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Biomedical subjects

J Rodés

Publications and source records attributed to J Rodés.

At least 361 records · Page 20Linked to original sources
PubMed1990

[Hepatitis B at an open institution for the mentally retarded. Immunogenic effect of a recombinant anti-hepatitis-B vaccine].

The diffusion of hepatitis B virus was investigated in an open institution for mentally retarded patients, where 24 patients with Down's syndrome (DS) and 94 with other types of mental retardation (OMR) were being cared for. The immunogenic response to a recombinant vaccine intramuscularly injected to the deltoid muscle at a dosage of 20 mcg in the months 0, 1 and 6 was also evaluated. Seropositivity for some hepatitis B serum marker was found in 19.4% of patients (12.5% of those with DS and 21.2% of those with OMR). HBsAg was found in 8.3% of patients with DS and in 4.2% of those with OMR. The seroconversion to antiHBs induced by the vaccine 8 months after the first dose was found in 72.3% of DS and in 100% of OMR. The poor immunogenic response in DS was attributed to age, as in patients younger than 20 years it was 91.6% while in those over that age it was only 33.3%. It was concluded that in open institutions for mentally retarded patients there is a risk of hepatitis B infection, also shown in closed institutions, and that recombinant hepatitis B vaccine is highly immunogenic in this population, although it has been found that in patients with DS the age has a very marked negative influence on the response to the vaccine.

Adolescent↗
PubMed1990

Factors influencing the development of metabolic bone disease in primary biliary cirrhosis.

The prevalence, type, and factors that may influence the development of bone disease in primary biliary cirrhosis, have been investigated in 20 consecutive patients, who, in addition to liver function tests and mineral and vitamin D metabolism studies, were submitted to a transiliac bone biopsy after tetracycline double-labeling for quantitative histomorphometric examination. Intestinal calcium absorption was also assessed in 16 patients. Seven patients (35%) had reduced bone volume and were considered osteoporotic. Three also had bone mineralization impairment, but did not have criteria for osteomalacia. Bone formation was depressed in 15 patients, and bone resorption was low or normal in 19 cases. Eroded surfaces were reduced in all osteoporotic patients. Duration of primary biliary cirrhosis was significantly longer in patients with osteoporosis (6.3 +/- 0.6 yr) than in those without osteoporosis (2.6 +/- 0.6, p = 0.004). Moreover, osteoporosis was more prevalent in postmenopausal women, and in those who had intestinal calcium malabsorption, which was present in 80% of osteoporotic patients but in only 18% of nonosteoporotic patients (p = 0.03). Osteoporosis and mineralization bone impairment were unrelated to the severity of cholestasis. 25-Hydroxyvitamin D was significantly lower in those patients with intestinal calcium malabsorption. The results of this study indicate that osteodystrophy in primary biliary cirrhosis is characterized mainly by "low-turnover" osteoporosis, which is related to the duration of the liver disease, postmenopausal condition, and calcium malabsorption.

Adult↗
PubMed1989

[Severe acute hepatitis as initial manifestation of chronic hepatitis B virus infection].

Chronic hepatitis B virus (HBV) infection was revealed by a severe acute hepatitis with positive HBsAg in a patient. The positivity of IgM anti-HBc antibody, the rapid negativization of DNA-HBV, the early normalization of liver function tests and the exclusion of other causes of acute hepatitis favored the diagnosis of recent HBV infection and were predictive of a rapidly favorable outcome. However, immunohistochemical study of a transjugular hepatic biopsy sample discovered HBsAg within the liver, with a characteristic topographic distribution of chronic HBV infection. The patient's evolution confirmed this diagnosis, because 20 months later he had chronic active hepatitis with persistent replicative activity of HBV. This case illustrates the heterogeneity of HBV infections, emphasizing the need of an accurate diagnosis and a careful follow up until the complete resolution of each case of acute hepatitis with positive HBsAg.

Acute Disease↗
PubMed1989

Comparison of rifampicin with phenobarbitone for treatment of pruritus in biliary cirrhosis.

The anti-pruritic effects of rifampicin (10 mg/kg) and phenobarbitone (3 mg/kg) were assessed in 22 patients with primary biliary cirrhosis in a crossover randomised clinical trial. Each agent was given for 14 days, with a 30-day washout period between treatments. 21 patients completed the course of rifampicin and 18 that of phenobarbitone; rifampicin was withdrawn from 1 patient when anaemia and renal failure developed, whereas 3 patients stopped taking phenobarbitone because of a rash and the 4th merely refused the drug. Rifampicin had a greater anti-pruritic effect than phenobarbitone. The symptom improved in 19 patients taking rifampicin and in 8 taking phenobarbitone, the degree of improvement being greater with rifampicin than with phenobarbitone. Pruritus disappeared in 9 patients receiving rifampicin, and three of them were free of itch when switching over to phenobarbitone. Both drugs were equally effective in inducing hepatic microsomal function but rifampicin has the additional effect of reducing cholestasis. Its anti-pruritic effect should be tested in long-term clinical trials.

Adult↗
PubMed1989

Hemodynamic effects of blood volume restitution following a hemorrhage in rats with portal hypertension due to cirrhosis of the liver: influence of the extent of portal-systemic shunting.

The present study investigated whether, in rats with portal hypertension due to cirrhosis of the liver induced by carbon tetrachloride, blood volume restitution following a hemorrhage produces an increase of portal pressure beyond control values, as observed in rats with prehepatic portal hypertension. Since carbon tetrachloride-induced cirrhosis caused mild portal-systemic shunting, in some of the cirrhotic rats (12 of 29 rats) portal-systemic shunting was enhanced by a transient (4 days) partial constriction of the portal vein, which was removed 1 week prior to the study. After baseline measurements of portal pressure and arterial pressure, 15 ml per kg of blood were withdrawn at a rate of 0.3 ml per min and reinfused 15 min later. After blood reinfusion, portal pressure and arterial pressure were measured again, and cardiac output, regional blood flows and portal-systemic shunting were determined using radioactive microspheres. Portal-systemic shunting was 78 +/- 11% of total blood flow in the cirrhotic rats that had temporary portal vein constriction, but only 5 +/- 2% (p less than 0.001) in those that did not. Blood volume restitution in low-portal-systemic shunting rats did not produce any significant modification in splanchnic or systemic hemodynamics. However, in rats with high portal-systemic shunting, blood volume restitution produced a significant increase in portal pressure (from 9.9 +/- 0.9 to 13.5 +/- 0.9 mmHg, p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Beta-blockade with propranolol and hepatic artery blood flow in patients with cirrhosis.

In patients with cirrhosis and portal hypertension, propranolol administration reduces heart rate and cardiac output and diminishes portal pressure and collateral blood flow. However, there is little information on the possible effects of propranolol on hepatic artery blood flow. The present study addressed this question in 12 cirrhotic patients with end-to-side portacaval shunt, in whom all of the liver blood flow represents the hepatic artery blood flow. Hepatic artery blood flow (continuous infusion of indocyanine green), cardiac output (thermal dilution), heart rate and mean arterial pressure were measured before and 20 min after the intravenous infusion of 10 to 15 mg of propranolol. beta-Adrenergic blockade caused a significant reduction of cardiac output (from 9.1 +/- 2.1 to 7.1 +/- 1.4 liters per min, p less than 0.001) (mean +/- S.D.) and heart rate (from 85 +/- 10 to 71 +/- 7 beats per min, p less than 0.001), and a significant increase of systemic vascular resistance (from 9.0 +/- 2.1 to 11.7 +/- 2.7 mmHg per liter per min, p less than 0.001), whereas mean arterial pressure did not change (77 vs. 78 mmHg). Propranolol significantly reduced hepatic artery blood flow (from 0.65 +/- 0.20 to 0.55 +/- 0.14 liters per min, p less than 0.01). However, reduction of hepatic artery blood flow (-12.9 +/- 7.3%) was significantly less than reduction of cardiac output (-21.1 +/- 5.2%, p less than 0.01). As a result, the fraction of the cardiac output delivered to the liver was significantly greater after propranolol (8.0 +/- 1.7%) than before (7.3 +/- 1.7%, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗
PubMed1989

Endotoxin-induced ascites formation in the rat: partial mediation by platelet-activating factor.

Systemic endotoxemia has been observed in patients with acute and chronic liver failure, and bacterial endotoxin is known to increase vascular permeability. We investigated in the normal rat the effects of intraportal endotoxin administration and the possible mediation of these effects by platelet-activating factor. Injection of endotoxin lipopolysaccharide (10 and 25 mg per kg) in the rat resulted in rapid ascites formation, as well as systemic hypotension, hemoconcentration and acute erosions of the gastrointestinal mucosa. These effects were significantly attenuated by pretreatment with L652,731 and CF-3988, specific platelet-activating factor antagonists. Administration of 25 mg per kg endotoxin also resulted in significant elevations of platelet-activating factor biosynthesis in vitro by samples of duodenum, liver and lung. The effects of endotoxin were mimicked by intraportal infusion of platelet-activating factor (50 ng per kg per min), which induced ascites and gastrointestinal lesions. Platelet-activating factor reduced circulating plasma volume and increased peritoneal permeability to albumin as assessed by the ascites to plasma ratio of labeled albumin. These results, therefore, support a role for platelet-activating factor in mediating endotoxin-induced ascites and gastrointestinal erosions.

Animals↗
PubMed1989

Propranolol decreases portal pressure without changing portocollateral resistance in cirrhotic rats.

Propranolol decreases portal pressure by reducing portal blood inflow. Studies in rats with prehepatic portal hypertension due to portal vein stenosis (a model with extensive portosystemic shunting) have shown that propranolol increases the portocollateral resistance, which hinders the fall in portal pressure. The present study examined the effects of propranolol on splanchnic and systemic hemodynamics in rats with portal hypertension due to cirrhosis of the liver, a model which is characterized by mild portosystemic shunting. Two groups of rats with CCl4-induced cirrhosis were studied: the propranolol group (n = 8), which received a propranolol infusion of 2 mg per 15 min, and controls (n = 9), which received a placebo (saline) infusion. Hemodynamic measurements were done using radiolabeled microspheres. Propranolol-treated rats had significantly lower cardiac output (-31%) and heart rate (-26%) than controls (p less than 0.001). Hepatic artery flow was not modified by propranolol. Propranolol caused splanchnic vasoconstriction, manifested by increased splanchnic resistance (+57%) and by a significant fall in portal blood inflow (4.8 +/- 0.4 vs. 6.3 +/- 0.5 ml per min.100 gm in controls, p less than 0.05). In contrast with rats with prehepatic portal hypertension, propranolol did not increase portal resistance in cirrhotic rats [2.0 +/- 0.2 vs. 2.0 +/- 0.1 mmHg per ml per min.100 gm body weight (not significant)]. Hence, the fall in portal pressure (-19%) was expected from the decrease in portal inflow (-24%). These results suggest that increased portal resistance in rats with prehepatic portal hypertension may represent an intrinsic effect of propranolol on the portocollateral vessels, since beta-blockade does not modify portal vascular resistance in cirrhosis.

Animals↗
PubMed1989

Association of transdermal nitroglycerin to vasopressin infusion in the treatment of variceal hemorrhage: a placebo-controlled clinical trial.

The aim of this study was to evaluate, using a double-blind technique, the efficacy of the association of transdermal nitroglycerin to vasopressin infusion for the treatment of variceal bleeding. Sixty-nine cirrhotic patients with active variceal bleeding were randomly allocated to receive vasopressin (0.4 to 0.8 unit per min until variceal bleeding has been controlled for 12 hr) associated with nitroglycerin administered transdermically in a slow-release preparation (10 mg in 24 hr) or placebo. An initial control of variceal hemorrhage was achieved in 83% of the patients receiving vasopressin-nitroglycerin and in 74% in the vasopressin-placebo group. Owing to a lower frequency of recurrent bleeding during therapy (18 vs. 42%, p = 0.11), vasopressin-nitroglycerin achieved a definitive control of bleeding in a higher proportion of patients than vasopressin-placebo (73 vs. 54%, p = 0.13). The group treated with the drug combination showed favorable results in relation to transfusion requirements (2.9 +/- 0.4 vs. 4.2 +/- 0.5 units, p = 0.05), total dose of vasopressin required (453 +/- 47 vs. 587 +/- 50 units, p less than 0.05), need of balloon tamponade (6 vs. 15, p less than 0.05) and requirement for emergency surgery (0 vs. 4, p = 0.07). There were no significant differences in the undesirable effects associated with treatment, observed in 37 and 49% of cases, respectively. Hospital mortality was similar (33 vs. 25%). This study demonstrates that transdermal nitroglycerin improves the effectiveness of vasopressin for controlling variceal hemorrhage.

Administration, Cutaneous↗
PubMed1989

Diagnostic accuracy of fine-needle aspiration biopsy in patients with hepatocellular carcinoma.

The present study was undertaken to investigate the diagnostic usefulness of fine-needle aspiration biopsy (FNAB) in a large series of patients with hepatocellular carcinoma (HCC) seen over a 1-year period. During 1986, ultrasonographically guided percutaneous FNAB was performed in 72 patients with suspected HCC. A final diagnosis of HCC was made in 58 patients. The presence or absence of HCC was ascertained by histological examination and/or by other diagnostic procedures (alpha 1-fetoprotein, computed tomography, arteriography) and by clinical follow-up (repeated ultrasonographic controls) and/or by surgery or necropsy. A total of 61 FNABs were carried out in these 58 patients. Only 42 (69%) of the 61 FNABs allowed the diagnosis of HCC. This moderate diagnostic sensitivity was not related to tumor size. Only one false positive result was observed in the non-HCC group. Therefore, the diagnostic specificity of FNAB for HCC was 93%, with a positive predictive value of 97% and a negative predictive value of 40%. These results show that FNAB is a useful diagnostic technique in patients with HCC. However, these data also show that there is a large proportion (31%) of subjects with false negative results. Therefore, we suggest that further efforts should be made to improve the diagnostic accuracy of this procedure.

Adult↗
PubMed1989

Influence of liver disease on hepatic alcohol and aldehyde dehydrogenases.

The hepatic activities and the isoenzyme patterns of both alcohol dehydrogenase and aldehyde dehydrogenase have been studied in 60 alcoholics with varying degrees of liver damage (from normal tissue or minimal changes to cirrhosis with alcoholic hepatitis) and in 24 nonalcoholics with chronic hepatitis or cirrhosis in order to ascertain their association with liver damage. In alcoholics both alcohol dehydrogenase and low-Km aldehyde dehydrogenase activities decreased proportionally with the severity of liver disease. In contrast, in nonalcoholics, there was a reduction of low-Km aldehyde dehydrogenase activity related to the severity of liver injury, but alcohol dehydrogenase was similar in patients with chronic hepatitis and nonalcoholic cirrhosis. There were no significant changes in total and high-Km aldehyde dehydrogenase activities among the different histologic groups studied, although the lowest activities were observed in patients with more severe liver injury. The prevalence of atypical alcohol dehydrogenase was similar in alcoholic (6.6%) and in nonalcoholic (8.3%) liver disease. All patients exhibited isoenzyme aldehyde dehydrogenase II, whereas isoenzyme I was not detected in 39.5% of the alcoholic patients and in 9.5% of those with nonalcoholic liver disease. The lack of aldehyde dehydrogenase I was observed in cases with the lowest enzymatic activities. These results suggest that the decrease of alcohol and aldehyde dehydrogenase activities in alcoholics is not a primary defect and, therefore, their decrease is secondary to liver damage. It is speculated that the diminution of alcohol dehydrogenase, found particularly in alcoholics, could be due to centrilobular cell necrosis.

Alcohol Dehydrogenase↗
PubMed1989

Reduction of portal pressure by isosorbide-5-mononitrate in patients with cirrhosis. Effects on splanchnic and systemic hemodynamics and liver function.

The results of a study to characterize the effects of the oral administration of isosorbide-5-mononitrate (Is-5-Mn), the active metabolite of isosorbide dinitrate, on portal hypertension in 23 patients with cirrhosis are reported. Patients received 20 mg of Is-5-Mn (n = 10), 40 mg (n = 9), or a placebo (n = 4). No significant changes were observed after the administration of the placebo. However, both doses of Is-5-Mn significantly reduced portal pressure, as evaluated by measurements of the hepatic venous pressure gradient. The fall in portal pressure averaged 10% after the 20-mg dose and 18% after 40 mg and was maintained for the 2 h of observation. Reduction of portal pressure was due to a decrease in the wedged hepatic vein pressure, with no changes in the free hepatic venous pressure. After the 20-mg dose, the decrease in portal pressure was associated with an increase in hepatic blood flow (16%), suggesting a fall in hepatic vascular resistance. However, after the 40-mg dose, a reflex splanchnic vasoconstriction elicited by the fall in arterial pressure (-19%) appeared to contribute to the greater reduction in portal pressure, as suggested by a significant decrease in azygos blood flow (-15%). These beneficial effects on portal pressure were not associated with adverse effects on liver function, as evaluated by measurements of the hepatic clearance of indocyanine green and the hepatic intrinsic clearance. Neither dose of Is-5-Mn caused significant changes in these quantitative parameters of liver function. These findings suggest that Is-5-Mn could be a potentially useful and safe agent in the treatment of portal hypertension.

Adult↗
PubMed1989

Blockade of the hydroosmotic effect of vasopressin normalizes water excretion in cirrhotic rats.

Water retention in cirrhosis has classically been considered to be due to a low distal fluid delivery secondary to increased proximal sodium reabsorption. However, recent studies showing high plasma vasopressin levels in patients and rats with cirrhosis, ascites, and dilutional hyponatremia suggest that a nonosmotic vasopressin hypersecretion could be an alternative mechanism. To investigate the role of vasopressin in water retention in cirrhosis, the renal ability to excrete a water load (50 ml/kg body wt), as estimated by the minimum urinary osmolality and the percentage of the water load excreted during 3 h, was assessed in 10 control rats and in 20 cirrhotic rats with ascites and impaired water excretion and high urinary excretion of vasopressin. Twenty-four hours later, the same procedure was repeated in cirrhotic rats 20 min after the subcutaneous injection (30 micrograms/kg body wt) of d(CH2)5Tyr(Et) VAVP, an antagonist of the hydroosmotic effects of vasopressin (10 rats), or the vehicle (10 rats). Treatment with the vasopressin antagonist normalized water excretion in 9 of the 10 rats. No significant changes in renal water metabolism were observed in the group of rats given the vehicle. These results indicate that vasopressin hypersecretion is the predominant mechanism of the impairment in water excretion in rats with experimental cirrhosis and ascites.

Animals↗
PubMed1989

Role of altered systemic hemodynamics in the blunted renal response to atrial natriuretic peptide in rats with cirrhosis and ascites.

The natriuretic effect of pharmacological doses of atrial natriuretic peptide (ANP) is markedly reduced in cirrhosis with ascites. The current study, which includes two protocols, was carried out to investigate whether this phenomenon is related to the altered systemic hemodynamics present in cirrhosis. In protocol A, the administration of ANP (2.5 micrograms.kg-1 as a bolus followed by a constant infusion of 0.1 microgram.kg-1.min-1) to 10 rats with carbon tetrachloride-induced cirrhosis and ascites produced a significantly lower increase in diuresis (13.4 +/- 1.3 microliters/min) and natriuresis (2.3 +/- 0.3 mu Equiv/min) than in 10 control rats (56.3 +/- 1.4 microliters/min and 8.7 +/- 0.5 mu Equiv/min, respectively), indicating a renal resistance to the effect of ANP in this experimental model of cirrhosis. The reduction of arterial pressure induced by ANP was similar in both groups. However, since baseline mean arterial pressure was significantly lower in cirrhotic rats, the degree of hypotension during ANP infusion was also greater in this group of animals (82 +/- 3 vs. 109 +/- 2 mmHg). The aim of protocol B was to assess whether normalization of arterial pressure in cirrhotic rats increases the renal response to ANP. This protocol includes two groups of 10 rats with cirrhosis and ascites infused with a glucose solution containing norepinephrine (CT-NE rats) or angiotensin II (CT-AII rats) at doses to normalize arterial pressure and an additional control group of 10 cirrhotic rats with ascites receiving only glucose solution (CT rats). Angiotensin II, but not norepinephrine or glucose solution administration, was associated with a significant increase in urine volume and sodium excretion. During ANP infusion, CT rats showed a blunted diuretic and natriuretic response. In contrast, the ANP-induced increase in urine volume and sodium excretion observed in CT-NE (53.6 +/- 10.4 microliters/min and 9.3 +/- 2.2 mu Equiv/min) and CT-AII rats (98.3 +/- 11.6 microliters/min and 15.5 +/- 2.9 mu Equiv/m), was similar or even greater than that showed by the healthy rats of protocol A. The degree of hypotension during ANP administration was also similar (CT-NE, 104 +/- 2; CT-AII, 108 +/- 5 mmHg). These results suggest that the blunted response to pharmacological doses of ANP in cirrhosis with ascites is related to altered systemic hemodynamics of cirrhosis, which further deteriorates during the infusion of the peptide.

Angiotensin II↗
PubMed1989

Treatment of ascites and renal failure in cirrhosis.

Ascites is a frequent complication in patients with liver cirrhosis. The accumulation of fluid in the abdominal cavity is associated with disturbances of systemic and splanchnic haemodynamics and of kidney function, which contribute to the poor prognosis of these patients. Classically, the treatment of ascites in patients with cirrhosis has been based on the combination of a sodium-restricted diet and the administration of diuretics. However, this treatment is not entirely satisfactory, since it is associated with a relatively high incidence of side-effects, and about 20% of patients hospitalized for the treatment of an episode of ascites do not respond to such therapy. In the last two decades, alternative therapies to diuretics have been introduced. PVS is an effective method of treating ascites. The high incidence of complications observed in early studies may be reduced by adequate perioperative management and careful selection of patients. The role of the PVS in the treatment of cirrhotics with ascites, however, still remains to be established. Recently, paracentesis has emerged as an alternative method of treating ascites in patients with cirrhosis. Several studies have shown that therapeutic paracentesis plus i.v. albumin infusion is more effective than conventional diuretic therapy and is associated with a lower incidence of complications. It has also been demonstrated that therapeutic paracentesis without the i.v. administration of albumin is associated with a marked increase in plasma renin activity, suggesting an impairment of effective blood volume, and with the development of hyponatraemia and/or renal failure in 20% of cases. Therefore, the i.v. administration of albumin is an essential measure in preventing the impairment of systemic haemodynamics and renal function that frequently follows the mobilization of ascites by paracentesis.

Ascites↗
PubMed1989

Portal hypertension.

Portal hypertension is a frequent syndrome characterized by a chronic increase in portal venous pressure and by the formation of portal-systemic collaterals. Its main consequence is massive bleeding from ruptured esophageal and gastric varices. Bleeding is promoted by increased portal and variceal pressure, and is favored by dilatation of the varices. The evaluation of the portal hypertensive patient should include the assessment of portal vein patency by ultrasonography, endoscopic evaluation of the presence, size, and extent of esophageal varices, and hemodynamic studies with measurements of portal pressure and of portal-collateral blood flow. The preferred techniques are hepatic vein catheterization and measurement of azygos blood flow. Endoscopic measurements of variceal pressure and estimations of portal blood velocity by the Doppler technique have recently been introduced, but are still research procedures. Acute variceal hemorrhage should be treated under intensive care. Specific therapy to arrest variceal bleeding includes balloon tamponade, vasopressin, somatostatin, sclerotherapy, and emergency surgery. Treatment of portal hypertension is aimed at preventing variceal hemorrhage and bleeding-related deaths. Pharmacologic prophylaxis is based on the use of drugs that cause a sustained reduction in portal pressure; most studies have used propranolol. Surgery and endoscopic sclerotherapy can also be used to prevent rebleeding.

Acute Disease↗
PubMed1989

Comparison of snare and large forceps biopsies in the histologic diagnosis of gastric vascular ectasia in cirrhosis.

To compare snare and large forceps biopsies in the histologic diagnosis of gastric vascular ectasia (GVE) in cirrhosis, two groups of patients were studied: (a) 8 cirrhotic patients in whom endoscopy disclosed multiple gastric red spots (GRS), and (b) 5 cirrhotic patients with no GRS. Histologic examination of snare specimens identified dilated capillaries in the mucosa of the stomach in 75% of the cirrhotic patients with GRS, while large forceps specimens enabled the diagnosis of GVE only in 20% of the cases (p less than 0.05). Morphometric analysis of snare specimens demonstrated a significantly greater mean mucosal capillary cross-sectional area in cirrhotic patients with GRS than in cirrhotic patients without these lesions (p less than 0.05), while no differences in this parameter was observed in large forceps specimens. These findings indicate that gastric mucosal specimens obtained with large forceps are not useful for establishing the histologic diagnosis of GVE in cirrhotic patients with GRS.

Aged↗