PubMed Health⌕ Search

Biomedical subjects

J Rodés

Publications and source records attributed to J Rodés.

504 records · Page 28Linked to original sources
PubMedDate not supplied

Noninvasive measurement of the pressure of esophageal varices using an endoscopic gauge: comparison with measurements by variceal puncture in patients undergoing endoscopic sclerotherapy.

Measurements of variceal pressure with a noninvasive endoscopic pressure gauge and by direct variceal puncture were performed in 20 cirrhotic patients with portal hypertension in the course of the first session of therapeutic sclerotherapy following an episode of variceal bleeding. Endoscopic gauge measurements of the pressure of esophageal varices gave similar values (15.5 +/- 2.7 mm Hg) than measurements by variceal puncture (15.4 +/- 2.4 mm Hg; not statistically significant), and there was a highly significant linear correlation between both measurements (r = 0.9, p less than 0.001). Azygos blood flow, that was markedly increased in these patients (852 +/- 399 ml per min), was directly related to variceal pressure (r = 0.73, p less than 0.01). Variceal pressure was significantly lower than portal pressure (18.8 +/- 5.0 mm Hg) (p less than 0.05), indicating that measurements of variceal pressure cannot substitute measurements of portal pressure. The study demonstrates that the noninvasive endoscopic gauge technique allows an accurate estimation of variceal pressure in patients with portal hypertension. This technique may provide additional useful information in the evaluation of portal hypertension as well as on the mechanism of variceal bleeding.

Adult↗
PubMedDate not supplied

Effects of metoclopramide and domperidone on azygos venous blood flow in patients with cirrhosis and portal hypertension.

The effects of pharmacological manipulation of the lower esophageal sphincter pressure on the esophageal circulation in patients with cirrhosis and portal hypertension were investigated in 33 patients by measuring the azygos venous blood flow, which is an index of blood flow through esophageal varices and periesophageal collaterals draining into the azygos venous system. Measurements were performed in baseline conditions and after the blind administration of metoclopramide (20 mg i.v.) (12 patients), domperidone (10 mg i.v.) (12 patients) and placebo (9 patients). Both metoclopramide and domperidone caused a significant reduction of azygos blood flow, that decreased by 11.5% (p less than 0.01) and 15.6% (p less than 0.02) respectively, while no change was observed in patients receiving placebo (+1.4%, not statistically significant). Reduction of azygos blood flow represents a selective effect of metoclopramide and domperidone on the esophageal circulation, since portal pressure, hepatic blood flow, cardiac output, heart rate and arterial blood pressure were unchanged by the administration of metoclopramide, domperidone or placebo. These results indicate that the administration of drugs that increase the lower esophageal sphincter pressure may reduce the inflow of blood into the esophageal varices in cirrhotic patients with portal hypertension.

Azygos Vein↗
PubMedDate not supplied

Compensated cirrhosis: natural history and prognostic factors.

To investigate the natural history of compensated cirrhosis, 293 consecutive patients without previous major complications (ascites, jaundice, encephalopathy or gastrointestinal hemorrhage) were studied in terms of morbidity (probability of developing decompensated cirrhosis during follow-up) and survival. Patients were diagnosed by liver histology between 1968 and 1980. Median follow-up was 63 months. Decompensation of cirrhosis was considered when a patient first developed one of the major complications of the disease. Ten years after diagnosis, the probability of developing decompensated cirrhosis and the survival probability rate were 58 and 47%, respectively. A multivariate survival analysis (Cox's regression model) using clinical, biochemical and histological data obtained at diagnosis disclosed seven factors that predicted prognosis: serum bilirubin; serum gamma-globulin concentration; hepatic stigmata; prothrombin time; sex; age, and alkaline phosphatase. According to the contribution of each one of these factors to the final model, a prognostic index was constructed that allows calculation of the estimated survival probability. The predicting value of this index was validated by a split sample testing technique.

Adult↗
PubMedDate not supplied

Sclerotherapy vs. distal splenorenal shunt in the elective treatment of variceal hemorrhage: a randomized controlled trial.

One hundred and twelve consecutive Child Class A and B cirrhotic patients were included in a prospective controlled trial aimed at investigating the efficacy and safety of endoscopic sclerotherapy vs. distal splenorenal shunt in the elective treatment of hemorrhage from esophagogastric varices. Fifty-seven patients were randomly allocated to splenorenal shunt and 55 to endoscopic sclerotherapy. Since only 4 of the 55 patients assigned to endoscopic sclerotherapy had to be excluded after randomization and before treatment as compared to 14 of the 57 patients assigned to splenorenal shunt, it is suggested that the applicability of endoscopic sclerotherapy is greater than that of splenorenal shunt. One patient in each group died within 30 days of the procedure and two in the endoscopic sclerotherapy group were lost to follow-up just after discharge. Variceal rebleeding during follow-up occurred in 37.5% (18/48) of patients in the endoscopic sclerotherapy group and in 14.3% of those in the splenorenal shunt group (6/42) (p less than 0.02), whereas hepatic encephalopathy was more frequent in patients submitted to splenorenal shunt (10/42, 24%) than in those treated by endoscopic sclerotherapy (4/48, 8%) (p less than 0.05). The therapeutic modality was the only variable with independent predictive value for rebleeding during follow-up, whereas for hepatic encephalopathy, the therapeutic modality, and the presence of encephalopathy related to the bleeding episode each showed independent predictive value. Early and long-term mortality, did not differ between the two therapeutic groups, being the 2-year survival was 71% for splenorenal shunt and 68% for endoscopic sclerotherapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Clinical Trials as Topic↗
PubMedDate not supplied

Recurrence of spontaneous bacterial peritonitis in cirrhosis: frequency and predictive factors.

We investigated whether spontaneous bacterial peritonitis in cirrhosis is a recurrent process and attempted to identify possible predictors of recurrence in 75 consecutive cirrhotics who had recovered from a first episode of spontaneous bacterial peritonitis between January, 1981 and December, 1984 and who were followed closely throughout their illness (follow-up period 10 +/- 13 months; mean +/- S.D.). Thirty-eight patients (51%) developed one or more episodes of spontaneous bacterial peritonitis during follow-up, the probability of recurrence (Kaplan-Meier's method) being 43% at 6 months, 69% at 1 year and 74% at 2 years. Twenty-three variables (age, sex, etiology of cirrhosis, standard liver and renal function tests and characteristics of the first spontaneous bacterial peritonitis) were analyzed as possible predictors of recurrence of spontaneous bacterial peritonitis. In univariate analysis (curves of Kaplan-Meier compared with Mantel-Cox's method), serum bilirubin greater than 4 mg per dl, prothrombin less than or equal to 45% and protein concentration in ascitic fluid less than or equal to 1 gm per dl were significantly (p less than 0.05) associated with a high risk or recurrence of spontaneous bacterial peritonitis. In multivariate analysis (Cox multiple regression model), only ascitic fluid protein concentration (p = 0.005) and prothrombin activity (p = 0.009) were found to be independent predictors of recurrence of spontaneous bacterial peritonitis. Fifty-nine patients (79%) died during follow-up, 18 of them (31%) secondary to spontaneous bacterial peritonitis. The 1-year survival probability in the whole series of patients was 38%.(ABSTRACT TRUNCATED AT 250 WORDS)

Bacterial Infections↗
PubMedDate not supplied

Comparative study of aminoglycoside nephrotoxicity in normal rats and rats with experimental cirrhosis.

Several authors have suggested that the risk of developing aminoglycoside nephrotoxicity is greater in cirrhotic patients than in the noncirrhotic population. However, this has not been confirmed by other investigators. To compare the intensity and characteristics of aminoglycoside nephrotoxicity in cirrhotic and normal rats, 31 rats with carbon tetrachloride-induced cirrhosis with ascites and 35 control rats were treated with gentamicin. Each group of rats was divided into two subgroups in order to receive 10 or 40 mg per kg per day of gentamicin, and different subsets of animals were killed on Days 4, 8 and 12 of treatment for renal histological examination and determination of renal tissue gentamicin concentration. Urine volume, osmolality, sodium excretion and N-acetyl-beta-D-glucosaminidase activity were measured daily throughout the study. Creatinine clearance and trough plasma concentration of gentamicin were determined in each animal immediately before killing. There were no significant differences between cirrhotic and control rats in relation to the magnitude of changes in urine volume, osmolality, sodium excretion and N-acetyl-beta-D-glucosaminidase activity and creatinine clearance during gentamicin administration. The values of a histopathological score semiquantitatively assessing the renal morphological changes observed by light microscopy were not significantly different in cirrhotic and control rats. In addition, similar trough plasma and renal cortical tissue concentrations of gentamicin were observed in both groups of animals. These results suggest that, in this experimental model, cirrhosis does not increase the risk for aminoglycoside nephrotoxicity.

Acetylglucosaminidase↗
PubMedDate not supplied

Effects of verapamil on hepatic and systemic hemodynamics and liver function in patients with cirrhosis and portal hypertension.

The effects of verapamil on hepatic and systemic hemodynamics and on liver function were investigated in 10 patients with portal hypertension due to advanced micronodular cirrhosis to verify whether, as it has been suggested, this calcium channel blocker may improve liver function and reduce portal pressure in these patients. The oral administration of 100 mg of verapamil caused systemic vasodilation, evidenced by a significant reduction in mean arterial pressure (-8.1 +/- 7.6%, p less than 0.025) and systemic vascular resistance (-12.5 +/- 9.5%, p less than 0.001), and increased heart rate (+13.9 +/- 10.4%, p less than 0.01). However, no beneficial effect was noted on portal pressure evaluated by hepatic vein catheterization (baseline 19.8 +/- 4.0, verapamil 20.2 +/- 3.6 mmHg, NS), hepatic blood flow (1.45 +/- 0.64 vs. 1.47 +/- 0.62 liters per min, NS) and hepatic vascular resistance (1.314 +/- 611 vs. 1,266 +/- 513 dyn per sec per cm-5, NS). Similarly, no change was observed in portal blood flow, measured in six patients by pulsed Doppler flowmeter (0.94 +/- 0.30 vs. 0.89 +/- 0.35 liter per min, NS). In addition, verapamil did not increase the hepatic intrinsic clearance of these patients (0.20 +/- 0.07 vs. 0.19 +/- 0.06 liter per min, NS). This study suggests that verapamil is of no beneficial effect in patients with advanced cirrhosis of the liver.

Adult↗
PubMedDate not supplied

Effects of vasopressin on the intravariceal pressure in patients with cirrhosis: comparison with the effects on portal pressure.

The present study investigated to what extent measurements of wedged and free hepatic venous pressures adequately reflect the effects of vasopressin at the esophageal varices in patients with cirrhosis. Eleven patients undergoing therapeutic sclerotherapy were studied by measuring wedged hepatic venous pressure, intravariceal pressure, free hepatic venous pressure, superior vena cava pressure and the intravascular pressure gradients wedged hepatic venous pressure-free hepatic venous pressure and intravariceal pressure-superior vena cava pressure, prior to and after vasopressin injection (1 IU, iv). Vasopressin caused a significant reduction in intravariceal pressure (from 22.5 +/- 9.4 to 19.2 +/- 8.4 mm Hg, p less than 0.001). Measurement of wedged hepatic venous pressure and free hepatic venous pressure closely reflected the reduction in variceal pressure. Thus, wedged hepatic venous pressure decreased by 16 +/- 11%, which is close to the 14 +/- 7% change in intravariceal pressure, and the 23 +/- 12% fall in the pressure gradient wedged hepatic venous pressure-free hepatic venous pressure was mirrored by the 26 +/- 10% change in intravariceal pressure-superior vena cava pressure. These pressure gradients decreased more than the absolute pressures (intravariceal pressure and wedged hepatic venous pressure) due to concomitant increases in superior vena cava pressure (1.9 +/- 1.9 mm Hg) and free hepatic venous pressure (0.6 +/- 1.9 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMedDate not supplied

Autoantibodies against nuclear envelope-associated proteins in primary biliary cirrhosis.

An antinuclear immunofluorescence pattern displaying a thin ring confined to the nuclear envelope was assessed in sera from 38 patients with primary biliary cirrhosis and in sera from a control group of 277 patients with other antinuclear antibody-positive diseases. This rim-like antinuclear reactivity was present in sera from 20 primary biliary cirrhosis patients (52.6%) but in only two patients from the control group (0.7%) (p less than 0.001). Furthermore, this autoantibody was present in three of four primary biliary cirrhosis patients without antimitochondrial antibodies. Presence of this rim-like pattern in primary biliary cirrhosis did not correlate with the presence of associated autoimmune diseases nor with other clinical, biochemical, nor histological features of the disease. The antigenic specificity of sera displaying this antinuclear immunofluorescence pattern was characterized by Western blot analysis using an antigenic extract containing nuclear envelope proteins purified from rat liver. Sixteen of the 20 positive sera showed a common pattern of reactivity with a set of nuclear envelope-associated proteins approximately 200 kD in size. In conclusion, sera from primary biliary cirrhosis patients showing a rim-like fluorescent nuclear pattern have antinuclear autoantibodies that react specifically with components of the nuclear envelope. The high specificity of these new autoantibodies in primary biliary cirrhosis indicate that they might be a serological marker of the disease, particularly useful in patients without antimitochondrial antibodies.

Antibody Specificity↗
PubMedDate not supplied

Peripheral arterial vasodilation hypothesis: a proposal for the initiation of renal sodium and water retention in cirrhosis.

Renal sodium and water retention and plasma volume expansion have been shown to precede ascites formation in experimental cirrhosis. The classical "underfilling" theory, in which ascites formation causes hypovolemia and initiates secondary renal sodium and water retention, thus seems unlikely. While the occurrence of primary renal sodium and water retention and plasma volume expansion prior to ascites formation favors the "overflow" hypothesis, the stimulation of the renin-angiotensin-aldosterone system, vasopressin release and sympathetic nervous system associated with cirrhosis is not consonant with primary volume expansion. In this present article, the "Peripheral Arterial Vasodilation Hypothesis" is proposed as the initiator of sodium and water retention in cirrhosis. Peripheral arterial vasodilation is one of the earliest observations in the cirrhotic patient and experimental animals with cirrhosis. Arterial vasodilators and arteriovenous fistula are other examples in which renal sodium and water retention occur secondary to a decreased filling of the arterial vascular tree. An increase in cardiac output and hormonal stimulation are common features of cirrhosis, arteriovenous fistula and drug-induced peripheral arterial vasodilation. However, a predilection for the retained sodium and water to transudate into the abdominal cavity occurs with cirrhosis because of the presence of portal hypertension. The Peripheral Arterial Vasodilation Hypothesis also explains the continuum from compensated to decompensated cirrhosis to the hepatorenal syndrome.

Animals↗
PubMedDate not supplied

Complete characterization of the 3' region of the human and mouse hereditary hemochromatosis HFE gene and detection of novel splicing forms.

The human HFE gene was identified in 1996 as the gene whose mutations are responsible for hereditary hemochromatosis in most patients. Expression analysis by Northern blot indicated that the gene was approximately 4.1 kb in length. However, the cDNA reported was only 2716 bp. These results implied that at least 1.4 kb of the mRNA remained to be identified. In the present study, we detected several 3' EST clones while screening the genomic region of the gene in search of potential additional HFE mRNA sequences. Subsequent sequencing of these EST clones and RT-PCR experiments revealed that exon 7 of the HFE gene has, in fact, a length of 1944 bp and it presents two polyadenylation signals. The new human HFE exon 7 region has been screened in non-C282Y HH patients in search for new putative mutations. Mouse 3' RACE experiments also further extend the previously reported mouse HFE exon 6 sequence. Additionally, we report two novel end forms of the human HFE gene detected by 3' RACE experiments and several novel splicing forms identified in the HepG2 cell line.

3' Untranslated Regions↗
PubMedDate not supplied

Gene expression of endothelin-1 and ET(A) and ET(B) receptors in human cirrhosis: relationship with hepatic hemodynamics.

Previous experimental studies have suggested that the paracrine endothelin system may participate in the regulation of hepatic hemodynamics in cirrhosis. The present study assesses the relationship between increased portal pressure and preproET-1, ET(A) receptor and ET(B) receptor gene expression in human cirrhosis. PreproET-1, ET(A) receptor and ET(B) receptor mRNA abundance was estimated by quantitative PCR in human hepatic tissue from subjects with normal liver and in cirrhotic patients in whom a hepatic hemodynamic study was performed. The expression of the three transcripts was significantly higher in liver samples of cirrhotic patients than in those obtained from subjects without any histological alteration. Moreover, while no significant correlation was found between preproET-1 mRNA abundance and portal pressure, there was a highly significant direct relationship between ET(A) and ET(B) receptor gene expression and portal pressure in cirrhotic patients. These results indicate that the liver paracrine endothelin system is overactivated in human cirrhosis and that a direct relationship exists between endothelin receptor mRNA abundance and the degree of portal hypertension in these patients.

Animals↗
PubMedDate not supplied

[Pleural empyema caused by Cryptococcus neoformans in a patient with liver cirrhosis].

Gram negative infections, particularly by E. coli, are usually observed in cirrhotic patients while infections by Cryptococcus neoformans are commonly found in immunosuppressed patients. The case of a cirrhotic patient with hepatitis C virus infection who developed pleural infection by C. neoformans is presented. No disease other than cirrhosis was observed in the patient. The treatment with oral fluconazole was initiated with good clinical response and infection cure. The efficacy of fluconazole in infections by this microorganism has been reported in other cases, mainly in patients with acquired immunodeficiency syndrome. The fact that the patient may be a liver transplant candidate, given the hepatic cirrhosis, leads to speculation as to the need for chronic treatment with fluconazole to avoid reactivation of C. neoformans on initiation of pharmacologic immunosuppression.

Administration, Oral↗