Biomedical subjects
Publications and source records attributed to D Lebrec.
We report the case of a patient with transient hypertension in relation to acute veno-occlusive disease of the liver. Ascites and esophageal varices, both transient, occurred in this patient and a transient elevation of the gradient between wedged and free hepatic venous pressures was observed.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Continuous, oral administration of propranolol at doses which reduced the heart-rate by 25% produced a sustained decrease in portal venous pressure in cirrhotic patients with portal hypertension. This effect of propranolol might be useful in preventing recurrent bleeding due to ruptured oesophageal varices in patients with portal hypertension.
Explore the source record for details and available documents.
A procedure for catheterization of a right hepatic vein is described in the rat. The procedure is based on the observation that, when the posterior half of the body is bent to the left, a right hepatic vein is aligned with the axis of anterior vena cava and posterior vena cava. A catheter, inserted in the right jugular vein and fitted with a rectilinear mandrel, is guided into the right auricle, the suprahepatic segment of posterior vena cava and a right hepatic vein. Successful catheterization of a right hepatic vein has been obtained in 47 out of 50 animals in which the procedure has been performed.
The gradient between wedged and free hepatic venous pressures were measured in 10 unselected adult patients suffering from fulminant viral hepatitis. The gradient was increased in all the studied patients, ranging from 0.9 to 2.1 kPa; this finding indicates that portal hypertension was present in all these cases. Ascites was present in all the five patients having a gradient about 1.5 kPa and affected only two of the five patients having a gradient below 1.5 kPa; this observation suggests that portal hypertension plays a role in the mechanism of ascites in fulminant viral hepatitis. Portal hypertension in fulminant viral hepatitis is likely to be the consequence of an intrahepatic block due to massive necrosis of the liver cells.
We studied the relationship between the degree of portal hypertension measured by the gradient between wedged and free hepatic venous pressures, the size of esophageal varices, and the risk of gastrointestinal bleeding in a series of 100 unselected patients with alcoholic cirrhosis. The degree of portal hypertension was not different in patients with no visible, in those with small-sized, and in those with large-sized, esophageal varices. The degree of portal hypertension was not different in patients without and with gastrointestinal bleeding, whether the source of hemorrhage was ruptured varices or acute gastric erosions. The risk of gastrointestinal bleeding, whether due to ruptured varices or acute gastric erosions, was significantly higher in patients with large-sized, than in those with no visible or small-sized, esophageal varices. It is concluded that, in patients with alcoholic cirrhosis, (a) the degree of portal hypertension has no predictive value for the risk of gastrointestinal bleeding and (b) large-sized esophageal varices are associated with a high risk of occurrence or recurrence of gastrointestinal bleeding and could be taken into account for a better selection of patients for portacaval shunt.
The authors report the case of a patient suffering from ulcerative colitis, who had several episodes of digestive hemorrhage due to portal hypertension. Portal hypertension was secondary to chronic portal vein thrombosis. This diagnosis was made on the venous phase of celiac and mesenteric angiography. The authors review the published cases of ulcerative colitis with portal vein thrombosis and discuss the possible etiologic factors: hypercoagulability, thrombocytosis, and intraabdominal sepsis.
In order to perform a quantification of the hepatic RES function, a mathematical model of the colloids phagocytosis was constructed and validated in normal and partially hepatectomised rats. The experimental design consisted of the collection of successive blood samples for the measurement of radiocolloids time courses after the injection of different doses of gelatin colloids (0.075--5 mg of gelatin/100 g body wt). The unknown parameters were estimated by method of maximum likelihood using a second order algorithm. A good fit between experimental and simulated data was obtained for a large range of injected doses using a single set of parameters. Comparisons of parameters values between normal and hepatectomised rats were found to be -onsistent with the hepatectomy ratio. This computerised estimation of parameters provides a determination of both the total number of Kupffer cells and the mean time of a complete phagocytosis cycle which cannot be obtained by classical approaches.
We report the cases of two renal transplant recipients suffering from idopathic portal hypertension, a condition characterised by increased portal venous pressure in the absence of both histological lesion of the liver and obstruction of the portal vein. In these two patients, perisnusoidal fibrosis, invisible by light microscopy, was demonstrated by electron microscopy; it is suggested that partial obstruction of hepatic sinusoids by perisinusoidal fibrosis could be the mechanism for increased portal venous pressure in all the patients with idiopathic portal hypertension. In these two patients, who received 6-mercaptopurine and azathioprine, perisinusoidal fibrosis might be the consequence of prolonged administration of these drugs.
We report 9 patients with pulmonary hypertension complicating portal hypertension. The cause of portal hypertension was cirrhosis in 7 patients, nodular regenerative hyperplasia of the liver in 1, and portal vein obstruction in 1. Six patients had been treated by portal-systemic shunting before the clinical onset of pulmonary hypertension. The interval between the first manifestation of portal hypertension and the recognition of pulmonary hypertension ranged from 2 to 15 years. Histologic examination in 1 of these patients revealed medial hypertrophy, concentric intimal proliferation, and plexiform lesions affecting the small pulmonary arteries. Pulmonary hypertension might result from the effect of a vasoconstrictive agent on the small pulmonary arteries or of a substance toxic to the walls of these vessels that is produced in the splanchnic territory, destroyed by the liver in normal subjects, and reaches the pulmonary arteries through portal-systemic shunts in these patients.
Splanchnic and systemic hemodynamic observations in eight patients with cirrhosis and refractory ascites were compared to those of 25 patients with cirrhosis and responsive ascites. The refractory ascitic group was characterized by less portasystemic shunting from both the superior mesenteric and splenic vascular beds, a lower cardiac output, a higher systemic vascular resistance, a wider arterial-hepatic venous oxygen difference, and a tendency for a lower HBF and higher postsinusoidal resistance. Portal pressures assessed from hepatic vein catheterization were similar in the two groups. The absence of a well-developed portasystemic collateral bed in patients with refractory ascites could in part be caused by the tense ascites but could also be an important factor in the mechanism of refractory ascites.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Transvenous (transjugular) liver biopsy consists in taking a liver specimen through a needle introduced into the liver parenchyma from the lumen of a hepatic vein. This procedure was attempted 104 times in 98 patients in whom percutaneous needle liver biopsy was contraindicated because of massive ascites and/or bleeding tendency. A liver specimen was obtained in 100 out of these 104 attempts; the tissue specimens were unfragmented and large enough to allow correct evaluation of liver architecture in 57 biopsies. The procedure was followed by no or only minor complications in all out patients except one who suffered a fatal intraperitoneal hemorrhage in relation to perforation of liver capsule; perforation was due to an excessive front rotation applied to the needle, a maneuver which therefore must be avoided. It is concluded that transvenous liver biopsy is a workable, efficient, and acceptably safe procedure for obtaining liver specimens in patients with massive ascites and/or bleeding tendency.
Serum somatomedin (SM) activity, measured as sulphation factor on chick embryo cartilage, and growth hormone (GH) levels were measured in peripheral, hepatic and renal veins of 23 patients with a alcoholic cirrhosis. SM activity (mean +/- SEM) was 0.65 +/- 0.05 U/ml in peripheral vein, 0.59 +/- 0.04 U/ml in hepatic vein, and 0.74 +/- 0.07 U/ml in renal vein. Mean GH levels were respectively 2.8, 2.5 and 3.1 ng/ml. Compared to peripheral vein, SM increase in renal vein was 19% (P less than 0.05). Serum SM activity was significantly lower in 13 patients with alcoholic hepatitis associated with cirrhosis than in other 10 patients (P less than 0.02 in hepatic blood and P less than 0.05 in peripheral blood). The decrease of SM activity seems related to cytolysis and hepato-cellular insufficiency. At last, in patients with alcoholic hepatitis, SM activity was lower in the hepatic vein than in the peripheral vein (P less than 0.05). The cause of this difference remains under discussion, no SM inhibitors being found in the serum samples used in this study.