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Biomedical subjects

J Rodés

Publications and source records attributed to J Rodés.

At least 433 records · Page 24Linked to original sources
PubMed1986

Hepatic disease in the Spanish toxic oil syndrome. A thirty months follow-up study.

Clinical and biological evidence of liver disease was found in 99 out of 242 (40%) patients hospitalized with acute manifestations of the Spanish toxic oil syndrome. No patient was alcoholic. According to the severity of liver involvement, patients were classified in 3 groups and followed up for at least 30 months. Group I included 65 patients with a transient increase of serum aminotransferase activity as the only evidence of liver disease. This abnormality disappeared within 2 months in all these patients. Group II included 18 patients with raised aminotransferases and alkaline phosphatase. At the end of follow-up, liver tests remained slightly abnormal in 4 patients of this group (22%) and a liver biopsy revealed minor changes in 3 of them. Group III included 16 patients with raised aminotransferases, alkaline phosphatase and bilirubin. Thirty months after the acute episode, liver function tests remained abnormal in 8 patients (50%); a liver biopsy, performed in 5 cases, showed changes suggesting chronic biliary disease in 2, and fibrosteatosis, chronic hepatitis and minimal changes in each of the remaining 3. Pulmonary, cutaneous, vascular, neuromuscular and other extra-hepatic disturbances were noted in a large number of patients but no relationship was observed between the degree of hepatic disfunction and the presence and severity of systemic manifestations of the toxic oil syndrome.

Adult↗
PubMed1986

Urinary excretion of 6-keto-prostaglandin F1 alpha, thromboxane B2 and prostaglandin E2 in cirrhosis with ascites. Relationship to functional renal failure (hepatorenal syndrome).

The aim of the study was to investigate the urinary excretion of 6-keto-PGF1 alpha (a stable metabolite of PGI2), thromboxane B2 (TxB2; a stable metabolite of TxA2), and PGE2 in 18 normal subjects, 49 cirrhotics with ascites without renal failure (GFR = 90 +/- 4 ml/min, means +/- S.E.M.) and 20 cirrhotics with functional renal failure (FRF) (GFR = 36 +/- 3). The study was made after 5 days on a 50 mEq sodium diet and without diuretics. Plasma renin activity (PRA), plasma norepinephrine concentration (NE) and plasma antidiuretic hormone concentration (ADH) were also measured. Cirrhotics without FRF showed a significantly higher urinary excretion of 6-keto-PGF1 alpha, TxB2 and PGE, (15.9 +/- 1.7 ng/h, 3.0 +/- 0.3 ng/h, and 6.2 +/- 1.0 ng/h) than did normal subjects (9.2 +/- 0.9, 1.3 +/- 0.1 and 2.3 +/- 0.4). On the contrary, the urinary excretion of these prostaglandins was normal or reduced in patients with FRF (5.3 +/- 0.8, 1.3 +/- 0.2 and 1.9 +/- 0.4). PRA, NE and ADH were significantly increased in cirrhotics with FRF (15.2 +/- 3.9 ng/ml/h, 1026 +/- 149 pg/ml and 4.1 +/- 0.3 pg/ml) and in patients without FRF (8.0 +/- 1.4, 667 +/- 67 and 3.9 +/- 0.3) as compared to normal controls (1.3 +/- 0.2, 275 +/- 46 and 2.4 +/- 0.2). These results suggest that renal hemodynamics in cirrhosis depends upon a critical equilibrium between the activity of endogenous vasoconstrictor systems and the renal production of the vasodilator prostaglandins PGI2 and PGE2. In addition, they do not support FRF in cirrhosis being related to an increased renal production of the vasoconstrictor prostaglandin TxA2.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Influence of HBV replication and delta agent superinfection on T cell subsets and killer (Leu 7+) in chronic hepatitis B virus infection.

Peripheral blood T-lymphocyte subsets and cells reacting for Leu 7 antigen, which identifies a subset of killer and natural killer cells, have been examined in 32 patients chronically infected by the hepatitis B or D viruses (HBV, HDV) and in 28 normal subjects. The T8+ lymphocytes were increased and the T4/T8 ratio was decreased in patients with HBV replication (identified by the presence of HBcAg in liver and HBV-DNA in serum) and in patients with HDV infection (HDAg in liver). These patients had more active liver disease than patients without evidence of viral replication, B or D, who showed normal lymphocyte counts. Leu 7+ lymphocytes were also increased in patients with viral replication and active disease and correlated positively with alaninaminotransferase serum levels. These observations suggest the participation of both T8+ and Leu7+ cells in the pathogenesis of liver cell injury in HBsAg-positive chronic liver disease.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1986

Atrial natriuretic factor: reduced cardiac content in cirrhotic rats with ascites.

The present study was designed to investigate whether cirrhosis with ascites is associated with altered tissue content of atrial natriuretic factor. Atrial extracts from 14 cirrhotic rats with ascites and increased plasma renin activity (PRA) (14.4 +/- 4.6 ng X ml-1 X h-1) and aldosterone concentration (148.3 +/- 17.3 ng/dl) and from 10 control rats (PRA, 3 +/- 0.5 ng X ml-1 X h-1; aldosterone, 34.7 +/- 3.7 ng/dl) were intravenously injected into anesthetized normovolemic rats. Only one extract was assayed in each bioassay rat. Atrial extracts from control rats increased diuresis and natriuresis 513 +/- 91 and 3,029 +/- 752%, respectively (means +/- SE). In contrast, atrial extracts from cirrhotic rats increased urine volume 199 +/- 49% (P less than 0.001) and sodium excretion 546 +/- 132% (P less than 0.001). These results strongly suggest that atrial content of atrial natriuretic factor is reduced in cirrhotic rats as compared with control animals.

Animals↗
PubMed1986

Sulindac reduces the urinary excretion of prostaglandins and impairs renal function in cirrhosis with ascites.

In 5 patients with cirrhosis and ascites the glomerular filtration rate (GFR), free water clearance (CH2O) and urinary excretion of prostaglandin E2(PGE2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) were measured before and after a 3-day treatment with sulindac (400 mg/day). The administration of sulindac induced a marked fall of urinary excretion of PGE2 (from 24.2 +/- 5.5 to 3.8 +/- 1.1 ng/h; p less than 0.05), 6-keto-PGF1 alpha (from 19.9 +/- 2.9 to 5.6 +/- 1.1 ng/h; p less than 0.02) GFR (from 111 +/- 15 to 67 +/- 10 ml/min; p less than 0.01) and CH2O (from 7 +/- 1.5 to 3.7 +/- 1.3 ml/min; p less than 0.02) in all patients studied. The plasma concentration of the active metabolite sulindac sulfide in cirrhotics was 400% of that found in 6 healthy volunteers (9.6 +/- 1.7 vs. 2.4 +/- 0.6 ng/ml). Our results indicate that sulindac, at a dose of 400 mg/day, inhibits the renal synthesis of prostaglandins and impairs renal function in cirrhotics with ascites. These effects are probably related to the marked alteration of sulindac kinetics that occurs in these patients.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Hepatic disease associated with ground-glass inclusions in hepatocytes after cyanamide therapy.

In a retrospective review of 2400 consecutive liver biopsy specimens, 60 cases with ground-glass hepatocytes were identified, 41 specimens gave a positive reaction to orcein stain and 19 a negative staining. These 19 specimens were obtained from chronic alcoholics who had been admitted to a detoxication program that used aversive drugs and who were hepatitis B surface antigen negative. The use of cyanamide (Colme), an inhibitor of aldehyde dehydrogenase could be documented in 11 instances. In addition to ground-glass hepatocytes, which were periodic acid-Schiff positive and had a periportal or paraseptal distribution, these liver specimens showed a variety of hepatic lesions: cirrhosis in five cases, portal and periportal inflammation in six, triaditis in five, portal fibrosis in two, and minimal changes in one. Patients with shorter courses of cyanamide were those who had less severe histologic lesions. In three patients who had a liver biopsy carried out before the cyanamide treatment ground-glass hepatocytes were not found. These data indicate that ground-glass hepatocytes that stain with periodic acid-Schiff may develop after cyanamide treatment. They are associated with structural hepatic damage of varied severity in patients submitted to a long-term treatment.

Adult↗
PubMed1986

[Technics for the study of the renal excretion of free water in normal rats and those with experimental liver cirrhosis].

Different techniques to measure free water excretion in rats, administered an oral water overload and with measurement of its ability to excrete it into the urine have been studied. When 30 or 50 ml/kg b.wt. were administered and the urine excreted in 3 h was collected, a decrease on the urinary osmolality (UOSM) was observed with respect to the baseline UOSM, which was similar in both overloads, although the percentage of the overload excreted was significantly greater with 50 ml/kg. However, the UOSM obtained was hypertonic as compared to plasma osmolality (POSM) indicating that this determination was not useful to study free water excretion. In a further study it was investigated if there was any period of time in which all the animals excreted hypotonic urine. However, results indicated that the period for excreting a maximally diluted urine was very variable in time. The best technique to study free water excretion in these animals was the collection of each spontaneously voided urine independently, to measure the minimal UOSM. When a 50 ml/kg water load was administered and the minimal UOSM was determined it was observed to be lower than POSM in all the animals indicating that this technique was useful to study this derangement in these animals.

Animals↗
PubMed1986

[Determination of arginine-vasopressin in small volumes of rat plasma].

A radioimmunoassay to determine arginine-vasopressin concentration in rat plasma is described. This method was a modification from a previously described technique from which the incubation volume was reduced. It allows us to use only 300 microliter of plasma, 1/4 of the original volume, without any impairment to the sensitivity. The intra- and inter-assay coefficients of variation are 11% and 13% respectively. The accuracy ranges between 90 and 99%. To investigate the influence of sampling blood conditions on arginine-vasopressin levels, five groups of Sprague-Dawley rats are analyzed: Group I, decapitation; Group II, ether anaesthesia and cardiac puncture; Group III, ether anaesthesia and decapitation; Group IV, ketamine anaesthesia and cardiac puncture; Group V, ketamine anaesthesia and decapitation. Arginine-vasopressin levels in Group V (2.2 +/- 0.8 pg/ml) are significantly lower than those from the other four groups and similar to those obtained by other authors using a chronic catheter.

Animals↗
PubMed1985

Paracentesis versus diuretics in the treatment of cirrhotics with tense ascites.

72 cirrhotics with tense ascites were randomly assigned to treatment with either paracentesis plus intravenous albumin infusion (38 patients) or diuretics (34 patients). Paracentesis was not associated with significant changes in renal function. The clinical course of the disease was similar in the two groups of patients, both during their hospital stay and during follow-up.

Ascites↗
PubMed1985

Lymphocytotoxic antibodies in primary biliary cirrhosis.

Sera of 30 patients with primary biliary cirrhosis (PBC) and 72 normal subjects matched for age and sex were examined for the presence of lymphocytotoxic antibodies (LCAs) against B and T cells at 4 degrees C and 37 degrees C. Patients were prospectively screened for: Sjögren's syndrome, scleroderma, Hashimoto's thyroiditis, and rheumatoid arthritis, in which LCAs have been described. Seventeen patients with PBC (56.6%) had LCAs against B cells as compared with only 11 of the 72 normal subjects (P less than 0.001). Five PBC patients (16.6%) also reacted against T cells as compared with none in control group (P less than 0.01). Clinical and biochemical features and the histological stage of PBC were similar in patients with and without LCA. Sjögren's syndrome was present in 13 patients--two with scleroderma and another with Hashimoto's thyroiditis. No patient had rheumatoid arthritis. The prevalence of LCAs was similar in PBC patients with or without autoimmune associated disease (54% vs 59%). We conclude that in PBC a high incidence of LCA is unrelated to the presence of an associated disease. LCA in PBC might be a nonspecific marker of an immune disorder.

Adult↗