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Biomedical subjects

J G Joly

Publications and source records attributed to J G Joly.

At least 37 records · Page 2Linked to original sources
PubMed1978

Alcohol induced changes of carbohydrate metabolism [author's transl].

It is evident that ethanol by itself or one of its metabolites produces alterations in transport, metabolism and disposition of carbohydrates. Ethanol acts via changes in the redox state of co-factors; e.g. ethanol-induced hypoglycemia is due, partly, to the inhibition of hepatic gluconeogenesis by ethanol as a consequence of the increased NADH2/NAD ratio in patients whose glycogen stores are already depleted. On the other hand, hyperglycemia has also been described in patients with alcoholism. Although its mechanism is still obscure, abnormal hormonal secretion of insulin, catecholamines and glucocorticoids has been incriminated. Finally, structural changes of the liver and pancreas such as cirrhosis and pancreatitis produced by chronic alcohol consumption should also be considered as pathogenetic factors in a variety of clinical states involving deranged carbohydrate metabolism.

Alcoholism↗
PubMed1977

Treatment of resistant ascites by continuous ultrafiltration--reinfusion of ascitic fluid.

Eight patients with diuretic-resistant ascites due to cirrhosis were treated by reinfusion of concentrated ascitic fluid. In 11 procedures, with a mean duration of 21.9 hours, weight loss averaged 14.8 kg. Complications during reinfusion included septicemia in 1 procedure, left-sided heart failure in 5, pyrexia in 7 and coagulation abnormalities in 10. Ascites recurred within 2 months after reinfusion in all but one patient. Although this technique is an efficient and inexpensive method of treatment of ascites, it does not appear indicated in patients with cirrhosis and resistant ascites in view of the possibly serious complications associated with reinfusion and the poor long-term results.

Aged↗
PubMed1977

Effects of chronic ethanol administration in the rat: relative dependency on dietary lipids. II. Paradoxical role of linoleate in the induction of hepatic drug-metabolizing enzymes in vitro.

The effect of chronic ethanol administration on the hepatic microsomal cytochrome P-450 content and activities of NADPH - cytochrome P-450 reductase (EC 1.6.2.4), benzphetamine demethylase, aniline hydroxylase (EC 1.14.14.1), and of the microsomal ethanoloxidizing system were studied in various dietary models. When ethanol was given with linoleate as the only source of dietary lipid, the ethanol induction of these parameters was greater with diets containing 2 or 5% of total calories as linoleate than with diets containing 10% of total calories as linoleate. By contrast, when ethanol was given with high fat (35% of total calories) diets, the ethanol induction of these same parameters was slightly greater when linoleate provided 10% of total calories than when it provided 3% of calories. The apparent effect of dietary linoleate on the induction, by ethanol, of microsomal drug-metabolizing enzymes is markedly different when linoleate is given as the only source of dietary lipid as opposed to when it is given with other dietary lipids. Thus, conclusions on the effect of ethanol on hepatic microsomal drug-biotransformation enzymes, drawn from studies with dietary models in which linoleate provides the only source of dietary lipid, connot be extended to dietary modles of more complex lipid composition. When given as the only source of lipid, 2% of total calories in linoleate appears optimal for basal activity and inductibility, by ethanol, of mixed-function oxidases.

Alcoholism↗
PubMed1976

Chronic carriers of hepatitis B antigen (HBsAg). Histological, biochemical, and immunological findings in 31 voluntary blood donors.

Among 289 HBsAg carriers detected by the Montreal Red Cross Blood Transfusion Service and seen by our group, 31 submitted voluntarily to liver biopsy. These 31 carriers have now been followed for 10-33 months (mean: 23) and all remained positive for HBsAg. 15 of these 31 subjects had lived in institutions during infancy or childhood and none were drug users. Histological examinations revealed 24 cases of chronic persistent hepatitis (CPH), 2 cases of chronic aggressive hepatitis, 2 with steatosis, and 3 with normal liver. On repeated determination, 16 of the 31 subjects had at least one elevated transaminase level. Transaminases levels could not be correlated with the histological diagnosis. 4 cases had positive antinuclear antibodies, all in the CPH group, a finding that could not be correlated with any clinical, biological, or histological findings. The search for other autoantibodies and the immunoglobulin determinations were totally unrewarding. Thus, it appears that chronic HBsAg carriers in Montreal voluntary blood donors often have chronic hepatitis, usually persistent, occasionally aggressive; liver biopsy still remains the most useful approach in the evaluation of these HBsAg carriers. The HBsAg-carrier state seems to be well tolerated, but further long-term studies are needed to understand the natural history of this condition.

Adolescent↗
PubMed1976

Idiopathic portal hypertension.

Idiopathic portal hypertension is reported in five cases including one case of chronic arsenical intake and one case of chronic industrial vinyl chloride exposure. In all five cases the patients presented with gastrointestinal bleeding as the chief complaint. Physical examination was within normal limits except for splenomegaly in all. Results of liver function tests were normal, except for the relative clearance of sulfobromophtalein. A surgical liver biopsy specimen was obtained in all cases and showed moderate degrees of portal fibrosis, but no cirrhosis. Combined umbilicoportal, hepatic vein and superior mesenteric artery catheterization was performed in all cases. Hepatoportographies showed distortion of the intrahepatic portal venous system and cut-off of small portal venules. Porto-hepatic gradients ranged from 14.0 to 20.5 mm Hg. The portal hypertension was both sinusoidal and presinusoidal in nature but mainly presinusoidal. Hepatic extraction of indocyanine green and of albumin microaggregates was normal, thereby suggesting normal functional portal blood supply to the liver. The patients with arsenical or vinyl chloride exposure could not be differentiated from the other three patients with idiopathic portal hypertension. These results suggest that idiopathic portal hypertension may be related to domestic or industrial exposure to other hepatotoxins.

Adult↗
PubMed1973

Effect of chronic ethanol feeding on hepatic microsomal glycerophosphate acyltransferase activity.

The activity and submicrosomal distribution of alpha-glycerophosphate acyltransferase (GPAT) were studied in rats fed ethanol for 6 wk. GPAT activity was also measured in rats after 10 days of alcohol feeding, 22 days of phenobarbital administration, or 24 days on a high fat (71% of total calories) diet. After 6 wk of ethanol feeding, GPAT activity was increased 73% when expressed per milligram of protein and 133% when expressed per 100 g of body weight (P < 0.005). GPAT activity was more abundant in the smooth than in the rough microsomes of both control and ethanol-fed rats when expressed per milligram of microsomal protein and when expressed per gram of liver; the smooth microsomes accounted for most of the increased GPAT activity after ethanol. 10 days of ethanol feeding or 22 days of phenobarbital administration did not increase GPAT activity. Feeding a high fat diet for 24 days increased GPAT activity per milligram of protein to an extent similar to that observed after chronic ethanol administration. When expressed per 100 g of body weight, however, the increase was much greater after ethanol. The significance of these findings in vivo has not been elucidated. Increased GPAT activity might contribute to the persistence of alcoholic fatty liver and the development of hyperlipemia.

Alcoholism↗
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↗