased, supporting previous concepts that renal failure complicating hepatocellular disease may occur both without and with tubular necrosis. The lysozyme values were inversely related to the creatinine clearance, suggesting that the development of tubular necrosis may be determined by the level of renal perfusion. The validity of simpler laboratory tests often used to assess renal tubular integrity--namely, the urine sodium concentration, the urine:plasma osmolality ratio, and casts in the urine sediment--was evaluated by comparison with the lysozyme measurements. The urine sodium concentration was of most value and the findings in the sediment were of no value at all.
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PMID:Spectrum of renal tubular damage in renal failure secondary to cirrhosis and fulminant hepatic failure. 63 52

Twelve patients with cirrhosis, refractory ascites, and varying degrees of renal failure (creatinine clearance, 5 to 44 ml/min) were studied before and up to 2 weeks following peritoneovenous shunt. Creatinine clearance increased 60% or more in seven patients (group I) and 22% or less in five patients (group II). There were no significant differences in maximum urine output or sodium excretion between groups (group I, 4,272 ml/14 hr, 372 mEq/24 hr; group II, 3,722 ml/24 hr, 255 mEq/24 hr). Aldosterone and renin concentrations were higher in group I and showed a greater decrease after shunting. Renin substrate levels also were higher in group I and rose following shunt insertion, while group II remained low. Ascitic fluid was found to contain renin substrate in concentrations of approximately 25% to 50% of plasma concentrations. Patients with the greatest increase in creatinine clearance showed the largest rise in substrate concentration and fall in renin and aldosterone secretion, suggesting a dynamic relationship between these factors. That a diuresis could occur without significant change in these parameters in five of 12 patients suggests independent control mechanisms for renal salt and water excretion and glomerular filtration in the ascitic patient.
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PMID:Improved renal function and inhibition of renin and aldosterone secretion following peritoneovenous (LeVeen) shunt. 66 20

The value and effects of treating renal failure by dialysis are analyzed in a series of 84 patients with various types of liver disease. Although none of the 25 patients with cirrhosis survived, six of 50 with fulminant hepatic failure recovered completely as did seven of nine patients with renal failure secondary to extrahepatic biliary tract obstruction or with liver and renal damage following episodes of severe hypotension. Dialysis was required for seven weeks before diuresis occurred in one patient in the latter group. Both peritoneal and hemodialysis satisfactorily controlled plasma urea and creatinine levels, except in patients with fulminant hepatic failure in whom this was only achieved by hemodialysis. Complications of dialysis were most common in patients with cirrhosis and fulminant hepatic failure and included hypotension, gastrointestinal bleeding, and intraperitoneal sepsis. Overall, the results show that dialysis is only worth attempting in those patients in whom recovery of the underlying liver lesion is possible, and even then treatment for prolonged periods may be necessary.
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PMID:Dialysis in the treatment of renal failure in patients with liver disease. 88 9

Carnitine is synthesized from lysine and methionine. In the rat, inadequate intake of either of these essential amino acids causes carnitine depletion. Inasmuch as protein deficiency is common in the hospital population, we have investigated the possible occurrence of nosocomial carnitine deficiency. Fasting serum carnitine concentration was measured in 16 normal and 247 patients in 16 disease groups. Normal range of carnitine was 55-103 muM. Only the cirrhotic group showed significant (P < 0.05) hypocarnitinemia. 14 of 36 hospitalized cirrhotics had subnormal values for serum carnitine. The creatinine/height index, midarm muscle circumference, and triceps skin-fold thickness indicated protein-calorie starvation in the 14 hypocarnitinemic liver patients. In six of the hypocarnitinemic cirrhotics (average serum level 50% of normal), spontaneous dietary intakes of carnitine, lysine, and methionine were measured and found to be only 5-15% as great as in six normocarnitinemic, healthy controls. When these six cirrhotic and six normal subjects were given the same lysine-rich, methionine-rich, and carnitine-free nutritional intake, the normals maintained normal serum carnitine levels and excreted 100 mumol/day, whereas the cirrhotics' serum level fell to 25% of normal, and urinary excretion declined to 15 mumol/day. Seven hypocarnitinemic cirrhotics died. Postmortem concentrations of carnitine in liver, muscle, heart, kidney, and brain averaged only one-fourth to one-third those in corresponding tissues of eight normally nourished nonhepatic patients who died after an acute illness of a 1-3-day duration. THESE DATA SHOW THAT CARNITINE DEPLETION IS COMMON IN PATIENTS HOSPITALIZED FOR ADVANCED CIRRHOSIS, AND THAT IT RESULTS FROM THREE FACTORS: substandard intake of dietary carnitine; substandard intake of lysine and methionine, the precursors for endogenous carnitine synthesis; and loss of capacity to synthesize carnitine from lysine and methionine.
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PMID:Deficiency of carnitine in cachectic cirrhotic patients. 89 75

The protease inhibitor aprotinin was given a) in experimental septic shock, and b) in patients with hepatic cirrhosis and ascites, since in both conditions, activation of the plasma kallikrein-kinin system is associated with pathological systemic vasodilatation, which may trigger reflex neuroendocrine activation and renal solute retention. Given early in experimental sepsis, aprotinin maintained the arterial pressure, systemic vascular resistance (SVR), creatinine clearance and sodium excretion, all of which fell in controls. Aprotinin also blocked increases in pulmonary artery pressure and plasma renin activity (PRA). Given late in sepsis, aprotinin caused a rapid rise in arterial pressure and SVR towards baseline levels. In cirrhosis, aprotinin increased SVR in patients with low baseline values, and improved glomerular filtration rate, renal plasma flow and sodium excretion in all subjects; PRA was suppressed by aprotinin. Aprotinin reverses pathological systemic vasodilatation in these two conditions, and this is associated with a reduction in renin release and improved renal function.
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PMID:Vasoactive effects of aprotinin. 128 72

As part of an infection control program in ICU, we studied prospectively 1500 consecutive patients admitted to a medical and surgical ICU from January 1988 to July 1990. Over this period of time, 69 patients developed septic shock, and 38 of them died (55.1%). Primary source of infection was the lower respiratory tract or intraabdominal in more than 50% of cases, and were related to a high mortality rate, however SS arising from a biliary tract infection is associated with a mortality rate below 20%. In the univariate analysis, nosocomial origin (p = 0.0001), creatinine serum level > 175 mumol/l (p = 0.005), multiple organ failure in the first 24 hours after shock started (p = 0.02), underlying cancer disease (p = 0.02) or liver cirrhosis (p = 0.03) were associated with a statistically significant higher risk for dying. No differences were found regarding age, sex, admission date, coma, recent surgery, prior cardiac arrest, diabetes, organ transplantation, corticosteroid therapy, cancer chemotherapy, absence of fever, bacteriology of the infection and appropriate antibiotic therapy. The multivariate analysis further identified that creatinine serum level > 175 mumol/l (p = 0.004), underlying cancer disease (p = 0.005), liver cirrhosis (p = 0.02) and nosocomial-acquired infection (p = 0.02) were independently associated to a higher risk for dying. These data allows the identification of factors related to a worst outcome. The high mortality rates recorded for septic shock still recommends the rapid transfer of the patient to an ICU as well as the use of aggressive therapy in all cases.
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PMID:[Septic shock: epidemiology and prognosis]. 129 99


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