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Biomedical subjects

Y Israel

Publications and source records attributed to Y Israel.

At least 127 records · Page 7Linked to original sources
PubMed1980

Hepatic vein oxygenation, liver blood flow, and the rate of ethanol metabolism in recently abstinent alcoholic patients.

To determine whether hepatic hypoxia is associated with hepatocellular necrosis in alcoholics, oxygen tension in the hepatic vein and hepatic blood flow were determined in thirteen patients without overt clinical liver disease. Ethanol metabolic rate was also assayed as an index of liver metabolism. Hepatic blood flow and ethanol metabolic rate were also determined in six normal volunteers. According to liver histology patients were separated into two groups, with and without hepatocellular necrosis. Alcoholics with necrosis showed a higher (P less than 0.002) ethanol metabolic rate (4.05 +/- 0.23 mmol/kg/h) than those without necrosis (2.46 +/- 0.34). Hepatic blood flow in the total group of alcoholics was not significantly different from controls; in the group with necrosis it was lower (651.7 +/- 44.6 ml/min/m2) than in the group without necrosis (878.3 +/- 81.6; P less than 0.025). Hepatic vein pO2 was lower (P less than 0.01) in patients with hepatocellular necrosis (31.7 +/- 0.68 mmHg) than in patients without necrosis (35.7 +/- 0.99). In the whole group, a significant negative correlation (r = 0.76, P less than 0.003) was observed between hepatic vein pO2 and ethanol metabolic rate. Acute administration of ethanol (21.7 mmol/kg) did not alter hepatic blood flow in six normal individuals nor in five alcoholic patients, although an increase in hepatic vein pO2 was observed in the latter. The changes observed in hepatic vein pO2 functional hepatic blood flow, and ethanol metabolic rate which correlate with hepatocellular necrosis, may be of pathogenic importance in alcoholic liver disease.

Adult↗
PubMed1980

Identification of alcohol abuse: thoracic fractures on routine chest X-rays as indicators of alcoholism.

In a retrospective study, rib and thoracic vertebral fractures were found to be present on posteroanterior and lateral routine chest x-rays of 57 (28.9%) of 198 alcoholic male patients and in 4 (1.8%) of 218 nonalcoholic male control subjects. The magnitude of the increased prevalence (16-fold; p < 0.001) of rib and vertebral fractures in alcoholics suggest that routine chest x-rays should be useful in the identification of problem drinking and may be used, along with other indices, in population screening for alcoholism.

Adult↗
PubMed1980

Mitochondrial function following chronic ethanol treatment: effect of diet.

Rats were fed liquid diets containing 36% of the calories as ethanol either in a high fat, adequate protein or in a high protein, low fat diet, with pair-fed controls receiving an isocaloric amount of sucrose replacing ethanol. Liver mitochondria were isolated in a fatty acid free albumin containing medium. Mitochondrial respiration respiratory control and ADP/O ratios were measured either using a glutamate-malate mixture or succinate. In rats fed the high fat adequate protein diet chronic ethanol treatment resulted in a reduction in the respiratory rates in states 3 and 4 with both substrates. However, such changes did not occur in rats fed high protein low fat diets. Using the NAD-linked substrates, but not with succinate, the respiratory control ratio was significantly decreased following ethanol treatment with the high fat adequate protein but not the high protein low fat diet. ADP/O ratios were not affected by the ethanol treatment with either diet. Ethanol metabolism rate increased by 70% in rats treated with ethanol containing high protein low fat diets and by 50% with ethanol containing high fat adequate protein diets.

Alcoholism↗
PubMed1979

Serum triiodothyronine and other clinical and laboratory indices of alcoholic liver disease.

Admission serum triiodothyronine (T3) values in 124 patients hospitalized for alcoholic liver disease were correlated with clinical and laboratory indices of liver function and commonly used determinants of thyroid function. Patients with low admission serum T3 levels had significant alterations in serum albumin, bilirubin, prothrombin time, and alkaline phosphatase associated with clinical signs of portal hypertension and collateral circulation, with little difference in serum glutamic-oxaloacetic transaminase, serum gamma glutamyl transpeptidase, or serum ornithine carbamyl transferase. This group also had a significant decrease in free T3 index despite an increase in T3 uptake; the slight reduction in total thyroxine (T4) was associated with an increase in free T4 index and no change in serum thyrotropin (TSH). For patients with alcoholic liver disease, low admission serum T3 and free T3 index values when accompanied by normal serum T4, free T4 index, and TSH levels appear to be indicative of severe liver dysfunction and increased mortality risk.

Humans↗
PubMed1979

Effect of short-term therapy with propylthiouracil in patients with alcoholic liver disease.

The effect of propylthiouracil (PTU; 300 mg/day) on alcoholic liver disease was evaluated in 133 patients in a short-term randomized double-blind trial. Severity of the disease was assessed by a composite clinical and laboratory index (CCLI). A normalization rate (NR) representing the rate of improvement in CCLI was calculated. Patients with alcoholic hepatitis, with and without cirrhosis, showed a significantly higher NR on PTU (43.6 +/- 4.6) than on placebo (19.8 +/- 3.3; P less than 0.001). A similar effect was observed in patients with abnormal prothrombin (no biopsy): NR was 32.9 +/- 6.9 on PTU and 2.6 +/- 3.7 on placebo (P less than 0.005). The effect of PTU on each clinical and laboratory component of the CCLI was also compared in these two groups. In 38 patients with alcoholic hepatitis and in 25 with abnormal prothrombin, those on PTU showed a greater improvement in 15 of 15 items (P less than 0.001) and 14 of 15 (P less than 0.01), respectively. When patients were divided according to the severity of the disease into those in the lower and upper halves of the CCLI range (81 and 52 patients, respectively), PTU was shown to have a significant effect only in the latter: The NR was 41.4 +/- 3.8 on PTU and 22.5 +/- 4.2 on placebo (P less than 0.005). PTU was ineffective in patients with inactive cirrhosis.

Double-Blind Method↗
PubMed1979

Thyroid hormones in alcoholic liver disease. Effect of treatment with 6-n-propylthiouracil.

The relationship between alcoholic liver disease and circulating thyroid hormones was investigated in 124 hospitalized patients treated with placebo or propylthiouracil (PTU) for a maximum of 46 days in a double-blind study. Serum triiodothyronine (T3) levels on admission were significantly (P less than 10(-6) and inversely correlated with the severity of alcoholic liver disease. After hospitalization, changes in T3-levels in patients with low admission T3 significantly correlated (P less than 0.001) with the degree of spontaneous improvement of liver function (placebo group). Treatment with 300 mg of PTU daily (Orrego et al. Gastroenterology 76:105--115, 1979) markedly increased the rate of improvement in severely ill patients with low T3 on admission. In this group, serum T3-levels were also increased after PTU, but this increase did not correlate with the change in the patient's condition. It is suggested that the known inhibitory effect of PTU on peripheral deiodination of T4 to T3 is marked by a more marked improvement in liver function in this group. PTU treatment in this group reduced the free T4-index and increased TSH levels markedly (16%; P less than 0.02) toward levels found in hypothyroidism. PTU did not improve the condition of mildly ill patients with normal admission T3-levels, nor did it alter free T4-index or serum TSH levels in these patients. Serum T3-levels provide a sensitive indicator of the severity of alcoholic liver disease and of its response to conventional treatment. Serum T3-levels also distinguish between a group of patients, in whom low-dose PTU administration results in a beneficial effect, and another group, in whom no therapeutic effect of PTU is observed.

Humans↗
PubMed1977

Ethanol metabolism, oxygen availability and alcohol induced liver damage.

The rates of ethanol oxidation in various species are linked to the rates of general metabolism, and more specifically that of O2 utilization by the liver. After chronic ethanol administration, increased oxidation of ethanol is accompanied by increased total hepatic O2 utilization, as studied in the whole animal, the perfused liver, and isolated liver slices. The correlation is particularly striking in the spontaneously hypertensive rat. This linkage makes the liver of the chronically ethanol-consuming rat abnormally vulnerable to hypoxic damage. Exposure to 5% oxygen atmosphere for 6 hours produced major elevations of SGOT and SOCT activities and marked centrilobular necrosis, in alcohol-treated animals but not in controls. The same differential susceptibility was found to acute anemia produced by bleeding. The possible relation of these findings to alcoholic liver damage in humans is discussed.

Alcoholism↗
PubMed1976

Protection by propylthiouracil against carbon tetrachloride-induced liver damage.

Rats given a single intragastric dose of carbon tetrachloride (CCl4), 0.25, 0.50, or 1.0 ml per kg) showed a dose-dependent increase in SGOT, serum ornithine carbamyltransferase, and liver necrosis (graded histologically as 0 to 4+) 24 hr after the treatment. Daily intubation with propylthiouracil (PTU) for 10 days in doses of 5 to 50 mg per kg significantly reduced the elevation of SGOT activity, completely suppressed the serum ornithine carbamyltransferase changes, and reduced the degree of necrosis found 24 hr after the intragastric administration of CCl4. Similar protection was found when CCl4 was given intraperitoneally. When PTU was given in liguid diets for 6 days, protection against CCl4 was increased. PTU did not affect the absorption or covalent binding of 14CCl4 to lipids or proteins. Also, control and PTU-treated rats did not differ with respect to glucose-6-phosphatase activity and conjugated diene production after CCl4. Thus, it has been observed that PTU affords partial protection against some end-stage consequences of CCl4 liver injury such as cell necrosis and release of intracellular enzymes. However, PTU afforded no protection against early chemical effects such as covalent binding of CCl4 carbon, lipid peroxidation, or loss of glucose-6-phosphatase. Therefore, it is concluded that the mechanism of the PTU effect comes into play after the initial effects of CCl4 are exerted and in some unknown manner modulates the expression of these early effects.

Animals↗
PubMed1975

Experimental alcohol-induced hepatic necrosis: suppression by propylthiouracil.

We have previously reported that a hypermetabolic state, resembling that produced by thryoid hormones, exists in the livers of animals treated chronically with ethanol. We propose that this alteration produces a relative hypoxia in the centrilobular zone of the liver which, if severe enough, leads to cellular death and to the production of hepatitis. Rats consuming ethanol for 30 days, given with a nutritionally adequate diet, and exposed to reduced oxygen tensions for only 6 hr, developed histological and biochemical evidence of hepatocellular necrosis and inflammatory lesions confined to the centrilobular zone. The severity was proportional to the degree of hypoxia. Pair-fed (nonalcohol) controls showed no such lesions. Treatment of the animals with propylthiouracil for 3-10 days abolished the hypermetabolic state of the liver in ethanol-consuming animals, and drastically reduced the histological and biochemical effects of hypoxia in them. These findings may have implications for pathogenesis and treatment of alcoholic hepatitis in man.

Animals↗