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Biomedical subjects

A Viallet

Publications and source records attributed to A Viallet.

At least 37 records · Page 2Linked to original sources
PubMed1976

Detection of surface and core antigens of hepatitis B virus in the liver of 164 human subjects. A study by immunoperoxidase and orcein staining.

The surface (HBsAg) and core (HBcAg) antigens of hepatitis B virus (HBV) have been searched by optic microscopy in the liver specimens from patients hospitalized for various conditions and from 38 HGsAg chronic carriers. The study was done blindly using Shikata et al.'s orcein staining on fixed and frozen material and direct immunoperoxidase on frozen material with antisera specific for surface (anti-HBs) and core (anti-HBc) antigens of HBV. No liver staining could be found in the 98 HBsAg seronegative patients. Among the 28 HBsAg seropositive patients, only 3 showed positive staining: 1 patient with acute viral hepatitis showed nuclear staining with anti-HBc; 2 patients with postnecrotic cirrhosis showed cytoplasmic staining with anti-HBs and/or orcein, and one of them also showed nuclear staining with anti-HBc. In contrast, among the 38 chronic carriers, 25 showed positive cytoplasmic staining with anti-HBs and/or orcein, while one of them (with chronic aggressive hepatitis) also showed nuclear staining with anti-HBc. Anti-HBs and orcein staining are equally sensitive and specific for the detection of HBsAg in hepatocytes; discrepant results can be attributed to sampling error of distribution of HBsAg in small liver fragments.

Hepatitis B Antigens↗
PubMed1975

Hepatitis B antigen in Montréal blood donors: childhood institutionalization as an epidemiologic factor.

In 1971 the Canadian Red Cross blood tranfusion service instituted routine screening for HBAg of all blood donors, using nationwide a standardized counterimmunoelectrophoretic technique. The prevalence of carriers in the Province of Québec is unusually high (0.51%), being 3 to 12 times higher than in the other nine provinces. Among the carriers found in the Montréal area 289 volunteered to be seen by our group for an extensive interview and a series of laboratory tests. There were 243 men and 46 women; their ages ranged from 18 to 55, 90% being less than 40. Twenty-nine were of foreign origin and 260 were born in Canada. The epidemiologic data revealed that the reservoir of HBAg carriers among the blood donors of the Montréal area was found predominantly in the autochthonous population of French origin. Moreover, it appeared that 149 (52%) had lived in institution when they were infants or children: 127 were orphans and had been placed in institutions as newborns or babies, and 22 others had lived in institutions for at least 1 year between the ages of 5 and 10. This was by far the most important single epidemiologic factor that could contribute to the explanation of the abnormally high prevalence of HBAg carriers in the population studied.

Adolescent↗
PubMed1975

Hemodynamic evaluation of patients with intrahepatic portal hypertension. Relationship between bleeding varices and the portohepatic gradient.

Between January 1970 and December 1974, 389 patients presenting an upper gastrointestinal hemorrhage had an emergency fiberoptic esophagogastroscopy at the time of bleeding. In 103 cases, esophageal and/or gastric varices were visualized and in 46 of these cases, bleeding originiated from varices. Hemodynamic data was available in 19 cases of intrahepatic portal hypertension who had bled from varices. Combined hepatic and umbilicoportal catherterization was perform in 17 cases whereas only hepatic vein catherterization was possible in 2. The portohepatic gradient (FPVP-FHVP or WHVP-FHVP) was utilized as an index of portal hypertension. In the 19 patients studied, the portohepatic gradient ranged from 12 to 24.5 mm Hg with a mean of 18.4 mm Hg; only one patient had a portohepatic gradient of less than 14.5 mm Hg. The present data strongly suggest that in intrahepatic portal hypertension, bleeding varices are observed only if significant portal hypertension exists. Hemodynamic studies may thus be helpful in evaluating bleeding patients with varices particularly when the origin of the bleeding cannot be determined at endoscopy. The finding of a portohepatic gradient of less than 12 mm Hg would strongly suggest that varices were not the source of bleeding and in these cases, shunt surgery should not be considered.

Adult↗
PubMed1975

Noncirrhotic presinusoidal portal hypertension associated with chronic arsenical intoxication.

A 39-year-old male with bleeding esophageal varices due to portal hypertension was observed. The patient had taken an arsenical preparation during a period of 12 yr because of psoriasis and subsequently developed keratotic changes of the palms and soles of his feet and an epithelioma of the scrotum. Physical examination was unremarkable except for splenomegaly and skin lesions. Liver function tests were normal; a needle biopsy of the liver (right lobe) showed nonspecific changes. Combined hepatic and umbilicoportal catheterization revealed, on splenography and portography, huge esophageal varices and patent portal vein; dilation, distortion, and cut-off of many intrahepatic portal branches were found. A marked gradient existed between the free portal venous pressure (25 mm Hg) and the wedged hepatic venous pressure (9.5 mm Hg). Hepatic blood flow, portal PO2, cardiac output, cardiac index, and blOOD volume were within normal range. Arteriographies did not reveal arteriovenous shunts in the splanchnic or splenic vessels. A splenorenal shunt were performed and a wedged biopsy of the liver (left lobe) revealed nonspecific changes. Three years later the patient had not experienced any episode of hemorrhage or hepatic encephalopathy but developed an epithelioma of the tongue. No known cause could be incriminated in the pathogenesis of the portal hypertension. However, there was unequivocal chronic arsenic intoxication. Toxic hepatitis, cirrhosis, noncirrhotic portal hypertension, and hemangiosarcoma of the liver have been reported with the intake of arsenicals. Thus, it is suggested that in this patient, presinusoidal portal hypertension was secondary to chronic arsenical intake associated with marked intrahepatic vascular changes seen on portography.

Adult↗
PubMed1975

Combined hepatic vein, umbilicoportal vein, and superior mesenteric artery catheterization in portal hypertension: estimation of the portal fraction of total hepatic blood flow in cirrhotic patients.

Hemodynamic data were obtained in 13 cirrhotic patients with severe portal hypertension, undergoing combined hepatic vein, umbilicoportal vein, and superior mesenteric artery catheterization. The relative clearance of indocyanine green, the portohepatic gradient (difference between the free portal venous pressure and the free hepatic venous pressure), and the estimated hepatic blood flow were measured. The portal fraction (PF) of total hepatic blood flow was calculated in all patients using indicator dilution curves obtained from the portal bifurcation, a right hepatic vein, and when possible a left hepatic vein (six cases) after injection of (51)Cr-labeled red blood cells ((51)Cr RBC) into the superior mesenteric artery. Flows were overestimated because of loss of indicator through spontaneous portosystemic shunts; however, the ratio between hepatic and portal indicator dilution curves can be used to calculate the portal fraction of total hepatic blood flow since no extrahepatic shunts existed after the bifurcation of the portal vein (as shown on portography). In 10 patients, 15 series of curves were calculable and the PF varied between 30.1 and 100% (mean ± SE: 71.1 ± 6.2%). In the three other patients, only delayed activity from recirculation was detected from portal and hepatic vein samples and PF was 0%; in these three cases, portography and arteriography revealed spontaneous portacaval shunting with reverse and/or stagnant circulation in the portal vein. In the 13 patients, no correlation existed between PF and the relative clearance of indocyanine green or the portohepatic gradient, parameters generally used as indices of severity in cirrhosis. In 10 patients, no correlation was found between PF and the estimated hepatic blood flow.These data indicate that (51)Cr RBC dilution curves can be used for the estimation of the portal fraction of total hepatic blood flow in conscious cirrhotic patients before portacaval shunts. Using this methodology, it could be assessed whether any critical level of portal fraction exists above which poor clinical results occur after portacaval shunting. This measurement could eventually be helpful in determining the appropriate surgical procedure to be applied in individual cases.

Adult↗
PubMed1975

Portal and systemic effects of selective infusion of vasopressin into the superior mesenteric artery in cirrhotic patients.

Selective infusion of vasopressin (0.2 U per min) was performed in 8 cirrhotic patients with portal hypertension who underwent umbilicoportal catheterization. There was a significantly decreased (9.6%) of the free portal venous pressure from 27.0 plus or minus 1.4 mm Hg to 24.4 plus or minus 1.4 mm Hg. In all patients, the portal PO2 significantly decreased with a mean fall of 18.8%. However, in all patients, significant systemic effects were noted: an increase in arterial blood pressure and a decrease in the arterial PO2. In 3 patients, a marked fall of the cardiac output (greater than 2.0 liters per min) was recorded during the selective infusion of vasopressin. It is concluded that if selective infusion of vasopressin into the superior mesenteric artery is efficacious in the control of bleeding varices, the therapeutic effect cannot be totally explained by the lowering of the portal venous pressure in cirrhotic patients with portal hypertension. The risk of vascular thrombosis, the decreased portal PO2, and the systemic effects have to be considered when this approach is used in cirrhotic patients with ruptured esophageal and/or gastric varices.

Blood Pressure↗
PubMed1973

Detection of Australia antigen in liver biopsies by immunofluorescence.

A search for Australia antigen (AuAg) was made by immunofluorescence in 105 liver biopsies obtained from the same number of patients. No specific fluorescence was observed in 38 cases of acute viral hepatitis (19 of them seropositive for AuAg) or in 55 seronegative patients with various liver disorders or in 8 seronegative patients with histologically normal livers. However, specific fluorescence was seen in two cases: in the single case of chronic aggressive hepatitis seropositive for AuAg and in one of three cases of chronic persistent hepatitis with AuAg-positive sera. The fluorescence observed was mainly intranuclear when cellular suspensions were used, but cytoplasmic fluorescence was more prominent when observations were made on cryostat sections. The finding of AuAg by immunofluorescence in liver cells in chronic but not in acute forms of hepatitis seropositive for AuAg is consistent with the hypothesis of an important role of cellular immunity directed against infected cells in the pathogenesis of viral hepatitis.

Acute Disease↗
PubMed1971

Bleeding from esophageal varices in cirrhosis of the liver. Hemodynamic and radiological criteria for the selection of potential bleeders through hepatic and umbilicoportal catheterization studies.

Combined hepatic and umbilicoportal catheterization was performed in 38 compensated cirrhotics. Portohepatography with opacification of the coronary vein was obtained in all cases. The free portal venous pressure (FPVP) and the wedged (WHVP) and free (FHVP) hepatic venous pressures were recorded. The portohepatic gradient (FPVP-FHVP) was used as an index of portal hypertension. The coronary vein was separately re-evaluated for varices and graded as 1+ to 4+.Eighteen patients had varices graded as 3+ or 4+ (Group A) and all had a portohepatic gradient of 10 mm. Hg or more. The other 20 cirrhotics (Group B) had varices graded as 1+ or 2+ and 15 had a portohepatic gradient of less than 10 mm. Hg. The difference between gradients of Group A and Group B was highly significant.Of the 38 cirrhotics studied, eight had bled from varices and all are included in Group A. There is no significant difference between the gradients of both bleeders and non-bleeders of Group A.There is a significant correlation between the presence of large varices with a portohepatic gradient of 10 mm. Hg or more and a high risk of variceal bleeding. The radiological and hemodynamic data obtained by combined hepatic and umbilicoportal catheterization in cirrhosis of the liver can be of significant help in the selection of potential bleeders.

Adult↗