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D Valla

Publications and source records attributed to D Valla.

At least 145 records · Page 8Linked to original sources
PubMed1988

Peliosis hepatis induced by 6-thioguanine administration.

A patient with acute myeloblastic leukaemia developed jaundice revealing peliosis hepatis after receiving 6-thioguanine for two months. Peliosis hepatis was severe and was associated with mild lesions of centrilobular veins. Withdrawal of 6-thioguanine was followed by a progressive improvement of liver dysfunction. This report shows that 6-thioguanine, a thiopurine already reported to be responsible for veno-occlusive disease of the liver, can induce peliosis hepatis. This suggests that some liver vascular disorders caused by thiopurines (6-thioguanine, azathioprine and 6-mercaptopurine), particularly peliosis hepatis, veno-occlusive disease, sinusoidal dilatation and perisinusoidal fibrosis, might be related syndromes caused by similar lesions at different sites.

Chemical and Drug Induced Liver Injury↗
PubMed1988

Comparative haemodynamic effects of betaxolol and propranolol in patients with cirrhosis.

The acute effects of betaxolol (10 mg, intravenously), a new cardioselective beta-blocker, and propranolol (15 mg, intravenously) on splanchnic and systemic circulations were studied in two matched groups of six patients with portal hypertension due to cirrhosis. Similar decreases in hepatic venous pressure gradient and azygous blood flow--an estimation of superior portosystemic shunts--were observed after both drugs, whereas hepatic blood flow was not modified. The decreases in heart rate and cardiac index were also similar after betaxolol and propranolol. Both drugs induced a significant decrease in the fraction of cardiac output flowing through superior portosystemic shunts. These findings confirm that the marked effect of beta-adrenoceptor blocking agents on splanchnic circulation results both from the reduction in cardiac output and from a vasoconstriction of the portal vein territory, and demonstrate that this vasoconstriction of the portal vein area does not necessitate a beta 2-blocking activity of the drug. The similar efficiency of the two agents in decreasing the hyperkinetic circulation suggests that betaxolol merits further long-term study in the pharmacologic treatment of portal hypertension.

Adrenergic beta-Antagonists↗
PubMed1987

Reversal of adrenaline-induced increase in azygos blood flow in patients with cirrhosis receiving propranolol.

In patients with cirrhosis, endogenous catecholamines may influence the circulatory effects of propranolol. We intended to evaluate the interaction of adrenaline and propranolol on azygos blood flow, an estimate of blood flow in the superior portosystemic collateral circulation. We investigated 6 patients with cirrhosis, 5 with good liver function, receiving an intravenous infusion of adrenaline (50 ng/kg/min) before and after administration of propranolol. The median value for baseline azygos blood flow was increased from 700 ml/min (range 340-1 470 ml/min) to 1 050 (range 570-1 840 ml/min) with adrenaline alone (P less than 0.05), and decreased to 610 ml/min (range 260-1 190 ml/min) with propranolol alone (P less than 0.05). The infusion of adrenaline given after propranolol further reduced azygos blood flow to a median value of 530 ml/min (range 200-730 ml/min) (P less than 0.05). Thus, following beta-adrenergic blockade, there is a reversal of the effects of adrenaline on azygos blood flow, which corresponds to a potentiation of the effects of propranolol. Similar endogenous adrenaline-propranolol interactions may play a role in preventing recurrent variceal bleeding in cirrhotic patients.

Adult↗
PubMed1987

Failure of haemodynamic measurements to predict recurrent gastrointestinal bleeding in cirrhotic patients receiving propranolol.

In an attempt to identify the haemodynamic factors predicting the recurrence of gastrointestinal bleeding in cirrhotic patients receiving propranolol, haemodynamic measurements were prospectively collected. Systemic and splanchnic haemodynamics were assessed before propranolol administration. Among 77 patients receiving propranolol, 24 re-bled and 53 did not re-bleed in a follow-up period of 30-730 days (median 540). There was no difference between patients with and without recurrent bleeding with regard to the initial value of heart rate, mean arterial pressure, cardiac index, and hepatic venous pressure gradient. A subgroup of 43 patients was further investigated for the haemodynamic response to one single dose of 40 mg of propranolol. No difference was observed in the propranolol-induced changes of heart rate, mean arterial pressure, cardiac index or hepatic venous pressure gradient, between patients with (n = 14) and those without (n = 29) recurrent bleeding while taking propranolol. In conclusion, systemic haemodynamics and hepatic venous pressure gradient have no predictive value in evaluating the risk of recurrent bleeding in cirrhotic patients receiving propranolol. Furthermore, therapeutic efficacy of propranolol cannot be predicted from the haemodynamic response to a single first dose of this substance.

Adult↗
PubMed1987

Cholangitis in the acquired immunodeficiency syndrome: report of two cases and review of the literature.

We report the cases of one patient with the acquired immunodeficiency syndrome as a result of human immunodeficiency virus type 1/lymphadenopathy associated virus type 1/human T-cell lymphotrophic virus type III (HIV-1/LAV-1/HTLV-III) infection and of another patient with AIDS related complex caused by human immunodeficiency virus type 2/lymphadenopathy associated virus type 2 (HIV-2/LAV-2) infection, who were suffering from cholangitis. The manifestations and possible mechanisms for cholangitis in these patients and in 10 previously reported similar cases are reviewed.

Acquired Immunodeficiency Syndrome↗
PubMed1987

Hepatic sarcoidosis with portal hypertension. A report of seven cases with a review of the literature.

We have reviewed the clinical, histological and hemodynamic features of sarcoidosis complicated by portal hypertension in seven patients and in 40 previously reported cases. Young black patients of either sex and white females over 40 years were selectively affected. In 12 of these 47 patients, portal hypertension appeared to be a consequence of cirrhosis due to longstanding intrahepatic cholestasis; in white patients, this condition was clinically, histologically, and serologically indistinguishable from primary biliary cirrhosis. In most of the other patients, portal hypertension was the predominant and often the presenting symptom of hepatic sarcoidosis; in these patients portal hypertension was due to a presinusoidal block probably determined by portal granulomas, with or without superimposed sinusoidal block determined by fibrosis. Corticosteroids did not prevent the development of portal hypertension.

Adult↗
PubMed1987

[Dynamic study of plasma and urine amino acid patterns after an oral load of tryptophan. Application to a patient with a complex deficiency syndrome].

The aim of this work was to show that the dynamic study of the amino acid pattern in plasma and urine following an oral load of tryptophan might confirm anomalies suggested by inconsistent clinical data and below-normal biological values. Such oral loads were administered to five control subjects and one patient who had recovered from a celiac condition but was suffering from a complex deficiency syndrome associating a polyneuritis due to a lack of folic acid and the excretion of blue-colored transpiration. Thirty minutes following the load a slowing in the rate of tryptophan absorption was observed (p less than 0.05) and, during the first 6 hours, increased urinary excretion of tryptophan (p less than 0.01) and indican (p less than 0.05). Similarly, changes in the metabolism of other amino acids were either revealed or accentuated by this oral load test (ornithine, glycine, lysine, phenylalanine). It is probable that in this patient a problem of tubular re-absorption led to tryptophan being less available for metabolization along the kynurenine pathway, accounting for the increase in urinary excretion of the amino acids concerned. The diagnosis put forward is that of an unexpressed form of Hartnup's disease in association with a folic acid deficiency.

Adult↗
PubMed1987

Hepatic vein thrombosis in paroxysmal nocturnal hemoglobinuria. A spectrum from asymptomatic occlusion of hepatic venules to fatal Budd-Chiari syndrome.

In a series of 40 patients with Budd-Chiari syndrome, 5 (12%) were found to be afflicted with paroxysmal nocturnal hemoglobinuria. The clinico-pathological features in these 5 patients and in 26 well-documented previously reported cases could be ascribed to three groups of increasing severity: thrombosis limited to small-sized hepatic veins with no or transient ascites, partial thrombosis of large-sized hepatic veins with chronic ascites, and complete thrombosis of large-sized hepatic veins with a life-threatening course. These three groups did not differ with regard to sex, age, and duration and characteristics of paroxysmal nocturnal hemoglobinuria. In view of the relationship between prognosis and the extent of hepatic vein obstruction, we suggest that early therapy directed toward limiting the extension of thrombosis, or toward dissolving formed thrombi, should improve the prognosis of this severe complication of paroxysmal nocturnal hemoglobinuria.

Adult↗
PubMed1986

Risk of hepatic vein thrombosis in relation to recent use of oral contraceptives. A case-control study.

In a case-control study, we evaluated the relative risk of hepatic vein thrombosis among recent oral contraceptive users as compared with nonusers. Thirty-three cases of hepatic vein thrombosis affecting women aged 15-45 yr were collected between 1970 and 1983, and individually matched to 3 or 4 controls interviewed in 1982-1984. There were 18 recent oral contraceptive users among the 33 cases, and 44 recent oral contraceptive users among the 128 case-matched controls. The relative risk of hepatic vein thrombosis was 2.37 (95% confidence interval: 1.05-5.34, p less than 0.02). The relative risk of hepatic vein thrombosis is close to that of stroke, myocardial infarction, and venous thromboembolism among oral contraceptive users as compared with nonusers.

Adolescent↗
PubMed1986

Circulatory actions of vasopressin in anaesthetized rats with portal hypertension subjected to haemorrhage.

To assess the influence of vasopressin on splanchnic and renal circulatory changes induced by haemorrhage in portal hypertension, we studied 4 groups of 7 rats with chronic portal vein stenosis. Two groups received saline (C and H) and two groups vasopressin, 0.01 IU/kg/min (VP and VP-H). Ten minutes after starting drug infusion, group H and VP-H animals were allowed to bleed from the superior mesenteric vein. Both haemorrhage and vasopressin alone, decreased portal venous tributary blood flow and pressure but their association was not additive (as reflected by comparable bleeding rate in groups H and VP-H). By contrast, vasopressin increased renal perfusion in bleeding and non-bleeding animals whereas haemorrhage alone decreased renal perfusion. These results indicate that the effects of vasopressin on the splanchnic circulation in bleeding anaesthetized animals differ from the effects observed when blood volume is normal. Therefore, in patients with cirrhosis the effects of vasopressin during bleeding might also differ from those observed in patients in stable condition.

Anesthesia↗
PubMed1986

Influence of the degree of liver failure on systemic and splanchnic haemodynamics and on response to propranolol in patients with cirrhosis.

Systemic and splanchnic haemodynamics were studied in patients with cirrhosis who had been classified in three groups (A, B, and C) according to the degree of liver failure (modified Pugh's classification). In patients of group A, cardiac index was significantly lower than that of group C and systemic vascular resistance was higher, but not significantly so, than that of patients with liver failure. Wedged hepatic venous pressure was significantly lower in the former group than in the latter. In patients in group B, corresponding values fell between those of groups A and C. Azygos blood flow averaged 0.477 +/- 0.242 l/min (mean +/- SD) in group A and it was significantly lower than in groups B and C (0.642 +/- 0.224 and 1.061 +/- 0.476 l/min, respectively). In the three groups, acute administration of propranolol induced statistically significant changes in systemic and splanchnic haemodynamics. In patients of group C but not of group B, the mean value of azygos blood flow after propranolol remained significantly higher than in group A. Moreover, the fraction of azygos blood flow to cardiac output decreased in groups A and B while slightly increased in group C. This study shows that in patients with cirrhosis, the degree of liver failure may be a determinant for the haemodynamic responses to drugs acting on portal hypertension.

Female↗
PubMed1986

Domperidone-induced increase in lower oesophageal sphincter pressure does not affect azygos blood flow in patients with cirrhosis.

An increase in lower oesophageal sphincter pressure induced by domperidone has previously been reported to decrease superior portosystemic collateral flow in patients with portal hypertension owing to cirrhosis. Although a 10-mg intravenous dose of domperidone was effective in increasing lower oesophageal sphincter tone in a group of six patients with cirrhosis, the same dose failed to affect azygos blood flow in a matched group of six patients. The results do not support the hypothesis that an increase in lower oesophageal sphincter tone can decrease flow through oesophageal varices in patients with cirrhosis.

Domperidone↗
PubMed1986

Role of portasystemic shunts in the hyperkinetic circulation of the portal hypertensive rat.

We evaluated the role of portasystemic shunts in the hyperkinetic circulatory state in rats with portal hypertension. Cardiac output and regional blood flow were measured by the radioactive microsphere technique in rats with portal hypertension caused by portal vein stenosis, in rats with end-to-side portacaval shunts, and in sham-operated rats. Cardiac output was significantly higher in rats with surgical shunts than in those of the two other groups and was significantly lower in sham-operated rats compared with portal hypertensive rats. Portal tributary blood flow and hepatic arterial blood flow expressed in absolute flow as well as in percentage of cardiac output were significantly increased in rats with surgical shunts compared with other groups. These blood flows were also significantly higher in portal hypertensive rats than in sham-operated animals. A significant correlation was found between cardiac output and portal tributary blood flow in rats with portal vein stenosis and in rats with surgical shunts; this correlation was absent in sham-operated rats. This study shows that the hyperkinetic circulatory state in rats with portal hypertension and a normal liver is related to the presence of portasystemic shunts but not to portal hypertension per se.

Animals↗
PubMed1985

Effect of propranolol on hepatic blood flow in patients with cirrhosis.

The effect of propranolol on systemic and hepatic hemodynamics was studied in patients with cirrhosis. One hour after 40 mg propranolol by mouth as well as during continuous oral dosing at doses that reduced heart rate 25%, cardiac output and the hepatic venous pressure gradient fell significantly, whereas arterial pressure and hepatic blood flow did not change significantly. In six patients with cirrhosis and surgical end-to-side portacaval shunts, cardiac output and the hepatic venous pressure gradient also decreased 15 minutes after intravenous propranolol (5 mg), whereas hepatic blood flow did not change significantly. In the patients with surgical shunts, systemic vascular resistance rose significantly but hepatic arterial vascular resistance fell. Our data show that in patients with cirrhosis, propranolol induces an increase in the fraction of cardiac output reaching the liver.

Administration, Oral↗