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Biomedical subjects

F A Oski

Publications and source records attributed to F A Oski.

At least 91 records · Page 5Linked to original sources

Vitamin E deficiency and enhanced platelet function: reversal following E supplementation.

Marked platelet hyperaggregability to adenosine diphosphate, epinephrine, and collagen was demonstrated in two children with vitamin E deficiency, with complete reversal following E supplementation. No clinical thrombotic tendency was observed during the E-deficient state. The action of vitamin E in the schema of platelet arachidonate peroxidation appears to be at the step of phosphilpase A activation, or the conversion of arachidonic acid into the cyclic endoperoxides, since the peroxidation product malonaldehyde was increased during the E-deficient state with normalization following E sufficiency.

Adenosine Diphosphate↗

Metabolism and physiologic roles of vitamin E.

Antioxidant effect of vitamin E averts hemolytic anemia in low-birthweight infants fed formula rich in polyunsaturated fatty acids and iron. Tocopherol supplementation has also been shown to decrease the incidence and severity of retrolental fibroplasia and the development of bronchopulmonary dysplasia. Although the vitamin lowers platelet hyperaggregability, its role as an antithrombotic agent is still unclear.

Anemia, Hemolytic, Congenital↗

Vitamin E and neonatal hemolysis.

A study was designed to determine if the presence of vitamin E deficiency during the first week of life played a contributory role in the shortened red cell life span observed in the premature infant. Carboxyhemoglobin values were used as an index of hemolysis. Ten infants received vitamin E administered intramuscularly in a total dose of 125 mg/kg during days 3 to 7 of life; ten infants served as controls. The mean percent carboxyhemoglobin level fell significantly from day 3 to day 8 in the treated group (1.08% to 0.78%) whereas the mean value remained unchanged at 0.96% in the control group. The administration of vitamin E appears to reduce but not eliminate the accelerated red cell destruction that characterizes the preterm infant. Pediatrics, 59:995-997, 1677, VITAMIN E, HEMOLYSIS, PREMATURE INFANT, CARBOXYHEMOGLOBIN.

Apgar Score↗

Iron absorption from human milk, simulated human milk, and proprietary formulas.

Studies from our laboratory have shown that iron is better absorbed from human milk than from cow milk and that human milk can provide insufficient iron for infants during their first year. We compared iron availability from human milk with that from other formulas and determined the factors responsible for its superiority. Adults were fed 100 ml of human milk, simulated human milk, simulated human milk containing added lactoferrin, two commercial formulas containing iron, 12 mg/qt, and human milk that had been boiled. The simulated human milk resembled human milk in concentration of protein, fat, carbohydrate, iron, total minerals, calcium, and phosphorus. Iron 59 was added to each feeding and iron incorporation into RBCs was determined 14 days after each feeding. Percent iron absorption was highest from human milk and lowest from the commercial formulas. The simulated human milk supported a 9.0% absorption; addition of lactoferrin reduced this to 4.7%. Net iron absorption was 0.12 mg/liter from human milk and 0.40 and 0.37 mg/liter from the iron-enriched commercial formulas. Absorption of iron from boiled human milk was the same as from the unboiled milk. This study confirms the unique ability of human milk to promote iron absorption. Simple manipulation of the protein, fat, lactose, calcium, phosphorus, or lactoferrin content of proprietary milk did not reproduce the iron absorption demonstrated with human milk.

Adult↗

The role of exchange transfusion in the management of low-birth-weight infants with and without severe respiratory distress syndrome. I. Initial observations.

Exchange transfusions within the first 8 hours of life, as an adjunct to conventional therapy, were evaluated in two groups of infants: (1) infants with birth weights of less than 1,250 gm without severe respiratory distress and (2) infants of any birth weight with evidence of severe respiratory distress syndrome. A total of 63 infants were studied in Group 1. Infants who received an exchange transfusion had a survival rate of 86% as contrasted with a survival rate of 57% in the control group (p less than 0.01). A total of 82 infants were studied in Group 2. Infants who received an exchange transfusion had a 59% survival rate as compared with a 39% survival rate for the control group (p less than 0.04). The mechanism by which early exchange transfusion improves survival rate is unknown.

Birth Weight↗

The role of exchange transfusions in the management of low-birth-weight infants with and without severe respiratory distress syndrome. II. Further observations and studies of mechanisms of action.

Exchange transfusion, as a form of therapy, was contrasted with the use of fresh frozen plasma or conventional supportive care alone in the management of 19 infants with birth weights of less than 1,000 gm, without severe respiratory distress, and in the management of 82 infants, birth weights less than 2,000 gm, with severe respiratory distress whose disease manifested itself within the first 24 hours of life. Survival for more than five days was similar, regardless of therapy, in infants weighing less than 1,000 gm without severe RDS. In contrast, the use of exchange transfusion significantly decreased the case fatality rate of infants with severe RDS. In the groups receiving exchange transfusion, the mortality rate was 41%, whereas the groups receiving either plasma or supportive care alone the mortality was 80%. Study of coagulation factors and red cell concentrations of fetal hemoglobin and of 2,3-DPG failed to demonstrate any relationship between either improvement in coagulation or oxygen unloading and the improved survival of infants receiving exchange transfusion. Following exchange transfusion there was a significant decrease in the ratio of FIO2 to PaO2, suggesting that pulmonary perfusion and/or ventilation was improved by the procedure.

Acidosis, Respiratory↗

Malabsorption of iron in children with iron deficiency.

Inability to absorb oral iron is believed to be an extremely rare cause of therapeutic failure in the treatment of iron deficiency anemia. Six patients who had failed to respond to oral iron therapy were studied by a simple oral absorption test and contrasted with 25 patients with untreated iron deficiency anemia and 10 normal subjects. All six of the patients who were therapeutic failures demonstrated impaired iron absorption in the absence of other clinical evidence of gastrointestinal disease. In the 25 newly diagnosed patients with iron deficiency. 24 demonstrated elevated iron absorptions while 10 ironreplete normal subjects had minimal elevations in their serum iron values following the administration of the test dose of 1 mg of elemental iron per kilogram. When the therapeutic failures were treated with parenteral iron, all had a therapeutic response. In addition, after treatment the impaired absorption of iron improved transiently. All children who absorbed iron readily responded to oral iron therapy.

Administration, Oral↗

Iron sufficiency in breast-fed infants and the availability of iron from human milk.

Four infants were studied who had been exclusively breast-fed for periods varying from 8 to 18 months. All had grown sufficiently to have exhausted their prenatally acquired iron endowment with respect to meeting current needs for maintaining normal hemoglobin levels. All infants had normal hemoglobin values and normal serum iron values. Studies of iron absorption from breast milk and cow's milk were performed in ten normal adults. The absorption of iron from the human milk was significantly higher. These findings suggest that the iron present in human milk is sufficient to meet the iron requirements of the exclusively breast-fed infant until he approximately triples his birthweight.

Adult↗

A simple nonradioisotope technic for the determination of platelet life-span.

Acetylsalicylic acid was shown both in vivo and in vitro to prevent the platelet lipid peroxidation normally induced by the aggregating agents thrombin and epinephrine, and the sulfhydryl inhibitor N-ethylmaleimide. After aspirin ingestion, there was a significant reduction (p smaller than 0.005) in platelet lipid peroxidation, with a gradual return to base-line values over a 10-day period. With these values, a normal platelet survival curve was constructed with a mean half-life of 4.4 days (range of 2.9 to 5.9 days). These values agree with the standard 51-Cr survivals in three patients with chronic idiopathic thrombocytopenic purpura. Half-lives of 1.0, 2.5, and 4.1 days by lipid peroxide technic compared with 1.9, 2.5, and 3.9 days by the concurrent use of 51-Cr. Thus, the technic may be used to measure platelet survival.

Aspirin↗

Role of dietary iron and fat on vitamin E deficiency anemia of infancy.

Thirty-five infants weighing less than 1500 g at birth were fed four commercial formulas (A-D) varying in polyunsaturated fatty acid composition (32 per cent linoleic acid in A and B and 12 per cent linoleic acid in C and D) and in iron content (smaller than 1.0 in A and B; 12 to 12 mg per liter in B and D). Infants receiving formula B showed significantly lower hemoglobins (p smaller than 0.01) and higher reticulocyte counts (p smaller than 0.005) than infants fed the other three formulas. Infants receiving the two formulas with higher concentrations of unsaturated fatty acids (A and B) showed significantly greater hydrogen-peroxide-induced hemolysis (p smaller than 0.001) than those given diets containing lower amounts. Infants in groups A and B also had lower serum tocopherol concentrations. Infant red-cell membranes are altered by the increased amounts of polyunsaturated fatty acids and iron in the diet. It appears that the development of vitamin E deficiency anemia occurs in infants receiving iron supplementation.

Anemia, Hemolytic↗

Impact of a system of computer-assisted diagnosis. Initial evaluation of the hospitalized patient.

Computer assisted diagnosis was evaluated for its ability to hasten the time to initial diagnosis and reduce laboratory studies. The time to diagnosis averaged 2.8 days for a control group and 1.9 days for the group in which the computer printout was made available. In a small group in whom the diagnosis was not established until after 48 hours, there was a further trend to reduction in number of days to diagnosis and irrelevant laboratory studies. The ability of the computer to include the final diagnosis in the initial list of differential diagnoses remained unchanged for patients whose conditions were diagnosed before or after 48 hours, while the physicians' ability decreased. In a university hospital setting, computer-assisted diagnosis may be most beneficial for patients whose conditions have not been diagnosed within 48 hours of admission.

Child↗