PubMed Health⌕ Search

Biomedical subjects

M Navasa

Publications and source records attributed to M Navasa.

At least 127 records · Page 7Linked to original sources
PubMed1989

Evaluation of the portal hypertensive patient.

Portal hypertension is characterized by a chronic increase in portal venous pressure. This is initiated by an increased vascular resistance to portal blood flow. In advanced stages, however, blood flow increases and contributes to worsen and maintain portal hypertension. Increased pressure and blood flow within the portal system promotes the appearance and dilation of portal-systemic collaterals and oesophageal varices, which are responsible for the main complication of portal hypertension: massive gastrointestinal haemorrhage. In recent years there have been several major innovations in the evaluation of portal hypertension. These include the application of new endoscopic, ultrasonographic and haemodynamic techniques that allow a better evaluation of the portal hypertensive patient, especially when prophylactic medical therapy is considered. Ultrasonography is very useful to assess the patency of the portal vein. The association of a pulsed Doppler flowmeter increases its accuracy and allows the non-invasive estimation of the direction and magnitude of portal blood flow. In addition to the measurement of portal pressure, measurement of azygos venous blood flow has proven very useful in the haemodynamic evaluation of portal hypertension. Azygos blood flow represents an index of blood flow through gastro-oesophageal collaterals and varices draining in the azygos vein. Its main application has been the assessment of the effects of pharmacological therapy. Endoscopic measurements of variceal pressure, either by direct puncture or using non-invasive pressure gauges, have contributed significantly to the understanding of the mechanism of variceal haemorrhage. This technique allows the calculation of the variceal wall tension as the product of the transmural pressure at the varices and the radius of the varix.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1989

Endoscopic measurement of variceal pressure in cirrhosis: correlation with portal pressure and variceal hemorrhage.

This study evaluated the clinical application of a pressure-sensitive gauge that allows the noninvasive measurement of the pressure of esophageal varices at endoscopy. The study was performed in 70 patients with cirrhosis and portal hypertension. Among them, 47 had bled from the varices and 23 had varices but had not bled. In addition to measurements of variceal pressure, the size of the varices was estimated semiquantitatively at endoscopy. This allowed an estimate of the tension on the wall of the varices as the product of the transmural pressure and the estimated radius of the varices. Most patients had a standard hemodynamic evaluation of portal hypertension, with measurements of wedged and free hepatic venous pressures, and of azygos blood flow. These were performed within 24 h of the variceal pressure measurements. Variceal pressure was significantly higher in bleeders than in nonbleeders (15.7 +/- 2.8 vs. 12.1 +/- 2.6 mmHg, p less than 0.001) in spite of a similar portal pressure in both groups (20.1 +/- 5.1 vs. 20.4 +/- 7.6 mmHg, NS). More than 60% of the bleeders, but only 22% of the nonbleeders had a variceal pressure greater than or equal to 15 mmHg (p less than 0.005). Among nonbleeders, variceal pressure was higher in patients with large varices (13.9 +/- 2 mmHg, n = 9) than in those with small varices (10.9 +/- 2.4 mmHg, n = 14) (p less than 0.01). Estimates of variceal wall tension further exaggerated the differences between bleeders and nonbleeders (66.1 +/- 22.6 vs. 32.0 +/- 19.8 mmHg.mm, p less than 0.001). More than 50% of bleeders, but just 9% of nonbleeders had an estimated variceal tension greater than 50 mmHg.mm (p less than 0.001). Our findings support the role of an increased variceal pressure in the pathogenesis of variceal hemorrhage, and suggest that this noninvasive technique can be valuable in assessing the risk of variceal hemorrhage in patients with portal hypertension.

Endoscopes↗
PubMed1988

Steady-state extrarenal sorbitol clearance as a measure of hepatic plasma flow.

Hepatic plasma flow was assessed with sorbitol (hepatic extraction = 0.96) at steady state. After infusion of 50 mg/min for 3 h, total and renal sorbitol clearances were calculated, and the extrarenal clearance was obtained by taking the difference between the two. In normal volunteers, the mean (+/- SD) extrarenal sorbitol clearance was 10.6 +/- 2.1 ml/min.kg. In patients with various liver diseases, it was correlated more closely to the fractional clearance of indocyanine green (r = 0.83, n = 57) than the galactose elimination capacity (r = 0.66, n = 55). Hepatic vein catheterization showed that the hepatic extraction of sorbitol was always much higher than the extraction of indocyanine green; there was no evidence for extrahepatic, extrarenal sorbitol elimination. On the basis of these findings, sorbitol is kinetically superior to indocyanine green and, although the noninvasively determined extrarenal sorbitol clearance at steady state may not be equal to total hepatic plasma flow, it may at least be regarded as a measure of parenchymal liver plasma flow.

Adult↗
PubMed1988

Hyperglucagonism and glucagon resistance in cirrhosis. Paradoxical effect of propranolol on plasma glucagon levels.

Propranolol, a non-selective beta-blocker, is known to decrease glucagon release in normal subjects. The present study was aimed at investigating the effects of propranolol on the hyperglucagonism commonly observed in patients with cirrhosis. Eight cirrhotic patients and 6 matched healthy controls were studied. The plasma concentrations of glucagon, insulin, c-peptide and glucose were measured in basal conditions and after stimulating glucagon secretion by an i.v. infusion of arginine (0.4 g/kg/30 min). The study was repeated 24 h later after inducing beta-blockade by the i.v. infusion of propranolol (10 mg). In baseline conditions, patients with cirrhosis, despite normal levels of insulin and glucose, had a marked hyperglucagonism (654 +/- 303 pg/ml vs. 269 +/- 90 in controls, P less than 0.01). Prior to propranolol, arginine infusion caused greater glucagon release in cirrhotics (71 +/- 31 ng.h.ml-1) than in controls (33 +/- 17 ng.h.ml-1, P less than 0.02), but despite a similar insulin secretion (assessed from c-peptide), blood glucose did not increase. After propranolol, glucagon secretion decreased as expected in controls (29 +/- 12 ng.h.ml-1, P less than 0.05) but experienced a paradoxical increase in cirrhotics (113 +/- 64 ng.h.ml-1, P less than 0.05). Again, despite the marked increase in glucagon release, there was no increase in glucose production, providing further evidence of the glucagon resistance that accompanies hyperglucagonism in cirrhosis. Our results suggest that hyperglucagonism with glucagon resistance might be the initial disturbance in carbohydrate metabolism in patients with cirrhosis. Contrary to what could be expected, propranolol does not correct but further accentuates this disturbance.

Adult↗
PubMed1988

Effects of somatostatin in patients with portal hypertension.

Portal hypertension is a common complication of chronic liver disease. Conventional therapy consists of surgery and palliative measures for the hemodynamic problem. It has been recently reported that somatostatin may reduce portal pressure without altering the systemic circulation and so reducing hepatic blood flow. This peptide also causes a significant fall in azygos circulation in patients with esophageal varices. The mechanism of this effect is unclear although suppression of intestinal vasodilating hormones and of glucagon have been claimed to play a role. Comparative clinical studies have shown somatostatin to be superior to the standard vasopressin treatment. Recent findings suggest that the efficacy of somatostatin can be increased by administering this peptide in repeated intravenous bolus injections. New derivatives, specially long-acting peptides, may eventually prove beneficial in the chronic treatment of this complication.

Blood Pressure↗
PubMed1988

Diagnosis and evaluation of portal hypertension.

In the past recent years there have been several major innovations in the diagnosis and evaluation of portal hypertension. These include the application of new endoscopic, ultrasonographic and haemodynamic techniques that allow a better evaluation of the portal hypertensive patient, specially when prophylactic medical therapy is considered. Ultrasonography is very useful to assess the patency of the portal vein. The association of a pulsed Doppler flowmeter increases its accuracy and allows the non-invasive estimation of the direction and magnitude of portal blood flow. Endoscopic measurements of variceal pressure may help to understand the mechanism of variceal bleeding, and perhaps might permit to assess the risk of haemorrhage in the individual patient. In addition to the measurement of portal pressure, measurement of blood flow through the azygos vein has been the major innovation in the haemodynamic evaluation of portal hypertension. Azygos blood flow represents an index of blood flow through gastroesophageal collaterals and varices draining in the azygos vein. This technique has been very useful in the development of new forms of pharmacological therapy for portal hypertension.

Azygos Vein↗
PubMed1987

Effects of alpha-adrenergic stimulation and beta-adrenergic blockade on azygos blood flow and splanchnic haemodynamics in patients with cirrhosis.

The effects of beta-blockade with propranolol and of alpha-adrenergic stimulation with methoxamine, a powerful alpha-agonist, on azygos blood flow and on systemic and hepatic haemodynamics were investigated in 26 cirrhotic patients with portal hypertension. Beta-adrenergic blockade with propranolol (n = 12), evidenced by a significant reduction of heart rate (-17 +/- 1%, P less than 0.001) and cardiac index (-17 +/- 2%, P less than 0.001), caused a mild but significant decrease of hepatic venous pressure gradient (-10 +/- 2%, P less than 0.05) and a marked fall of azygos venous blood flow (-31 +/- 5%, P less than 0.05). Alpha-adrenergic stimulation with methoxamine (n = 14), manifested by a significant increase of mean arterial pressure (19 +/- 2%, P less than 0.001), mimicked the effects of propranolol on hepatic venous pressure gradient (-10 +/- 4%, P less than 0.05) and cardiac index (-11 +/- 2%, P less than 0.001). However, azygos blood flow was not significantly reduced by methoxamine (0.7 +/- 0.1 vs 0.6 +/- 0.1 l/min). On the contrary, hepatic blood flow was significantly reduced by methoxamine (-19 +/- 4%, P less than 0.01) but not by propranolol (-7 +/- 7%, ns). Similarly, in 8 patients who received methoxamine after being beta-blocked by propranolol, azygos blood flow, that was markedly reduced by beta-blockade, did not experience a further reduction but increased slightly by alpha-adrenergic stimulation, while hepatic blood flow, that was not reduced by propranolol, decreased significantly during the subsequent methoxamine infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Azygos Vein↗
PubMed1987

Portal hypertension in primary biliary cirrhosis. Relationship with histological features.

The prevalence and type of portal hypertension (PH) in primary biliary cirrhosis (PBC) and their relationship with liver lesions have been investigated in 32 patients with the disease. Portal hypertension was considered when oesophageal or gastric varices were observed by endoscopy and/or when hepatic venous pressure gradient measured by hepatic vein catheterization was greater than 6 mmHg. Within 3 days of endoscopy, a liver biopsy was performed for histological staging and semiquantitative grading (0 to 3+) of portal and sinusoidal fibrosis, portal inflammation, piecemeal necrosis, lobular necrosis, cholestasis, as well as the presence of granulomas and Mallory's hyaline. Twenty patients (62.5%) had portal hypertension, five of them showing presinusoidal PH (15.5%) and the remaining 15 (47%) with sinusoidal component. The four patients in stage IV had sinusoidal PH and the only patient in stage I had no PH. The prevalence of portal hypertension was similar in patients in stage II (57%) and stage III (55%), but presinusoidal PH was only observed in patients in stage II. Patients with PH showed significantly higher portal inflammation and piecemeal necrosis than patients without PH. By contrast, there were no differences in portal and sinusoidal fibrosis, nor in the other histologic features. These results indicate that portal hypertension is common in PBC and it may be present in the early stages of the disease. The fact that presinusoidal PH was only observed in patients in stage II suggests that portal hypertension is initially of presinusoidal type, and then as the disease progresses is joined by a sinusoidal component.

Adult↗
PubMed1984

Relapsing polychondritis with segmental necrotizing glomerulonephritis.

Glomerulonephritis is a very unusual feature of relapsing polychondritis. A 16-year-old woman presented with microscopic hematuria and severe renal insufficiency during the course of relapsing polychondritis. A renal biopsy specimen disclosed focal segmental proliferative glomerulonephritis with necrotizing lesions and crescent formation. Immunofluorescent studies suggested immune complex mediated glomerular injury. The renal involvement appeared during high-dose steroid therapy. Subsequently, she was treated by adding plasmapheresis and cyclophosphamide during 6 weeks, with sustained improvement. A regimen of plasmapheresis and immunosuppression warrants consideration for use in cases of relapsing polychondritis with glomerulonephritis.

Adolescent↗
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

Atrial natriuretic factor in cirrhosis with ascites: plasma levels, cardiac release and splanchnic extraction.

The aim of this study was to determine the plasma levels, cardiac release and splanchnic extraction of atrial natriuretic factor in cirrhosis with ascites. The plasma concentration of immunoreactive atrial natriuretic factor in samples obtained from an antecubital vein was measured in 18 healthy volunteers and in 35 cirrhotics with ascites. In 11 of these cirrhotics and in 11 patients admitted to the hospital for the study of a thoracic pain who had no clinical or hemodynamic signs of cardiac failure (control group), the plasma levels of immunoreactive atrial natriuretic factor in samples from the coronary sinus, right atrium, pulmonary artery, hepatic vein and femoral vein were determined and the coronary sinus blood flow measured by thermodilution. Cirrhotic patients showed significantly higher plasma levels of immunoreactive atrial natriuretic factor in each vascular territory studied than did control subjects (coronary sinus: 101.2 +/- 10.6 vs. 26.1 +/- 4.7 fmoles per ml; right atrium: 32.5 +/- 5.8 vs. 9.4 +/- 3.5; pulmonary artery: 36.8 +/- 10.1 vs. 7.5 +/- 2.4; hepatic vein: 10.7 +/- 2.0 vs. 2.7 +/- 0.8; femoral vein: 18.2 +/- 2.4 vs. 3.1 +/- 0.9; antecubital vein: 14.7 +/- 1.6 vs. 4.0 +/- 0.8). The coronary sinus blood flow was also higher in cirrhotics (200 + 22 ml per min) than in controls (105 +/- 7 ml per min). Consequently, the estimated cardiac release and cardiac production of immunoreactive atrial natriuretic factor were strikingly increased in cirrhotics (13,334 +/- 2,007 and 5,484 +/- 1,734 fmoles per min, respectively) as compared to control subjects (1,669 +/- 338 and 1,431 +/- 350 fmoles per min, respectively; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Ascites↗
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

Experience with cefotaxime in the treatment of spontaneous bacterial peritonitis in cirrhosis.

Spontaneous bacterial peritonitis (SBP) is a severe infectious complication in cirrhotic patients, and initial antibiotic therapy must be empirical. An initial study published in 1985 found that cefotaxime administered at a dose of 2 g every 4 h was more effective and safer than the combination of tobramycin-ampicillin. Since then, cefotaxime has been considered the agent of choice in the empiric therapy of SBP. Subsequent publications showed that a dosage of 2 g every 6 h was also adequate in this infection. More recent studies have demonstrated that the high efficacy of cefotaxime in SBP can be maintained by using lower dosages than those used in initial investigations. In one of these studies, a dose of 2 g every 8 h for 5 days was found to be as effective as the same dose for 10 days. Finally, a prospective, randomized multicenter trial aimed at comparing the efficacy of two different dosages of cefotaxime, 2 g every 6 h versus 2 g every 12 in a large series of cirrhotic patients with SBP, showed that both dosages resulted in similar rates of resolution of infection and survival. Despite the reasonably adequate rate of infection resolution in SBP patients, the in-hospital mortality rate remains high as a result of complications such as renal failure. Further studies should therefore be addressed to reducing the incidence of these complications and thus improving survival.

Bacterial Infections↗
PubMedDate not supplied

[Living donor liver transplantation in adults. Initial results].

AIM: To analyze the preliminary results of the implementation of a living donor liver transplantation program. PATIENTS AND METHOD: Between March and September 2000 we performed 7 living donor liver transplantations using the right hepatic lobe. The donors were 5 men and 2 women with a mean age of 39.3 11.5 years. Three donors were genetically related (daughter, mother, son). The mean relative liver volume transplanted was 58.8 2.5%. The mean age of the recipients was 50.4 16.5 years. Six patients presented hepatitis C virus-induced cirrhosis and one presented familial amyloidotic polyneuropathy. RESULTS: Three complications occurred in the donors: 1 slight infection and 2 biliary fistulae. Graft function was adequate in all recipients and there were three acute rejections. Four biliary leakages occurred of which two required reoperation. None of the patients developed vascular thrombosis. Two recipients died, 53 and 72 days after the operation, with a correctly functioning graft. CONCLUSION: Living donor liver transplantation constitutes a necessary complement to the current cadaveric donor program to increase the number of patients who can benefit from this treatment, which may represent 10% of the activity of our center. The technical complexity of this procedure is much greater than that of cadaveric transplantation. The right hepatic lobe provides sufficient hepatic mass for most adult recipients.

Adult↗