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Biomedical subjects

J Rodés

Publications and source records attributed to J Rodés.

At least 451 records · Page 25Linked to original sources
PubMed1985

Effects of prostaglandin inhibition on systemic and hepatic hemodynamics in patients with cirrhosis of the liver.

The role of prostaglandins in the pathogenesis of the circulatory abnormalities of cirrhosis was investigated by studying the effects of prostaglandin inhibition with indomethacin (50 mg/8 h for 24 h) on the systemic and splanchnic hemodynamics in 13 patients with cirrhosis of the liver. Indomethacin administration significantly reduced cardiac output (from 7.44 +/- 0.7 to 6.78 +/- 0.7 L/min, p less than 0.05) and increased peripheral vascular resistance (from 990 +/- 104 to 1155 +/- 140 dyn X s X cm-5, p less than 0.05). Arterial pressure was not modified. These changes in systemic hemodynamics were associated with a significant reduction in hepatic blood flow (from 1.88 +/- 0.43 to 1.48 +/- 0.3 L/min, p less than 0.05) and with a slight decrease of portal pressure (from 18.8 +/- 1.3 to 17.5 +/- 1.4 mmHg, p less than 0.05). These results suggest that endogenous prostaglandins contribute to the increased cardiac output and diminished vascular resistance observed in cirrhosis of the liver. In addition, by promoting splanchnic vasodilation, prostaglandins may contribute to increased portal pressure in these patients.

Adult↗
PubMed1985

Natural history of chronic persistent hepatitis B. Relationship between hepatitis B virus replication and the course of the disease.

The status of viral replication at diagnosis and its relationship to the changes occurring during the natural history of the disease have been investigated in 26 patients with chronic persistent hepatitis (CPH) type B. Liver HBcAg and serum HBeAg were found in 73% of patients. During follow-up, serum transaminases normalized in 13/17 HBeAg-positive patients 1-6 years after diagnosis and 11 of them developed anti-HBe. HBe seroconversion was closely preceded by a transient elevation of transaminases in 5 patients in whom a repeated liver biopsy showed prominent lobular hepatitis and marked reduction of liver HBcAg. Such changes resulted in long-lasting biochemical normalization but only 1 patient became HBsAg-negative. These observations indicate that prolonged viral replication occurs in type B CPH. Termination of replication frequently implies a transient worsening caused by lysis of HBcAg-containing hepatocytes which leads to inactivation of the disease and to development of a healthy HBsAg carrier state.

Adolescent↗
PubMed1985

Measurement of azygos venous blood flow in the evaluation of portal hypertension in patients with cirrhosis. Clinical and haemodynamic correlations in 100 patients.

Blood flow in the azygos vein, an index of blood flow through gastro-oesophageal collaterals, was measured by continuous thermal dilution in 100 patients with cirrhosis. Azygos blood flow was directly related to portal pressure (r = 0.54, P less than 0.001). Patients with portal hypertension had very high azygos blood flow (692 +/- 32 ml/min) in comparison with controls (n = 11, 174 +/- 29 ml/min). Patients with previous oesophageal bleeding had similar azygos blood flow as those without, but azygos blood flow was significantly greater in patients with massive or recurrent bleeding than in those with less severe haemorrhage, suggesting that the magnitude of collateral flow may influence the course of variceal bleeding. Patients with grade III varices had higher azygos blood flow than those with grades II or I. In addition, both oesophageal tamponade and vasopressin infusion, procedures of known value in variceal bleeding, markedly reduced azygos blood flow (-40% and -25%, respectively). Measurement of azygos blood flow allows evaluation of haemodynamic changes in the oesophageal collaterals of patients with portal hypertension, and provides useful information on the effect of therapeutic procedures aimed at arresting or preventing variceal haemorrhage.

Azygos Vein↗
PubMed1985

Localized sclerosing cholangitis?

Primary sclerosing cholangitis presenting as a localized stricture affecting a segment of the extrahepatic biliary tree is seldom found. This article describes the case of a 56-year-old male admitted with obstructive jaundice, in whom endoscopic retrograde cholangiography showed a localized and smooth stricture at the common hepatic duct, initially diagnosed as cholangiocarcinoma. However, the histological examination of the resected stricture, common bile duct and gallbladder, and a liver biopsy performed 3.5 years later were consistent with primary sclerosing cholangitis, affecting both the extrahepatic and intrahepatic biliary tree.

Aged↗
PubMed1985

Diagnosis of Caroli's disease by technetium-99m DISIDA cholescintigraphy. Report of three cases.

Three patients in whom Caroli's disease was diagnosed by cholangiographic methods were studied by scintigraphy with Tc-99m DISIDA. Cholescintigrams showed an intense concentration of the radionuclide in the form of round spots near the hepatic hilus in late images. In two patients with cholestasis, a delayed hepatic clearance of the radionuclide was observed, which improved when the exploration was performed after a choledocoduodenostomy. Tc-99m DISIDA is not only a good noninvasive method to diagnose Caroli's disease, but also a useful technique to evaluate the patency of the biliary tree during the follow-up of such patients.

Adult↗
PubMed1985

Chronic hepatitis: a possible etiology of fatty liver.

In a survey of the etiology of hepatic steatosis, none of the known causes of fatty liver was identified in 12 of 137 patients with severe fatty changes (more than 50% of hepatic cells containing fat vacuoles) diagnosed over a 4-year period. The retrospective analysis of the clinical records of these patients disclosed the absence of symptoms, liver biopsy being performed because of persistent hypertransaminasemia, which had been discovered fortuitously in 10 cases and after acute hepatitis in two. None had HBsAg in serum. In addition to fatty changes, lobular necrosis was found in 11 cases and chronic inflammation of portal tracts in eight. Patients remained asymptomatic and had raised transaminases during a follow-up ranging from 1 to 3 years. The clinical, biochemical and follow-up features of these patients closely resemble those of patients with chronic hepatitis in Mediterranean countries. Thus it can be suggested that in some cases fatty liver may be a prominent feature of chronic hepatitis.

Adolescent↗
PubMed1984

Evidence that renal prostaglandins are involved in renal water metabolism in cirrhosis.

Plasma antidiuretic hormone (ADH) and urinary prostaglandin E2 excretion (UPGE2V) were measured in basal conditions, after water restriction, and after water-loading in 10 normal subjects (free water clearance after the water load, CH2O, 9.6 +/- 0.8 ml/min) and in 27 patients with cirrhosis and ascites (13 with a positive CH2O: 3.6 +/- 0.5; 14 with a negative CH2O: -0.37 +/- 0.007). Plasma ADH and UPGE2V were significantly increased in patients with a positive CH2O as compared with normal subjects. Patients with a negative CH2O showed a significantly higher plasma ADH and a lower UPGE2V and GFR than did normal subjects and patients with the positive CH2O. In 18 additional subjects (6 normal and 12 with cirrhosis, ascites, and a positive CH2O) submitted to a sustained water overload, the i.v. administration of 450 mg of lysine acetylsalicylate (LAS) induced a marked reduction of UPGE2V, but it had no effect on plasma ADH. LAS did not alter GFR and CH2O in normal subjects; however, it reduced CH2O in all the 12 patients (from 5.1 +/- 0.4 to 0.6 +/- 0.3) and the GFR in only 6 of these patients. These results suggest (a) that renal PGE2 plays an important role in the maintenance of water excretion in cirrhosis with ascites, and (b) that impaired ability to dilute the urine in cirrhosis may be a consequence of the simultaneous occurrence of impaired renal hemodynamics, nonostomic hypersecretion of ADH, and reduced renal production of PGE2.

Arginine Vasopressin↗
PubMed1984

Role of spontaneous portal-systemic shunting in hyperinsulinism of cirrhosis.

The possible contribution of hepatocellular damage and portal-systemic shunting to hyperinsulinism in cirrhosis was studied in 23 cirrhotics, 8 of whom had a surgical portacaval shunt, and 16 controls by measuring insulin and the connecting peptide (C-peptide) concentrations in simultaneous samples of peripheral arterial and hepatic venous blood. The fractional hepatic insulin extraction (0.48 +/- 0.06, mean +/- SE) was normal in cirrhosis. The hepatic insulin elimination rate was directly related to arterial insulin levels (r = 0.91, P less than 0.001) even at very high circulating levels. Extrahepatic insulin metabolism was measured across the kidney and lower limb. There were no significant differences between cirrhotics and control subjects in relation to renal (0.25 +/- 0.05 vs. 0.23 +/- 0.04) and lower limb insulin extraction (0.14 +/- 0.07 vs. 0.19 +/- 0.04). While in the control group hepatic venous insulin (0.143 +/- 0.018 pmol/ml) markedly exceeded the peripheral insulin concentration (0.083 +/- 0.009 pmol/ml, P less than 0.01), the contrary was found in cirrhotics with end-to-side portacaval shunt in whom all the pancreatic venous effluent is shunted to the systemic circulation (hepatic venous insulin, 0.130 +/- 0.028 pmol/ml; peripheral, 0.234 +/- 0.037 pmol/ml; P less than 0.01). Portal-hypertensive cirrhotics without a surgical portacaval shunt also had hepatic venous insulin levels (0.132 +/- 0.029 pmol/ml) below peripheral arterial insulin concentrations (0.205 +/- 0.041 pmol/ml, P less than 0.01). The study suggests that hyperinsulinism in cirrhosis is not the result of an intrinsic defect of hepatic insulin metabolism but of the spontaneous shunting of portal blood to the systemic circulation.

C-Peptide↗
PubMed1984

Effect of demeclocycline on renal function and urinary prostaglandin E2 and kallikrein in hyponatremic cirrhotics.

8 cirrhotics with hyponatremia were given demeclocycline (DMC) 900 mg/day to investigate its effect on renal function, plasma renin activity, aldosterone and urinary excretion of prostaglandin E2 and kallikrein. In 7 patients DMC induced an increase of free water clearance (from -0.36 +/- 0.06 to 0.13 +/- 0.06 ml/min) and serum sodium concentration (from 125.4 +/- 0.09 to 131.1 +/- 1.0 mEq/l, mmol/l). In 5 of these patients DMC also induced a marked reduction of glomerular filtration rate (from 72.2 +/- 6.2 to 31,2 +/- 4.7 ml/min) and renal plasma flow (from 468 +/- 98 to 195 +/- 55 ml/min) which could not be explained on the basis of hypovolemia. In each case this renal impairment was not associated with changes in urinary concentration of beta 2-microglobulin, urinary casts excretion, fresh urine sediment or urine protein content and disappeared after discontinuation of the drug. DMC induced a marked increase in the urinary excretion of prostaglandin E2 (from 0.82 +/- 0.27 to 6.16 +/- 1.91 ng/min) in 6 out of the 7 patients who responded to DMC and a marked reduction in urinary kallikrein (from 16.1 +/- 4.4 to 4.2 +/- 1.6 pkat/min) in the 5 patients who developed renal insufficiency. The serum DMC concentration was greater than 5 micrograms/ml in all patients who responded to DMC, greater than 8 micrograms/ml in all cases who developed renal insufficiency and of 3 micrograms/ml in the case not responding to DMC. (ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1984

Fat digestion and exocrine pancreatic function in primary biliary cirrhosis.

Intestinal bile salt deficiency marginally impairs fat absorption in cholestatic patients. The finding of massive steatorrhea in some patients with primary biliary cirrhosis led us to systematically study and compare fat digestion in control subjects (n = 4) and patients with biliary cirrhosis with (n = 11) and without (n = 3) steatorrhea. The jejunum was anatomically and functionally intact in all subjects, as demonstrated by normal gastrointestinal radiology and xylose absorption, respectively. The intestinal contents were recovered during digestion of a fat meal. Lipolysis, pH, and trypsin activity were measured in whole intestinal contents, whereas bile salts, total lipid, and fatty acid were determined in both total and aqueous phases. The results obtained in controls and patients without steatorrhea were similar. Percentage of lipolysis and intraluminal pH were normal in controls and in both patient groups. The intestinal contents of the patients with steatorrhea had a significantly lesser capacity to solubilize both total lipid and fatty acid in relation to abnormally low aqueous bile salt concentrations. No bile salt deconjugation and only minimal bile salt precipitation were found, thus low aqueous bile salts were strictly related to bile secretory failure. Steatorrhea was always present when aqueous bile salt levels were below 3.0 mM. Intestinal trypsin activity was subnormal in patients with steatorrhea; decreased trypsin activity was related (r = 0.82, p less than 0.001) to reduced intestinal bile salt levels. One patient was found to have severe exocrine pancreatic failure. Administration of medium chain triglycerides was uniformly effective in improving nutrition in patients with steatorrhea, but the course of the disease was unaffected. These results indicate that overt pancreatic failure is uncommon in primary biliary cirrhosis, and that fat maldigestion and steatorrhea, regardless of what degree, are due mainly to low intestinal bile salt levels secondary to bile secretory failure. Finally, subnormal pancreatic function in this disease appears to be related to the bile secretory failure, suggesting either that the lack of bile or bile salts in the intestine depresses pancreatic exocrine function or that both biliary and pancreatic secretions decrease in parallel as part of a widespread secretory failure syndrome.

Adult↗
PubMed1983

Randomized comparative study of efficacy of furosemide versus spironolactone in nonazotemic cirrhosis with ascites. Relationship between the diuretic response and the activity of the renin-aldosterone system.

Loop and distal diuretics are the basic drugs for the treatment of ascites. Although pharmacologic studies indicate that the natriuretic potency of loop diuretics is much greater than that of distal diuretics, there are no studies comparing the efficacy of these drugs in cirrhosis. Forty nonazotemic cirrhotic patients with ascites and avid sodium retention were randomly allocated into two groups. Group 1 contained 21 patients treated with furosemide; group 2 contained 19 patients treated with spironolactone. The initial doses were 80 and 150 mg/day, respectively. These doses were increased to 160 and 300 mg/day, respectively, if there was no response. Cases not responding to furosemide and spironolactone were later treated with spironolactone and furosemide, respectively. In group 1, 11 of the 21 patients responded to furosemide, while in group 2, 18 of the 19 patients responded to spironolactone (p less than 0.01). Of the 10 patients in group 1 not responding to furosemide, 9 responded later to spironolactone. The diuretic response to furosemide and spironolactone was related to the activity of the renin-aldosterone system. Patients with higher renin and aldosterone did not respond to furosemide and required 300 mg/day of spironolactone to achieve a diuretic response. These results indicate that (a) at the dosages used in the study, spironolactone is more effective than furosemide in nonazotemic cirrhosis with ascites, and (b) the activity of the renin-aldosterone system influences the diuretic response to furosemide and spironolactone in these patients.

Ascites↗
PubMed1983

Acetylsalicylic acid suppresses the renal hemodynamic effect and reduces the diuretic action of furosemide in cirrhosis with ascites.

To investigate if lysine acetylsalicylate influences the hemodynamic and diuretic responses to furosemide in cirrhosis, 21 nonazotemic patients with ascites were studied. In 8 patients (group 1), the renal plasma flow and glomerular filtration rate were serially measured before and during three 30-min periods after the i.v. administration of lysine acetylsalicylate (450 mg). In 7 patients (group 2), renal plasma flow, glomerular filtration rate, urine volume, and sodium excretion were measured before and during three 20-min periods after the i.v. administration of furosemide (40 mg). After a 45-min period in which urinary losses were restored, a similar study was performed before and after a second injection of furosemide (40 mg). Six patients (group 3) were studied with an identical protocol as group 2, except that the second injection of furosemide was preceded by the administration of lysine acetylsalicylate (450 mg). In 6 patients of group 1, lysine acetylsalicylate caused a marked and reversible reduction of renal plasma flow and glomerular filtration rate. In groups 2 and 3, the i.v. injections of furosemide alone produced a significant increase in renal plasma flow and glomerular filtration rate, and a marked diuresis and natriuresis. In patients of group 3, pretreatment with lysine acetylsalicylate suppressed the renal hemodynamic effect and markedly reduced the diuretic effect of the second injection of furosemide. Lysine acetylsalicylate did not cause the appearance of renal insufficiency in any of these patients. These results suggest that prostaglandins are involved in the renal response to furosemide in cirrhosis with ascites and that furosemide protects these patients from developing renal insufficiency after acute administration of nonsteroidal antiinflammatory agents.

Aspirin↗