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Biomedical subjects

J Rodés

Publications and source records attributed to J Rodés.

At least 199 records · Page 11Linked to original sources
PubMed1996

Renal and neurohormonal changes following simultaneous administration of systemic vasoconstrictors and dopamine or prostacyclin in cirrhotic patients with hepatorenal syndrome.

BACKGROUND/AIMS: Intravenous ornipressin in cirrhotic patients with hepatorenal syndrome causes marked improvement of systemic hemodynamics and suppression of plasma renin and norepinephrine but only moderate improvement of renal function. This study was designed to investigate whether these beneficial effects could be enhanced by the simultaneous administration of dopamine. The renal effects of the i.v. infusion of norepinephrine plus prostacyclin in patients with hepatorenal syndrome were also assessed. METHODS: Renal plasma flow, glomerular filtration rate, free water clearance, sodium excretion and the plasma levels of renin and norepinephrine were measured in baseline conditions and during the administration of ornipressin (6 i.u./h) and ornipressin (6 i.u./h) plus dopamine (2 micrograms/kg.min) in nine patients with hepatorenal syndrome. Five additional patients with hepatorenal syndrome were studied prior to and following the administration of norepinephrine (0.45 +/- 0.1 microgram/kg.min) and norepinephrine (0.85 +/- 0.2 microgram/kg.min) plus prostacyclin (5 ng/kg.min). RESULTS: Despite a significant increase in arterial pressure and marked suppression of plasma renin activity during ornipressin and ornipressin plus dopamine administration, no significant improvement in renal function was observed. Norepinephrine and norepinephrine plus prostacyclin also failed to increase renal perfusion and glomerular filtration rate. CONCLUSIONS: The combined administration of systemic vasoconstrictors (ornipressin or norepinephrine) and vasodilators (dopamine or prostacyclin), at the doses used in the current study and for a short period of time, does not improve renal function in cirrhotic patients with hepatorenal syndrome. The current study does not confirm a potential role for ornipressin in the treatment of hepatorenal syndrome.

Antihypertensive Agents↗
PubMed1996

Diabetes mellitus after liver transplantation: prevalence and predictive factors.

AIMS/METHODS: To investigate the prevalence and risk factors for the development of diabetes mellitus after orthotopic liver transplantation, we reviewed 27 variables (including previous history of diabetes mellitus, data related to pre-transplant liver disease, and postoperative events) in 102 patients who survived longer than 1 year after orthotopic liver transplantation. RESULTS: Fourteen patients had diabetes mellitus prior to liver transplantation and all but one were alive 2 and 3 years after transplantation, with all survivors continuing to have diabetes mellitus 1, 2 and 3 years after transplantation. Among the 88 patients without pre-transplant diabetes mellitus, the prevalence of post-transplant diabetes mellitus was 27% at 1 year, 9% at 2 years and 7% at 3 years, probably related to a significant reduction in the daily prednisone dose (13 +/- 4 mg at 1 year, 7 +/- 6 mg at 2 years and 2 +/- 4 mg at 3 years, p < 0.001). Patients with post-transplant diabetes mellitus 1 year after transplantation had a higher number of rejection episodes during the first postoperative year than those without post-transplant diabetes mellitus (1.5 +/- 1.1 vs 1.1 +/- 0.7, p < 0.05) and also had higher, but not statistically significant, cumulative steroid dose and blood cyclosporine levels. Mortality of patients with post-transplant diabetes mellitus was significantly higher during the second postoperative year in comparison with patients without post-transplant diabetes mellitus: 4/24 vs 2/64 (17% vs 3%; p < 0.05). CONCLUSIONS: Liver transplantation does not significantly modify pre-transplant diabetes mellitus. Diabetes mellitus frequently develops de novo after liver transplantation, although this complication is usually transient and probably related to immunosuppressive drug administration. The prognosis of patients with post-transplant diabetes mellitus is worse than that of those without this complication.

Adult↗
PubMed1996

Mechanical pumping of portal blood to the liver: hemodynamic effects of a new experimental treatment for portal hypertension.

BACKGROUND/AIMS: It has been suggested that mechanical pumping of portal blood to the liver may correct portal hypertension while increasing portal flow to the liver, which may enhance liver function in cirrhosis. However, the hemodynamic effects of this procedure are unknown. The present study investigated these issues in rats with portal hypertension due to portal vein stenosis. METHODS: Mechanical pumping of portal blood to the liver was established by an extracorporeal shunt bypassing the portal vein stenosis, connected to a continuous withdrawal/infusion pump. Portal pressure, portal-systemic shunting (mesenteric injection of Cr-51 microspheres, n = 10), mesenteric artery blood flow (perivascular Transonic flowmeter, n = 7) and systemic hemodynamics and regional blood flows (left ventricle injection of Ce-141 microspheres, n = 15), were measured at pumping rates of 0, 3 and 6 ml.min-1. RESULTS: Mechanical pumping of portal blood to the liver caused a marked decrease in portal pressure (from 17 +/- 1 to 12.6 +/- 1 and 9.4 +/- .9 mmHg at pumping rates of 0, 3 and 6 ml.min-1) and portal-systemic shunting (from 97 +/- 4 to 70 +/- 4 and 51 +/- 6% respectively) (p < 0.001). However, there were no significant changes in mesenteric artery flow (5.5 +/- 3 vs 5.6 +/- 3 ml.min-1.100 g-1), suggesting that all blood pumped to the liver was withdrawn from that circulating through the collaterals. Moreover, there were no changes in mean arterial pressure, cardiac index, peripheral resistance and splanchnic arteriolar resistance. CONCLUSIONS: The short-term mechanical pumping of portal blood to the liver effectively decreases portal pressure and portal-systemic shunting and has no significant effects on systemic and splanchnic hemodynamics in portal hypertensive rats.

Animals↗
PubMed1996

Increased blood hemoglobin attenuates splanchnic vasodilation in portal-hypertensive rats by nitric oxide inactivation.

BACKGROUND & AIMS: Nitric oxide, which is quenched by hemoglobin, has been implicated in the pathogenesis of portal hypertension. The aim of this study was to investigate the effects of increasing blood hemoglobin concentration by erythropoietin treatment on the gastrointestinal vasodilation associated with portal hypertension. METHODS: Portal-hypertensive and sham-operated rats treated with erythropoietin were studied 2 weeks after surgery. Hemodynamic and rheological parameters were measured in baseline conditions and after N(G)-nitro-L-arginine methyl ester (L-NAME) or sodium nitroprusside treatment. RESULTS: In portal-hypertensive rats, erythropoietin attenuated the increase in gastric mucosal and superior mesenteric artery blood flows and the decrease in arterial blood pressure and splanchnic vascular resistances. Those parameters were not affected by erythropoietin in sham-operated rats. A direct vascular effect of erythropoietin was ruled out by the lack of changes in blood pressure or mesenteric blood flow after intravenous erythropoietin administration and by a similar in vitro relaxation to acetylcholine in mesenteric artery rings. In portal-hypertensive rats, erythropoietin blunted the blood pressure response to sodium nitroprusside and attenuated the gastric and mesenteric blood flow response to L-NAME. CONCLUSIONS: Gastrointestinal vasodilation associated with portal hypertension can be attenuated by increasing blood hemoglobin concentration. Inactivation of overproduced NO by hemoglobin may account for this effect.

Animals↗
PubMed1996

Acute and chronic cyclooxygenase blockage in portal-hypertensive rats: influence in nitric oxide biosynthesis.

BACKGROUND & AIMS: Prostacyclin and nitric oxide have been involved in the hyperkinetic syndrome in portal hypertension. The aim of this study was to investigate the relative contribution and possible interaction between prostacyclin and NO in this circulatory abnormality. METHODS: Portal vein-ligated and sham-operated rats received indomethacin and vehicle either on a short-term (5 mg/kg subcutaneously) or long-term basis (5 mk.kg-1.day-1, continuous 7-day infusion with an osmotic minipump). Measurements of arterial pressure and superior mesenteric arterial flow (mL.min-1.kg-1, ultrasonic flow probe) were then performed before and after NG-nitro-L-arginine methyl ester (L-NAME) injection (13 mg/kg intravenously). RESULTS: Short-term or long-term indomethacin treatment had no effect in sham-operated rats but significantly decreased mesenteric arterial flow in portal-hypertensive rats. Mesenteric flow remained higher after long-term than after short-term indomethacin treatment (54.5 +/- 2 vs. 46.1 +/- 2; P = 0.01). This blunted response to long-term indomethacin treatment was associated with an enhanced response to L-NAME, shown by greater increments in arterial pressure (29% +/- 3%) and mesenteric arterial resistance (209 +/- 22%) in indomethacin-treated rats than in rats receiving vehicle (19% +/- 2% and 130% +/- 20%; P < 0.05). CONCLUSIONS: Both prostacyclin and NO contributed to splanchnic hyperemia in portal-hypertensive rats. There was an enhanced release of NO after long-term prostacyclin inhibition, suggesting that both vasodilatory systems interact, promoting splanchnic hyperemia in portal hypertension.

Animals↗
PubMed1996

Physical exercise increases portal pressure in patients with cirrhosis and portal hypertension.

BACKGROUND & AIMS: In healthy subjects, exercise promotes marked hemodynamic and humoral changes characterized by an increase in cardiac output, a redistribution of blood flow to muscular territories under activity, and an increase in sympathoadrenergic activity. The aim of this study was to investigate the extent to which hemodynamic and humoral changes caused by exercise may influence portal and systemic hemodynamics in patients with cirrhosis. METHODS: In 8 patients with liver cirrhosis and portal hypertension, arterial pressure, cardiac output, portal pressure (as hepatic venous pressure gradient [HVPG]), and hepatic blood flow were measured before and at two steps of cycling exercise equivalent to 30% and 50% of their peak workload. RESULTS: Exercise (at 30% of peak work-load) significantly increased arterial pressure and cardiac output and decreased systemic vascular resistance. This was associated with a significant increase in HVPG (from 16.7 +/- 1.5 to 19.2 +/- 1.6 mm Hg; P < 0.01) and a significant reduction in hepatic blood flow (from 1291 +/- 216 to 1034 +/- 152 mL-min-1; P < 0.05). All of these changes were intensified at 50% of target workload. CONCLUSIONS: The present study shows that moderate exercise increases portal pressure and may therefore increase the risk of variceal bleeding in patients with esophageal varices. These findings suggest that cirrhotic patients with portal hypertension should be advised of potential risks during exercise.

Exercise↗
PubMed1996

Existence of a platelet-adhesion defect in patients with cirrhosis independent of hematocrit: studies under flow conditions.

A defect in hemostasis has been repeatedly reported in patients with cirrhosis. However, the nature of this defect has not been fully characterized. We explored adhesive and cohesive functions of platelets from cirrhotic patients at different stages of disease development. The response of platelets to standard activating agents was tested by aggregometric procedures. The interaction of platelets with subendothelial components was explored in a perfusion system in which blood was exposed (shear rate, 800/s; 10 minutes) to denuded segments of rabbit aorta. Platelet interactions in these perfusions were analyzed morphometrically. Results were always compared with those obtained in similar studies using blood obtained from healthy subjects. Aggregation studies showed abnormal responses for single or several agonists. Abnormalities in aggregation were more evident in patients with severe disease (Child-Pugh class C), although they occasionally were abnormal for single agonists (ADP or U46619) in patients with less severe disease (Child-Pugh classes A or B). All the patient classes showed impaired platelet-subendothelial interactions (P < .01 vs. healthy subjects) that were not justified by the relative thrombocytopenia present in the more severely affected patients. Experimental increases in hematocrit in patients at stages B and C did not improve platelet-subendothelial interactions. Platelets from cirrhotic patients interact defectively with subendothelial components under flow conditions. The adhesion defect is more evident and consistent than the aggregation defects and may already be present in patients with mild liver failure. This adhesion defect may contribute to the defective hemostasis observed in cirrhotic patients.

Adult↗
PubMed1996

Recurrent liver involvement in heatstroke.

We report the case of a young patient who presented two self-limited episodes of acute jaundice that developed immediately following a long distance run. Zone 3 necrosis was the most prominent histologic change of the liver during the second episode. The diagnosis of heatstroke with liver damage was based on the exclusion of known causes of acute hepatitis, the histopathologic changes and the circumstances preceding the onset of liver disease. This seems to be the first case of severe and recurrent liver impairment due to heatstroke.

Adult↗
PubMed1996

Comparative study of three methods for genotyping hepatitis C virus strains in samples from Spanish patients.

Hepatitis C virus (HCV) genotypes may be investigated by a variety of laboratory methods that target different parts of the HCV genome and have various degrees of technical difficulty. Since the choice of a particular method is difficult, we compared the performance of (i) a type-specific PCR with type-specific primers from the core region, (ii) molecular hybridization of the PCR-amplified 5' noncoding region to type-specific probes, and (iii) identification of type-specific antibodies against epitopes of nonstructural region 4 by enzyme-linked immunosorbent assay (ELISA). One hundred fifty-one patients with biopsy-proved chronic hepatitis and HCV RNA in serum were investigated. The HCV genotype was identified in 99%, 100%, and 85% of the cases by type-specific PCR, probe hybridization, and ELISA, respectively. The type-specific PCR disclosed infection with type 1a in 3%, type 1b in 74%, and type 3a in 4% of the cases and suggested infection with two or more HCV types, including 2a/2c and 2b, in the remaining 18%. Apparently mixed infections were more prevalent in patients with past intravenous drug use (P < 0.001), but cloning and sequencing of PCR products did not confirm a mixed infection in any of the four cases investigated. Concordant results were obtained by the three procedures with virtually all of the samples in which the type-specific PCR revealed a single HCV genotype. Type-specific hybridization and ELISA usually recognized the genotype producing the strongest DNA band in samples in which type-specific PCR suggested a mixed infection. In conclusion, the three procedures evaluated in this study are reliable for investigation of HCV genotype. Type-specific PCR provides information about HCV subtypes, but a mixed infection detected with this method should be interpreted with caution.

Enzyme-Linked Immunosorbent Assay↗
PubMed1996

Low dose alpha interferon therapy can be effective in chronic active hepatitis C. Results of a multicentre, randomised trial.

BACKGROUND: There is some controversy concerning the efficacy of low dose alpha interferon therapy in chronic hepatitis C. AIMS: To evaluate the effectiveness of treatment with low doses of alpha interferon in chronic hepatitis C. PATIENTS: One hundred and forty one patients with anti-HCV positive chronic active hepatitis C from six hospitals were enrolled in the study. METHODS: Patients were randomised to treatment with 5 MU (group A) or 1.5 MU (group B) injections. The dose was reduced in responders from group A or increased in non-responders from group B to maintain treatment with the minimal effective dose. Patients were treated for 48 weeks and followed up for 24 additional weeks with no treatment. Normalisation of alanine aminotransferase (ALT) was used to evaluate response. RESULTS: A sustained response was seen in eight patients from group A (12%) and in 15 (21%) from group B. This difference was not statistically significant. Increasing the dose of interferon led to sustained response in only five of 58 patients (9%) from group B who did not respond to 1.5 MU injections. In contrast, 15 of 21 patients (71%) in whom ALT remained normal with 1.5 MU injections developed a sustained response. By multivariate analysis sustained response seemed associated with young age and was more frequent in patients with genotype 3 HCV infection. Sustained response was preceded by a rapid normalisation of ALT and was inversely related to the amount of alpha interferon necessary to maintain ALT at low values during treatment. CONCLUSIONS: Some patients with chronic hepatitis C are very sensitive to alpha interferon and can be successfully treated with low doses. Treatment with higher doses may be effective in a minority of patients who do not respond to low doses.

Alanine Transaminase↗
PubMed1996

Cyclosporine-associated mutism in liver transplant patients.

Four liver transplant recipients treated with cyclosporine developed a reversible neurologic syndrome characterized by a speech disorder leading to mutism. This complication, previously reported in a few liver transplant recipients treated with the immunosuppressive drug FK506, had not been described with cyclosporine. Recognition of this syndrome should prompt withdrawal of the drug and avoidance of unnecessary diagnostic procedures.

Adult↗
PubMed1996

[Prevalence of hepatocellular carcinoma in cirrhotic patients with with portosystemic shunt. Cohort analysis].

The development of hepatocellular carcinoma is frequent in patients with hepatic cirrhosis of any etiology. Despite the suggestion that portosystemic shunt may increase the risk of developing this neoplasm there are scarce clinical evidence to confirm this suggestion. The present cohort study was aimed at analyzing the follow up data of 232 patients included in 3 prospective randomized controlled studies in which the efficacy of shunt procedures (group I: portocaval or splenorenal anastomosis) versus techniques other than shunt (group II: esophageal transection or variceal sclerosis) in the treatment of upper-6I bleeding secondary to rupture of esophageal-gastric varices were compared. After a mean follow up of 50 months, no differences were observed between the two groups in relation with the prevalence of hepatocellular carcinoma (group I: 17%; group II: 12%; relative risk: 1.41 [CI 95%: 0.72 - 2.75]; p = 0.41) or the actuarial probability of developing this neoplasm (group I: 2% at 2 years, 21% at 5 years; group II: 7% at 2 years, 14% at 5 years; p = 0.42). The results of this analysis suggest that the performance of portosystemic shunt does not increase the risk of developing hepatocellular carcinoma in patients with hepatic cirrhosis.

Adult↗
PubMed1996

[The efficacy of excluding anti-HVC-positive donors by ELISA 2 in the prevention of posttransfusion hepatitis].

To assess the efficacy of blood donor screening with a second generation ELISA for the detection of anti HCV the incidence of post transfusion hepatitis was prospectively determined in 190 patients submitted to cardiovascular surgery. An increase greater than 100 U/l of transaminases of serum activity was detected in five patients (2.6%), being found in four patients at 3 months of the transfusion and in one patient at 6 months. Serologic markers for HAV, HBV, HCV, CMV and EBV were not identified in any of these cases of post transfusion hepatitis and it is therefore assumed that they may have been caused by an, as yet unidentified, agent. It is concluded that second generation ELISA screening for anti HCV is very effective in the prevention of post transfusion hepatitis C.

Adult↗