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

Malignant ascites is often refractory to therapy and rapidly deteriorating the nutritional and physical state of the cancer patient. Nevertheless, ascites does not always implicate preterminal state of the cancer process (e.g. ovarian carcinoma). A short review is made of the pathophysiology of ascites in cirrhosis and in malignancy, and different modes of treatment are discussed. The results of medical therapy of malignant ascites (salt and water restriction, diuretics, intraperitoneal cytostatics or radiocolloids) are not convincing. The immunotherapy with OK-432, as worked out by Katano (16-46) has to prove its value. The best and most hopeful results in cases of massive previously resistant ascites, are obtained with a peritoneojugular shunt, improving immediately the nutritional status and life condition, providing excellent palliation. The superiority of the Denver shunt versus the Le Veen shunt has been assessed recently, especially for malignant ascites. Some technical and perioperative details merit more attention, to limit the high risk ratio. Control of the intrathoracic position of the catheter tip, the maintenance of the bloodflow in the jugular vein, the intramuscular tunnelisation of the peritoneal catheter, the discard of 3 or 5 liters ascitic fluid and the substitution of part of it by physiological fluid, perioperative prophylactic antibiotics and heparinisation, flow-rate control in the postoperative period by changing patients position, respiratory exercises, daily flushing, all those measures limit the risk of fibrinolysis (DIC), shunt occlusion, fluid overload and infection. The fear of metastasis by shunt is unfounded, since the survival of the primary tumor is mostly too short (41). The postoperative follow up in an intensive care unit is necessary during 24-72 hours.
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PMID:[The Denver shunt in malignant ascites]. 258 Apr 8

Some indices of central hemodynamics: cardiac and systolic indices, specific peripheral resistance and circulating plasma and blood volumes were studied in 136 patients with chronic liver diseases using radionuclide cardiography. I. Three hemodynamic types of blood circulation (hyper-, eu- and hypokinetic) were defined in patients with chronic liver diseases as well as in healthy persons. II. In liver cirrhosis and ascites the number of patients with the hyperkinetic type of circulation increased significantly, mainly at the expense of patients with hypervolemia. III. A significant decrease in circulating plasma and blood volumes was noted in patients with liver cirrhosis complicated by ascites, with the hypokinetic type of circulation. It should be borne in mind in administration of diuretics to such patients. The above results suggested that different types of circulation in patients with chronic liver diseases were formed under the influence of the disease against a background of existing constitutionally and genetically determined hemodynamic heterogeneity.
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PMID:[Changes in central hemodynamics in chronic liver diseases (radiocardiologic study)]. 358 7

Portal hypertension has been studied in the rat to see if it is associated to altered blood volume composition, as it has been shown in other species. Plasma volume was measured by isotope dilution using 99mTc labelled albumin in three groups of male Sprague-Dawley rats: normal rats (controls), partially ligated portal vein rats and rats with Cl4C induced cirrhosis. Plasma volume was significantly higher in rats with portal hypertension due to partially ligated portal vein and cirrhosis than in control animals. Similarly, the calculated blood volume was also significantly higher in the portal hypertensive animals than in control group. Portal hypertension in the rat, therefore, has been demonstrated to be associated to a marked hypervolemia and this finding should be taken into consideration in haemodynamic and pharmacokinetic studies in portal hypertensive rat models.
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PMID:Increased plasma volume in two models of portal hypertension in the rat: cirrhosis of the liver and partial portal vein ligation. 365 43

Necropsy findings of hepatobiliary system from 78 patients with end-stage renal disease maintained on hemodialysis are reported. Ninety percent of the patients exhibited some abnormalities. Multiple abnormalities often coexisted in each patient. Hepatomegaly was found in 50% of the patients and could be attributed to a discernible cause in all but two of the affected patients who had isolated hepatomegaly. Hepatic congestion was also prevalent and was complicated by fibrosis, cardiac cirrhosis, and centrilobular necrosis and hemorrhage in some patients. This was associated with chronic fluid overload, hypertension, and/or cardiovascular disease in the affected patients indicating the importance of adequate control of these factors. Mild periportal hepatic fibrosis, fatty metamorphosis, triaditis, hemosiderosis, and cystic changes were also seen with some frequency--the latter were associated with polycystic kidney disease and were complicated by massive intracystic hemorrhage and abscess formation, each in one patient. Chronic active hepatitis was found in three patients and was associated with chronic HBs antigenemia in one patient and presumed non-A, non-B infection in two. Nearly 22% of the patients showed either cholelithiasis at autopsy or before cholecystectomy due to complications. Significant negative findings included lack of acute viral hepatitis, silicone hepatosis, and recently described focal anoxic lesions associated with erythrocyte sludging. In conclusion, the present study has demonstrated the spectrum of hepatobiliary pathology in a large group of patients with end-stage renal disease maintained on hemodialysis.
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PMID:Hepatobiliary pathology in hemodialysis patients: an autopsy study of 78 cases. 375 41

Although an impairment in renal sodium and water excretion is a commonly encountered clinical problem in cirrhotic patients, the mechanisms responsible for this abnormality are uncertain. Norepinephrine (NE) levels are elevated in some patients with decompensated cirrhosis, but a causal relationship between these levels and impaired sodium and water excretion has not been established. Since in normal man, water immersion to the neck (NI) results in a preferential central hypervolemia, and since theoretical considerations suggest that central hypervolemia might suppress NE, we designed the present study to determine if the natriuretic and diuretic responses of cirrhotic patients to NI are mediated by a decrease in NE. 16 cirrhotic patients with ascites were studied on two occasions: during a seated control study and during 4 h of NI: NE, determined by radioenzymatic assay, was measured hourly. 15 of the 16 patients manifested a marked diuresis, and 12 had a natriuresis that equalled or exceeded that documented in normal subjects during NI. NI did not alter mean NE, with 9 subjects manifesting an increase of NE as compared with the prestudy hour. Furthermore, peak urinary sodium excretion and flow rate varied independently of prestudy NE (r = 0.163 and -0.173, respectively), change in NE (r = 0.256 and 0.239), as well as nadir NE levels (r = 0.118 and -0.039). The demonstration of a natriuresis and a diuresis in a majority of the subjects, occurring without concomitant suppression of plasma NE, suggests that NE does not constitute the prepotent determinant in the impaired sodium and water excretion of many patients with advanced liver disease.
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PMID:Effects of water immersion on plasma catecholamines in decompensated cirrhosis. Implications for deranged sodium and water homeostasis. 388 19

Although an impairment in renal water excretion is a commonly encountered clinical problem in cirrhotic patients, the mechanisms responsible for this abnormality are uncertain. ADH levels are elevated in some patients with decompensated cirrhosis, but a causal relationship between these levels and impaired water excretion has not been established. Since in normal man, water immersion to the neck (NI) results in a preferential central hypervolemia (CV), without plasma compositional change, and a resultant suppression of AVP, we designed the present study to determine if the diuretic response of cirrhotic patients to NI is mediated by a decrease in AVP. 17 cirrhotic patients with ascites were studied following 14 h of dehydration on two occasions: during a seated control study (C) and during 4 h of NI. AVP, determined by RIA, was measured every 30 min. 12 of the 17 patients manifested a diuresis that equalled or exceeded that documented in normal hydropenic subjects during immersion. NI did not alter mean AVP as compared with either the pre-study hour or those of the corresponding control study. Furthermore, peak V and CH2O varied independently of prestudy AVP (r = -0.116), mean change in AVP (r = -0.060), as well as nadir AVP levels (r = -0.122). The demonstration of a diuresis in some of the subjects, occurring without concomitant suppression of plasma AVP, suggests that ADH may constitute a permissive rather than pivotal factor in the impaired water excretion of many patients with advanced liver disease.
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PMID:Relationship between plasma arginine vasopressin and renal water handling in decompensated cirrhosis. 637 13

The influence of 1000 ml of 0.9% NaCl infusion induced hypervolemia on the water-electrolyte and hormonal balance was investigated in HBV-infected patients with chronic persistent hepatitis, chronic active hepatitis and compensated cirrhosis. All examined patients showed higher concentrations of vasopressin and atrial natriuretic peptide and the increased activity of RAA system before the trial. The induced hypervolemia caused the decrease of RAA system's activity and vasopressin concentration and increase of atrial natriuretic peptide's secretion, different in every group of patients. The latent deficiency of calcium and magnesium was found, too. The results showed that all determined patients had water-electrolyte and hormonal disorders, significantly increased in patients with chronic active hepatitis.
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PMID:[The influence of hypervolemia on the secretion of atrial natriuretic peptide, the renin-angiotensin-aldosterone system's activity and concentration of vasopressin, parathormone and calcitonin in hepatitis B virus infected patients with chronic liver diseases]. 759 80

We recently showed that patients with compensated cirrhosis can dispose of their fluid overload while reclining. In contrast, patients with ascites fail to develop supine-induced natriuresis. To assess the effect of reclining on renal sodium handling in patients with advanced cirrhosis and the mechanisms blunting natriuresis in this situation, renal function and plasma concentrations of atrial natriuretic factor, aldosterone and norepinephrine were evaluated in 10 nonazotemic patients with cirrhosis and ascites and 10 healthy controls standing for 2 h and reclining for 2 h. While standing, all patients showed marked sodium retention and significantly elevated plasma atrial natriuretic factor levels, aldosterone and norepinephrine. Glomerular filtration rate did not differ from healthy controls. The reclining increased renal sodium excretion in both groups, but this change was far less marked in patients; natriuresis only rose to the control range in two of them. An increase in atrial natriuretic factor and a depression of plasma aldosterone and norepinephrine was seen in both controls and patients. In the latter, despite the greater change in atrial natriuretic factor and aldosterone, the aldosterone to atrial natriuretic factor ratio, which was inversely correlated with natriuresis during both standing and reclining remained significantly elevated. In the two patients who achieved normal natriuresis during reclining, reclining was associated with both the normalization of the aldosterone/atrial natriuretic factor ratio, and with an increase in glomerular filtration rate. The supine-induced increase in atrial natriuretic factor was not only preserved but was even enhanced in cirrhosis with ascites.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal sodium handling in cirrhosis with ascites: mechanisms of impaired natriuretic response to reclining. 769 37

It seems that hypervolemia and vasodilatation coincide in compensated cirrhosis, but neither rank nor importance of these factors has been fully clarified in adaptive response to postural change. We studied, with gated equilibrium radionuclide angiography and thoracic electrical bioimpedance the hemodynamic status of 19 patients with compensated cirrhosis and 18 healthy subjects in upright and supine positions. In the upright position, the cirrhotic patients were hypotensive and had decreased peripheral vascular resistance despite increased cardiac output. The transition to the supine position was accompanied by a significant fall in the heart rate and an increase in the stroke volume in both controls (92 +/- 22 to 63 +/- 10 beats/min, and 38 +/- 9 to 62 +/- 19 ml/m2, respectively) and cirrhotic patients (101 +/- 20 to 79 +/- 13 beats/min, and 44 +/- 15 to 63 +/- 19 ml/m2, respectively). Besides, the diastolic arterial pressure fell in controls from 89 +/- 9 mmHg to 81 +/- 11 mmHg; p < 0.01, while it remained unchanged in cirrhotic patients (77 +/- 17 vs 82 +/- 13 mmHg). In the supine position, the cirrhotic patients presented tachycardia and left ventricular hyperkinesy (increased velocity of left ventricular filling and emptying). In conclusion, these results show that in compensated cirrhosis the decreased arterial tone and peripheral blood pooling are important factors of adaptive hemodynamic reaction to postural change.
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PMID:Cardiovascular status after postural change in compensated cirrhosis: an argument for vasodilatory concept. 906 72

The aetiology, biochemistry, clinical features and complications of histologically confirmed hepatic cirrhosis in 45 patients (26 females, 19 males) seen at the University Hospital of the West Indies, Jamaica, between 1984 and 1994 are presented. The age range was 1 to 72 years (mean 48 years). Abdominal swelling and weight loss were the commonest symptoms, occurring in 51% and 47% of patients, respectively. Jaundice was a presenting feature in 44%. Hepatomegaly was present in 71% of patients and splenomegaly in 33%. The aetiological factors were: alcohol (36%), bush tea (18%), chronic active hepatitis (11%), drugs (7%), and haemochromatosis (2%). Hepatitis B surface antigen was detected in 2 of 20 patients tested. 24% of the patients also had diabetes mellitus., 29% were anaemic, 29% were thrombocytopenic, 4% were leukopenic, and the prothrombin time was prolonged in 22%. The albumin/globulin ratio was reversed in 71% of the patients. The alkaline phosphatase was elevated in 56%, the aspartate aminotransferase was increased in 58% and the gamma glutamyl transpeptidase in 56%. 56% of the patients had macronodular cirrhosis; the liver showed a micronodular pattern in 18%; 7% had biliary cirrhosis; 7% chronic active hepatitis with cirrhosis; and 13% showed a mixed macro-micronodular pattern. Ascites and fluid overload developed in 44% of the patients. Hepatic encephalopathy occurred in 18% and upper gastrointestinal bleeding in 18%.
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PMID:Hepatic cirrhosis in Jamaica. 926 May 37


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