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Biomedical subjects

D Valla

Publications and source records attributed to D Valla.

At least 73 records · Page 4Linked to original sources
PubMed1998

Concurrent emergence of hepatitis B e antigen-negative hepatitis B virus variant and autoimmune hepatitis cured by adenine arabinoside monophosphate.

We report the case of a hepatitis B virus chronic carrier in whom features of severe autoimmune hepatitis developed concurrently with the emergence of a hepatitis Be antigen-negative variant. Corticosteroid administration failed to normalize serum transaminase activity and resulted in increased viral multiplication. Adenine arabinoside monophosphate treatment allowed simultaneous inhibition of hepatitis B virus multiplication and remission of autoimmune features. This observation indicates that hepatitis Be antigen-negative variants can induce autoimmune hepatitis and adds support to the hypothesis that autoimmune hepatitis can be triggered by hepatotropic viruses. Patients with both features should first be treated with adenine arabinoside monophosphate. This observation indicates that hepatitis Be antigen-negative variants can induce autoimmune hepatitis and adds support to the hypothesis that autoimmune hepatitis can be triggered by hepatotropic viruses. Patients with both features should first be treated with adenine arabinoside monophosphate.

Antiviral Agents↗
PubMed1998

Comparison of high initial and fixed-dose regimens of interferon-alpha2a in chronic hepatitis C: a randomized controlled trial. French Multicenter Interferon Study Group.

The efficacy of a high-dose de-escalating treatment regimen versus the standard, fixed-treatment regimen of interferon-alpha2a (IFN; Roferon-A) in chronic hepatitis C was evaluated in 291 patients who had elevated alanine aminotransferase (ALT) levels, for at least 6 months prior to the study, and histologically proven chronic hepatitis. Patients were randomized into two groups: 142 patients received IFN at a fixed dose (3 million international units (MIU) three times a week for 6 months) and 149 patients received 6 MIU three times a week for 3 months followed by 3 MIU three times a week for the next 3 months. The groups did not differ significantly with respect to age, gender or percentage of patients with cirrhosis. Response was evaluated by monitoring ALT levels monthly during treatment and during the 6 months post-treatment follow-up. Sixty-one per cent and 66% of the patients in the fixed and de-escalating treatment groups had a primary response (serum ALT normalization) during the treatment period; sustained-response rates at the end of follow-up were 20% and 29%, respectively (not significant). In non-cirrhotic patients, a primary response was recorded in 65% and 70% of the patients in the fixed and de-escalating groups; sustained-response rates were 22% and 33%, respectively. Overall, 62% of patients with a sustained response showed histological improvement. In univariate analysis, patients with sustained response tended to be non-cirrhotic and had lower initial serum gamma-glutamyl transpeptidase and ferritin levels. Multivariate analysis indicated that only ALT activity assessed at month 1 (P < 0.01) was a significant predictor of sustained response. These findings suggest that although the difference in the response rates between the de-escalating (6 MIU three times a week for 3 months; 3 MIU three times a week for 3 months) and fixed (3 MIU three times a week for 6 months) treatment regimens did not reach statistical significance, there was a clear trend towards higher response with the 6 MIU induction dose in patients without cirrhosis.

Adolescent↗
PubMed1998

Influence of transjugular intrahepatic portosystemic shunts (TIPS) on tissue oxygenation in patients with cirrhosis.

UNLABELLED: AIMS/BACKGROUNDS: The aim of this prospective study was to evaluate the influence of transjugular portosystemic intrahepatic shunts (TIPS) on tissue oxygenation in patients with cirrhosis and refractory ascites. METHODS: Five shunted patients were included in the study. The blood and tissue oxygenation values were analyzed 12 days and 4 months after TIPS procedure. The results were compared with those observed in patients treated by paracentesis. RESULTS: Unlike patients treated by paracentesis, PaO2 values remained unchanged throughout follow-up in shunted patients. After the TIPS procedure, there was a transient increase in systemic O2 transport and O2 uptake and a transient decrease in O2 saturation of hepatic oxyhemoglobin. After 4 months, TIPS resulted in an increase in PCO2 values and bicarbonate concentrations. CONCLUSIONS: The TIPS procedure seems to prevent the decrease in PaO2 observed in patients treated by paracentesis and may improve the respiratory alkalosis of cirrhosis.

Adult↗
PubMed1997

Studies of portal hemodynamics and hepatic oxygen consumption during acute liver allograft rejection.

Hemodynamics and oxygen variables, plasma cytokines, and histological features of a liver tissue sample obtained by transvenous biopsy were evaluated during 65 episodes of acute rejection. The hepatic venous pressure gradient was significantly higher in patients with acute rejection than in those without (5.1+/-0.3 vs. 3.1+/-0.2 mmHg, P<0.01). The increase in pressure gradient was related to the severity of rejection lesions. Hepatic blood flow was significantly lower in patients with than in those without acute graft rejection (1.28+/-0.11 vs. 1.75+/-0.13 L/min, P<0.05). Plasma interleukin-6 levels were significantly increased in patients with acute rejection and positively correlated with pressure gradient values. In patients with acute rejection, a significant decrease in hepatic venous oxygen content (-16%) was associated with a significant increase in hepatic oxygen consumption (+24%), whereas hepatic oxygen transport did not change significantly. In treated patients with a favorable response, the pressure gradient decreased significantly by 46%, but it remained elevated in patients who later developed chronic graft rejection. In conclusion, this study confirms that acute graft rejection may induce an increase in portal pressure, which is related to the severity of rejection lesions. It also shows that acute rejection decreases hepatic blood flow and increases hepatic oxygen consumption. In addition, it suggests that the hepatic venous pressure gradient might be useful to determine the outcome of rejection.

Acute Disease↗
PubMed1997

Hepatic venous outflow block caused by short-length hepatic vein stenoses.

In contrast with the well-recognized membranous obstruction of the inferior vena cava, short-length hepatic vein stenoses are not well-recognized causes of hepatic venous outflow block. The aim of this study was to ascertain the prevalence, causes, manifestations, and outcome of short-length hepatic vein stenoses. We performed a retrospective study of patients with short-length hepatic vein stenosis among 86 patients with hepatic venous outflow block who were seen between 1970 and 1992. There were 25 patients with short-length hepatic vein stenosis. A thrombogenic condition was identified in 14 patients (56%). The lesions of the accompanying hepatic veins in these patients were variable (short-length stenoses, thromboses, or nonspecific changes) and similar to that seen in patients without short-length hepatic vein stenosis. In 3 necropsied cases, the venous lesions were suggestive of fibrous sequela of prior thromboses. In patients with short-length hepatic vein stenosis, splenomegaly (28% vs. 55%, P < .05) and hypersplenism were significantly less common; serum transaminase (P < .001) and creatinine levels (P < .02) were lower, prothrombin was higher (P < .001), and 5-year survival was significantly better (Kaplan-Meier estimates: 80% vs. 50%, P < .05). In patients with hepatic venous outflow block, short-length hepatic vein stenosis is a common lesion that appears to be the sequela of localized thrombosis. Long-term anticoagulation and percutaneous angioplasty (with or without stenting) are potentially applicable in these lesions. The long-term results of these treatments merit further evaluation.

Adult↗
PubMed1997

Hypoxemia in patients with cirrhosis: relationship with liver failure and hemodynamic alterations.

BACKGROUND/AIMS: The relationship between hypoxemia, liver failure and the hemodynamic alterations in cirrhosis are unknown. This study examined the relationship between arterial hypoxemia, the severity of liver disease and hyperkinetic circulation in patients with cirrhosis. METHODS: Arterial blood gases, the severity of cirrhosis (Child-Pugh score), and splanchnic and systemic hemodynamics were measured in 120 patients with cirrhosis and without cardiopulmonary disease. Hypoxemia was considered to be present when PaO2 was < or = 70 mmHg. RESULTS: Seventeen patients had hypoxemia (14%). Hypoxemic patients had significantly lower pulmonary vascular resistance and a significantly higher alveolar-arterial oxygen gradient, Child-Pugh score and hepatic venous pressure gradient than non-hypoxemic patients. Cardiac index and right atrial and pulmonary pressures did not significantly differ between the two groups. CONCLUSIONS: Hypoxemia occurs mainly in patients with severe liver disease and is associated with pulmonary vasodilation.

Adult↗
PubMed1997

Natriuretic response to the combination of atrial natriuretic peptide and terlipressin in patients with cirrhosis and refractory ascites.

BACKGROUND/AIMS: Refractory ascites, which occurs in certain patients with cirrhosis, is associated with a blunted natriuretic response to exogenous atrial natriuretic peptide (ANP). Since this blunting seems to be related to ANP-induced arterial hypotension, a vasoconstrictor, such as terlipressin (a vasopressin analogue), may restore natriuresis to exogenous ANP. Moreover, since cirrhosis-elicited vasodilation is thought to play a role in sodium retention, a vasoconstriction caused by terlipressin alone may lead to an increase in sodium excretion. This study aimed to evaluate the natriuretic response to either a combination of ANP with terlipressin or terlipressin alone in patients with cirrhosis and refractory ascites. METHODS: Sixteen consecutive patients with cirrhosis and refractory ascites were randomly assigned to receive either a combination of terlipressin (1-2 mg, i.v. bolus) with ANP (35 ng/kg, i.v. bolus followed by 15 ng x kg(-1) x min(-1) for 60 min) (n=8) or terlipressin alone (1-2 mg, i.v. bolus) (n=8). Sodium excretion and urine output, systemic, splanchnic and renal hemodynamics and renal oxygen consumption were measured before and during treatments. RESULTS: Combined therapy did not change arterial pressure but significantly increased urinary sodium excretion and urine output. These effects were associated with a significant increase in glomerular filtration rate and a decrease in renal oxygen consumption. Terlipressin alone significantly increased arterial pressure but did not change urinary sodium excretion or urine output. Moreover, terlipressin did not change either glomerular filtration rate or renal oxygen consumption. CONCLUSIONS: The combination of exogenous ANP with terlipressin, but not terlipressin alone, increases sodium excretion in patients with cirrhosis and refractory ascites.

Adult↗
PubMed1997

Noncirrhotic portal hypertension.

This article reviews the different conditions leading to noncirrhotic intrahepatic portal hypertension, describes the related vascular lesions, and provides a review of the clinical characteristics, diagnosis, and treatment options available. Diseases associated with noncirrhotic portal hypertension are also specifically discussed.

Female↗
PubMed1997

Haemodynamic effects of octreotide in portal hypertensive rats receiving propranolol.

BACKGROUND: The aim of this study was to investigate short-term effects of propranolol (a non-selective beta-adrenergic antagonist), octreotide (a long-acting somatostatin analogue), or a combination of these substances on splanchnic and systemic haemodynamics and arterial blood gases in rats with portal vein stenosis. METHODS: Splanchnic and systemic haemodynamics were measured using the radioactive microspheres method. Eight rats first received an i.v. infusion of isotonic saline (10 microL/min for 15 min) and then an i.v. infusion of octreotide (8 micrograms.h/kg for 15 min). Eight other rats first received a bolus i.v. injection of propranolol (2 mg) and an i.v. infusion of octreotide 15 min later. RESULTS: Propranolol or octreotide alone significantly decreased portal pressure (both by 23%), portal tributary blood flow (35 and 10%, respectively) and cardiac index (36 and 26%, respectively). Octreotide administration in rats pretreated with propranolol significantly decreased cardiac index but did not change portal and arterial pressures or portal tributary blood flow. Propranolol significantly increased arterial oxygen tension. Octreotide alone or combined with propranolol significantly decreased oxyhaemoglobin saturation and pH and increased carbon dioxide tension. CONCLUSIONS: In rats with portal vein stenosis, the somatostatin analogue, octreotide, accentuates the short-term decrease in cardiac index due to propranolol. In addition, octreotide altered arterial blood gases and acid-base status. In contrast, octreotide does not further decrease portal pressure in animals receiving propranolol.

Adrenergic beta-Antagonists↗
PubMed1997

Haemodynamic responses to a combination of terlipressin and octreotide in portal hypertensive rats.

BACKGROUND: An enhancement of the haemodynamic effects of terlipressin by octreotide (and vice versa) may be useful in the treatment of portal hypertension. The aim of this study was to investigate the short-term effects of terlipressin, octreotide or a combination of these substances on splanchnic and systemic haemodynamics in rats with portal vein stenosis. METHODS: Eight rats received an intravenous (i.v.) infusion of isotonic saline (10 microL/min for 15 min). Eight rats received terlipressin first (0.05 mg/kg) and then an i.v. infusion of octreotide (8 micrograms.h/kg for 15 min) 15 min later. Eight other rats first received an i.v. infusion of octreotide and then terlipressin 15 min later. Splanchnic and systemic haemodynamics (radioactive microsphere method) were measured after saline, after terlipressin or octreotide alone, and after the combined treatments. RESULTS: Terlipressin and octreotide alone significantly decreased portal pressure, portal tributary blood flow and cardiac index. Terlipressin, but not octreotide, significantly increased heptocollateral vascular resistance and arterial pressure. Octreotide administration in rats pre-treated with terlipressin did not change portal pressure, caused portal tributary blood flow to increase and decreased hepatocollateral vascular resistance; it also decreased arterial pressure but not cardiac index. Terlipressin administration in rats pre-treated with octreotide further decreased portal pressure, portal tributary blood flow and increased hepatocollateral vascular resistance; terlipressin increased arterial pressure and further decreased cardiac index. CONCLUSIONS: In rats with portal vein stenosis, octreotide decreased short-term splanchnic and systemic vasoconstriction due to terlipressin. In contrast, terlipressin enhanced the splanchnic and systemic vasoconstriction due to octreotide. Thus, the haemodynamic responses to the combination of octreotide and terlipressin depend on the order of administration of these substances.

Animals↗
PubMed1997

[Influence of anemia on hemodynamic changes in patients with cirrhosis].

OBJECTIVE: The aim of this retrospective study was to evaluate the systemic and splanchnic hemodynamic changes induced by anemia in patients with cirrhosis. METHOD: 148 patients (Child-Pugh A: 46 patients, Child-Pugh B: 64 patients and Child-Pugh C: 38 patients) were included in the study. Anemia was defined by a blood hemoglobin level < 12 g/dL. A systemic and splanchnic hemodynamic study was performed in all patients. RESULTS: A significant elevation of the hepatic venous pressure gradient was observed in Child-Pugh A patients with anemia but not in Child-Pugh B and C patients. In the 2 latter groups, cardiac index was significantly increased and systemic vascular resistance decreased in patients with anemia. CONCLUSION: Anemia may worsen the hemodynamic changes associated with cirrhosis.

Adult↗
PubMed1996

Liver dysfunction in allogeneic bone marrow transplantation recipients.

Liver dysfunction is common in allogeneic bone marrow graft recipients, but no systematic studies of pre- and posttransplantation liver biopsies have been performed to identify and compare hepatic lesions. This study involved 25 consecutive patients who had undergone serial viral screening tests, liver tests, and pre- and posttransplantation liver biopsy. The aims were to ascertain the origin of liver disorders prior to bone marrow transplantation, to determine the mechanism and severity of liver dysfunction occurring early after transplantation, and to identify a possible relationship between pre-existing liver lesions and the frequency and nature of early liver dysfunction after transplantation. Pretransplantation biochemical liver tests were abnormal in 72% of patients, despite the absence of clinical liver disease. Eleven patients had chronic viral hepatitis B or C. Mild or moderate histological lesions were present in all the patients, with bile duct abnormalities in 48%, central vein abnormalities in 24%, sinusoidal fibrosis in 52%, portal fibrosis in 88%, portal necrosis in 52%, and parenchymal siderosis in 76%. After transplantation, fatal veno-occlusive disease occurred in two patients and biochemical abnormalities occurred in 24. Coded review of needle biopsy specimens failed to provide a single diagnosis. Histological lesions differed between pre- and posttransplantation biopsy specimens only by increased iron overload (96%, P<0.01). We conclude that pretransplant liver lesions contribute to hepatic dysfunction early after bone marrow transplantation, being very similar in nature and degree to lesions observed posttransplantation.

Adolescent↗
PubMed1996

[Indications and role of albumin, plasma volume expansion excluded, in the preoperative or postoperative management of portal hypertension].

Low serum albumin levels are common in patients with cirrhosis and liver failure. Decreased synthesis is the main but not the only mechanism leading to decreased serum levels. The consequences of low albumin concentrations are a decreased plasma colloid osmotic pressure and a decreased binding of liposoluble xenobiotics and endogenous substances. Besides the fluid accumulation in pleura and peritoneum, the complications directly related to low serum albumin levels have been only poorly assessed. An increase in serum albumin levels (by a few g.L-1) for a few days can be achieved by the infusion of large amounts of human albumin (approximately 120 g over 3 days). The efficacy of this treatment has been only tested in association with large paracentesis: albumin infusion, which induces volume expansion, reduced the incidence of hyponatremia and functional renal failure. No significant effect on ascites production rate or survival has been observed. Similar results were achieved through polygelin or dextran-70 infusions. No well-conducted controlled study on the value of albumin infusion in other circumstances apart from cirrhotic patients is available. In conclusion, albumin infusion should be reserved to the treatment of hyponatraemia or functional renal failure complicating cirrhosis with severe liver failure and marked hypoalbuminaemia, when the infusion of colloids failed to correct these anomalies.

Ascites↗
PubMed1995

[Treatment of digestive hemorrhages caused by non-cirrhotic portal hypertension].

Causes of gastrointestinal bleeding and principles for their treatment are very similar in non-cirrhotic portal hypertension to those in portal hypertension due to cirrhosis. When the cause of the block responsible for portal hypertension is a thrombogenic disorder, anticoagulation must be associated. The need for anticoagulation does not modify the general rules for management but may make it more difficult.

Gastrointestinal Hemorrhage↗