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Biomedical subjects

L Aledort

Publications and source records attributed to L Aledort.

32 records · Page 2Linked to original sources
PubMed1987

Assessment for evidence of non A-non B hepatitis in patients given n-heptane-suspended heat-treated clotting factor concentrates.

Nineteen patients, (2 adults, 17 children) with inherited bleeding disorders were infused with n-heptane-suspended-heated clotting factor concentrates. Twelve of the nineteen were previously untreated. Six patients were infused with Profilnine Heat-Treated and 13 with Profilate Heat-Treated. Five separate centers participated and were given various lots of concentrates for use. Blood from the seventeen children was sampled prior to entry, at infusion, 2 weeks, 6 weeks, 12 weeks and 6 months after the first infusion. The two adults were sampled every 2 weeks. Twelve of the 19 patients were followed beyond six months. Three patients demonstrated a rise in ALT during the first six months of observation with levels above 2.5 times the upper limit of normal. One of these patients showed a parallel increment in a-CMV IgM titer and a second patient, an adult, had previously received many units of single donor blood components. During the second 6 month observation interval, two patients showed a rise in ALT. One of these patients had been exposed to only one lot of concentrate with no other viral cause being determined. Two additional patients had a moderate increase in ALT up to 98 U/L (normal less than 50). No patients were clinically ill or showed jaundice during these episodes. The hepatitis episode at 11 months in the patient using one lot of concentrate, might suggest a non-viral mechanism in this instance. This study indicates that these concentrates may be associated with episodes of ALT above 2.5 times the upper limit of normal in approximately 20% of the patients treated, but the etiology of the raised ALT may not always be Non A-Non B hepatitis.

Adult↗
PubMed1986

HTLV-III/LAV antibody and immune status of household contacts and sexual partners of persons with hemophilia.

We evaluated the human T-cell lymphotropic virus type III/lymphadenopathy-associated virus (HTLV-III/LAV) antibody and immune status of 88 persons living with and/or sexual partners of 43 hemophiliacs, 12 of whom had AIDS, five of whom had AIDS-related complex (ARC), 17 of whom were clinically well but HTLV-III/LAV antibody positive, and nine of whom were well and HTLV-III/LAV antibody negative. No nonhemophilic household contacts (0/50) of healthy hemophiliacs were HTLV-III/LAV antibody positive; two of 33 nonhemophilic AIDS/ARC contacts were positive. One was a spouse and one a sexual partner of a hemophiliac. One of these antibody-positive contacts herself had AIDS, and one had ARC. Antibody-negative, nonhemophilic contacts of AIDS/ARC and of antibody-positive hemophiliacs had significantly lower numbers of lymphocytes, T helper lymphocytes, and T suppressor lymphocytes than did contacts of antibody-negative hemophiliacs. We conclude that risk of HTLV-III/LAV transmission may exist for spouses and/or sexual contacts of hemophiliacs with AIDS/ARC, but we cannot now determine the risk for contacts of asymptomatic hemophiliacs.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Immune status of blood product recipients.

Persons with hemophilia are at risk of the acquired immunodeficiency syndrome (AIDS), and clinically asymptomatic hemophiliacs have shown a high incidence of AIDS-like immune abnormalities, facts leading to speculation that many hemophiliacs have been exposed to the AIDS agent through their blood products. We therefore evaluated the immune status of three groups of blood product recipients without AIDS in New York City, including 47 persons with hemophilia A receiving factor VIII concentrate, 50 persons with homozygous beta-thalassemia, and 27 persons with sickle cell anemia receiving frozen-packed RBCs and 20 healthy persons who had not received a transfusion. Hemophiliac participants had significantly lower lymphocyte counts (median, 1,826/cu mm) than did the thalassemic (6,110/cu mm) or anemic (4,443/cu mm) participants, had lower numbers of T-helper lymphocytes (median, 533 cells/cu mm v 1,733 cells/cu mm and 1,554 cells/cu mm), and had a lower T-helper/suppressor ratio (median, 0.8 v 1.8 and 2.1). These differences remained after adjustment for age and sex. Thus, AIDS-like immune abnormalities were found in patients receiving factor concentrate, but not in those receiving RBCs. These defects could be due to both an immunosuppressive effect of the lyophilized factor itself and to contact with the AIDS agent.

Acquired Immunodeficiency Syndrome↗
PubMed1980

Hypertension and propranolol therapy: effect on blood pressure, plasma catecholamines and platelet aggregation.

The effects of propranolol on blood pressure, plasma catecholamine concentration and platelet aggregation were examined in 16 patients with uncomplicated primary hypertension. The patients were studied at rest, during isometric handrip stress and 48 hours after sudden discontinuation of propranolol therapy. Plasma catecholamine concentration and platelet aggregation studies were also carried out in 11 age-matched normotensive and healthy subjects at rest. Plasma catecholamine concentration and platelet aggregation were greater in the hypertensive than in the normotensive subjects, but the difference reached statistical significance for aggregation only. Exercise significantly increased catecholamines and platelet aggregability. The administration of propranolol (240 mg/day) produced a significant decrease in systolic and diastolic blood pressue and in aggregation (the percent of light transmission at 1 microM adenosine diphosphate, at rest) and a significant increase in catecholamine concentration. However, propranolol did not prevent the changes in all these variables with exercise. The abrupt discontinuation of propranolol was not associated with any subjective or objective untoward cardiovascular effect or abnormal changes in plasma catecholamines. However, in some patients the platelet aggregation studies demonstrated a hyperaggregable state, which may be due to a state of supersensitivity of platelets to circulating catecholamines.

Blood Pressure↗
PubMed1979

Platelet aggregation in relationship to plasma catecholamines in patients with hypertension.

Plasma catecholamine concentration and platelet aggregation were studied in 22 patients with uncomplicated primary hypertension and 13 age-matched normotensive, healthy subjects at rest and in some during isometric handgrip exercise. The effect of norepinephrine (NE) infusion upon platelet aggregation was also examined. Plasma catecholamine concentration was slightly higher in the hypertensive than the normotensive group, but the difference was not significant. However, platelet aggregation to ADP was significantly greater in the hypertensive than the normotensive subjects. Exercise increased significantly both catecholamines and aggregation in both groups. Platelet aggregation was correlated with age (r = 0.62, P less than 0.01) and plasma NE (r = -0.34, P less than 0.05 for the total group of subjects). The infusion of NE increased significantly plasma NE and platelet aggregation and there was an inverse correlation between NE increase and threshold decrease (r = -0.69, P less than 0.05). Thus, plasma catecholamines and important determinants of platelet aggregation. However, in our study, uncomplicated primary hypertension was not associated with abnormal plasma catecholamine concentration. It is likely that the observed abnormal platelet aggregability to ADP represents a secondary phenomenon, possibly related to more advanced atherosclerotic vascular changes in hypertensive than normotensive subjects.

Adult↗
PubMed1976

Amino acid metabolism of platelets in leukemia.

Platelets from patients with acute myelogenous leukemia, both before and after remission induction, were evaluated for their ability to incorporate D-[U-14C]glucose into the four amino acids, glutamine, asparagine, glutamic acid, and aspartic acid. Normal platelets incorporated about 80% of the activity into the amides, glutamine and asparagine, and only 20% into their respective amino acids, glutamic acid and aspartic acid. Platelets from patients with acute myelogenous leukemia in the acute stage showed a reversal of this pattern, which then returned to normal during remission. However, the concentration of amino acids was higher than normal, suggesting that remission platelets behaved like a young cell population. The abnormal pattern of labeling could be interpreted as a defect in the platelet citric acid cycle thereby compromising its energy source.

Amino Acids↗
PubMed1975

Functional changes in platelets during extracorporeal circulation.

An in vitro trauma test was conducted to determine the effects of extracorporeal circulation on platelet count and function. Fresh human blood was circulated in two identical in vitro circuits for six hours at a rate of 500 ml per minute (500 recirculations). One circuit included a G.E.--Peirce membrane lung and the other was a control. Platelet aggregation induced by adenosine diphosphate (ADP), epinephrine, or collagen was studied before and after six hours of perfusion. No important drop in platelet count occurred in the control circuit (Control-C) following bypass, but there was a 20% drop for the lung circuit (Lung-C). Platelet aggregation was reduced by about 30% for the control circuit and 65% for the lung circuit. The large decrease in platelet function accompanied by only a moderate decrease in platelet count is discussed in terms of loss of the youngest and most active platelets, platelet inhibition due to ADP released by red blood cell lysis, and platelet trauma.

Adenosine Diphosphate↗