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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To develop a more comprehensive index for predicting the prognous of liver cirrhosis. 300 consecutive patients with cirrhosis were studied in terms of survival from 1975 to 1986. Median follow-up period was 5.3 years. A multivariable survival analysis (Cox's regression model) using clinical biochemical data obtained at admission disclosed eight factors of value in predicting prognosis: age, frequency of previous GI bleeding, ascites, hepatic encephalopathy, serum albumin, serum bilirubin, hemoglobin and prothrombin time. A prognostic index was constructed for the calculation of the estimated survival probability.
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PMID:An analysis of prognostic factors in cirrhosis. 250 40

A 76-year-old woman, who had suffered from liver cirrhosis, was referred to our hospital because of pancytopenia. Her peripheral leukocyte count was 2,500/microliters with 43% myeloblasts, hemoglobin at 9.0 g/dl and platelet count of 0.9 x 10(4)/microliters. Aspirate from bone marrow showed hypercellular marrow with 52% myeloblasts. No chromosomal abnormality was detected. She was diagnosed as acute myelogenous leukemia (AML, M2). The diagnosis of liver cirrhosis was confirmed by laboratory data and findings of abdominal sonography. Moreover, she had valvular aortic stenosis. These complications made it difficult to treat her with combined chemotherapy containing anthracycline antibiotics, so she was given a small dose of cytosine arabinoside (Ara-C, 10 mg/body/12 hr) for 18 days. After severe myelosuppression, complete remission was achieved. The highest serum concentration of Ara-C was obtained at 15 min after subcutaneous injection of Ara-C; thereafter the Ara-C concentration decreased immediately within 60 min in a pattern similar to that observed in patients without liver cirrhosis. Thus, low-dose Ara-C regimen might be a useful treatment for aged patients with AML, even complicated with liver cirrhosis.
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PMID:[An aged patient with acute myelogenous leukemia complicated with liver cirrhosis: successful treatment with low-dose cytosine arabinoside]. 275 21

A double-blind, placebo-controlled multicenter trial was conducted to determine the efficacy of oral testosterone treatment (200 mg three times daily) in men with alcoholic cirrhosis. By skewed randomization (3:2), 134 patients received testosterone and 87 placebo. Patients were followed from 8 to 62 months (median = 28 months). In the testosterone group, 33 patients died (25%; 95% confidence limits = 18 to 33%) as compared to 18 (21%; 95% confidence limits = 13 to 31%) in the placebo group. Taking age and significant prognostic variables into consideration, this corresponds with a relative mortality risk of 1.17 (95% confidence limits = 0.65 to 2.15) in the testosterone group vs. the placebo group. Testosterone treatment did not significantly affect liver biochemistry, prevalence of complications to cirrhosis or causes of death. Patients treated with testosterone developed significantly (p less than 0.05) higher serum testosterone and blood hemoglobin concentrations and significantly (p less than 0.05) lower plasma IgM concentrations as compared to the placebo group. The prevalence of gynecomastia decreased significantly (p less than 0.05) in the testosterone group as compared to the placebo group. We conclude that oral testosterone treatment has no beneficial effect on survival and liver biochemistry in men with alcoholic cirrhosis, and adverse effects cannot be excluded.
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PMID:Testosterone treatment of men with alcoholic cirrhosis: a double-blind study. The Copenhagen Study Group for Liver Diseases. 287 27

To determine and to quantify the pulmonary and extrapulmonary contributors to hypoxemia in liver cirrhosis, we measured in 10 cirrhotics blood gases, P50, hemodynamics, ventilation, and the distribution of ventilation-perfusion ratios (VA/Q) using the multiple inert gas elimination technique. Seven patients had an arterial hypoxemia (PaO2 = 69 +/- 6 mm Hg, mean +/- SD), and three patients were normoxemic (PaO2 = 89 +/- 6 mm Hg). In each hypoxemic patient, the VA/Q distributions were characterized by the presence of low VA/Q units. A negative logarithmic correlation was found between the dispersion of the blood flow distribution and the arterial PO2. An acute inspiratory hypoxia (FIO2, 0.125) elicited an increase in pulmonary vascular resistance by 58.5% in the hypoxemic group and by 81.6% in the normoxemic one (p = NS between the two groups). The percent change in pulmonary vascular resistance induced by hypoxia was not correlated with the percent change in the dispersion of the blood flow distribution. A theoretical analysis showed that the mean arterial PO2 of 69 mm Hg of the hypoxemic group differed from a normal reference value of 96 mm Hg as a result of the combined effects of reduced hemoglobin (-4 mm Hg), increased P50 (+4 mm Hg), increased ventilation (+10 mm Hg), low VA/Q (-35 mm Hg), and true shunt (-2 mm Hg). These results show that the "hypoxemia of liver cirrhosis" is essentially caused by VA/Q mismatching, which is not explained by an abnormal hypoxic pulmonary vasoconstriction.
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PMID:Pulmonary and extrapulmonary contributors to hypoxemia in liver cirrhosis. 292 62

The effect of glucagon on hepatic regional hemodynamics was investigated in patients with chronic liver disease during peritoneoscopy with reflectance spectrophotometry. When glucagon was infused intravenously in patients with a non-cirrhotic liver, the regional hepatic tissue oxygen consumption, as estimated spectrophotometrically, increased significantly, whereas the index of hepatic tissue blood volume did not change appreciably, and consequently, the oxygen saturation of hemoglobin in the hepatic tissue blood decreased. In contrast, the administration of glucagon in patients with liver cirrhosis resulted in a significant increase in the index of hepatic tissue blood volume and produced a minor increase in hepatic tissue oxygen consumption. The oxygen saturation of hepatic blood hemoglobin tended to increase in the cirrhotics. The result suggests the presence of functional vasoconstriction at the presinusoidal and/or sinusoidal vessels in the cirrhotic liver, possibly due to a decreased vasomotor activity and/or an abnormal regulatory function of vasoactive substances, which are released by glucagon.
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PMID:Characterization of hepatic hemodynamics in cirrhotics and non-cirrhotics. Effect of glucagon infusion. 292 37

We investigated the estimated hepatic oxygen consumption by reflectance spectrophotometry during peritoneoscopy and the rate of in vitro oxygen consumption of liver slices obtained by liver biopsy using the oxygen electrode apparatus in patients with chronic liver diseases. The estimated hepatic oxygen consumption decreased concomitantly with the decrease in blood supply, expressed as the regional hepatic blood hemoglobin concentration, and it was significantly decreased in cirrhosis compared to chronic hepatitis. The estimated hepatic oxygen consumption also was significantly correlated with the serum albumin level, 15-min retention rate of indocyanine green, and prothrombin time. There was no correlation between the estimated hepatic oxygen consumption calculated from the reflectance spectra and the rate of in vitro oxygen consumption measured by the oxygen electrode apparatus. Most cirrhotic liver slices had a respiratory rate comparable to that in chronic hepatitis. Thus, it is concluded that the reduction of estimated hepatic oxygen consumption in cirrhosis of the liver is mainly due to the reduction of oxygen supply secondary to the decrease of hepatic blood flow.
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PMID:Estimated hepatic oxygen consumption in patients with chronic liver diseases as assessed by organ reflectance spectrophotometry. 293 79

As public health measures decrease the number of deaths due to infectious diseases, life expectancy will increase and chronic and degenerative diseases will claim a greater part of the public health resources. Moreover, many of these diseases are directly related to certain preventable risk factors, which it would be advantageous to identify and eliminate before they become major problems in developing countries. First, demographic analyses, using multiple decrement life tables, were performed to show 1) the survival experience of persons in the population who would die of a disease, given the current cause-specific mortality rates, 2) the life expectancy at any age in the table for a given cause of death, and 3) the gain in life expectancy among persons expected to die of the disease. Second, models were constructed for assessing the effects of risk factors and their change over time. The 1st part of this analysis used hazard functions to relate the risk of disease or death to the values of the risk factor; the 2nd part used linear regression equations to project future values of the risk factors as a function of their past values. Data for the life tables were drawn from World Health Organization cause-specific mortality profiles for cancer, diabetes, cirrhosis, stroke, and heart disease in highly developed, moderately developed, and less developed nations. Data for assessing the effects of various risk factor interventions were drawn from the Framingham Study of cardiovascular disease. Risk factors used were serum cholesterol, blood pressure, smoking, Quetelet index, blood sugar, hemoglobin, vital capacity and age. Demographic analysis showed that the effects of major noncommunicable diseases on life expectancy was not significantly different in developed and developing countries; there were differences in the proportions of deaths from the 5 diseases analyzed but not in the distribution of age at death. Moreover, numerically there are currently more chronic disease deaths in developing than in developed countries, and as life expectancy increases and fertility declines, the impact of noncommunicable diseases will rapidly increase in those countries. Analysis of risk-factor reduction by intervention, such as nonsmoking campaigns and low cholesterol diets, showed that such interventions would be cost-effective, but less so at some ages than at others. Nevertheless, such interventions would be worthwhile if they prevented unhealthful life styles from gaining a foothold in these countries.
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PMID:The global impact of noncommunicable diseases: estimates and projections. 323 13

The effect of intraportal infusion of norepinephrine (NE) on primary hemostasis in the cirrhotic rat was investigated at standardized liver trauma. Cirrhosis was induced by simultaneous administration of increasing amounts of carbontetrachloride (CCl4) and phenobarbitone. Infusion of norepinephrine took place after cannulation of the gastroduodenal vein. Intraportal infusion of NE resulted in a significant increase in arterial blood pressure and portal pressure in all animals. No difference was observed between cirrhotic and control rats. Cirrhotic animals bled longer and more profusely as compared with the controls. Infusion of NE resulted in significant decrease in bleeding time and blood loss. NE did not affect hematocrit, hemoglobin, platelet, or white cell count. Platelet aggregation was not influenced by the compound. In conclusion, intraportal infusion of NE proved effective in decreasing hemorrhage at liver trauma in cirrhotic rats.
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PMID:Control of traumatic liver hemorrhage in the cirrhotic rat by intraportal infusion of norepinephrine. 343 39

The clinical efficacy of ultrafiltration (UF) of ascitic fluid with hemofilter in the treatment of intractable ascites associated with chronic liver disease or intraabdominal malignancy was studied in fifteen patients. The ascitic fluid was reinfused into the peritoneal cavity after ultrafiltration. An average of 6.2 liters of fluid was removed during 4.4 hours of ultrafiltration with no significant change in blood pressure, central venous pressure, hemoglobin, platelets or plasma creatinine. Ascitic fluid albumin rose significantly immediately after the procedure (from 5.2 +/- 4.3 gm/L to 31.9 +/- 30.0 gm/L, P less than 0.01). The plasma albumin concentration increased significantly at the end of UF (P less than 0.001). Also there was a significant increase in urine output (P less than 0.001), urinary sodium excretion (P less than 0.001), and endogenous creatinine clearance (P less than 0.01) during the 48 hours following UF. There was no evidence of hemodynamic, renal or hematological dysfunction, and other complications, including encephalopathy, peritonitis and variceal bleeding were not experienced. Ultrafiltration of ascitic fluid with hemofilter may be safely used in the temporary relief of refractory ascites due to cirrhosis or intra-abdominal malignancy.
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PMID:Ultrafiltration by hemofilter--a new therapeutic measure in intractable ascites. 358 26

The records of 54 patients with documented cirrhosis who underwent colectomy between January 1970 and January 1984 were studied to assess the operative risk and to determine the preoperative predictive risk factors. In-hospital mortality was 24 percent (13 patients), and postoperative complications occurred in 48 percent (26 patients). The risk of surgical intervention was significantly increased if encephalopathy, ascites, anemia, or hypoalbuminemia was present before operation. A simple operative risk index involving the presence of encephalopathy and ascites and the levels of hemoglobin and albumin is proposed to help distinguish a low-risk subgroup in whom postoperative mortality was 12.8 percent from a high-risk subgroup in whom postoperative mortality was 53.3 percent.
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PMID:The surgical risk of colectomy in patients with cirrhosis. 359 74


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