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Biomedical subjects

C Chesney

Publications and source records attributed to C Chesney.

16 recordsLinked to original sources
PubMed1998

Lack of association between antiphospholipid antibodies and first-trimester spontaneous abortion: prospective study of pregnancies detected within 21 days of conception.

OBJECTIVE: To determine the role of antiphospholipid antibodies and anticardiolipin antibodies in first-trimester losses, addressing experimental pitfalls that preclude excluding the possibility that these antibodies reflect merely the selection bias of studying couples only after they have already experienced losses. DESIGN: Given that retrospective studies cannot exclude the possibility that such antibodies arise as a result of the fetal death, blood samples were obtained either before pregnancy or very early in pregnancy. Sera were obtained within 21 days of conception. SETTING: Multicenter university-based hospitals (National Institute of Child Health and Human Development collaborative study). PATIENT(S): Subjects for the current study were 93 women who later experienced pregnancy loss (48 diabetic; 45 nondiabetic), matched 2:1 with 190 controls (93 diabetic and 97 nondiabetic) who subsequently had normal live-born offspring. INTERVENTION(S): Sera from these 283 women were analyzed for antiphospholipid antibodies by enzyme immunoassay. In 260 of the 283 women (87 with pregnancy losses; 173 with live-born infants), sera were also available to perform assays for anticardiolipin antibodies by enzyme immunoassay. MAIN OUTCOME MEASURE(S): Pregnancy losses. RESULT(S): No association was observed between pregnancy loss and the presence of antiphospholipid antibodies or anticardiolipin antibodies. Levels of antiphospholipid antibodies were 6-19 PL/mL in 62.4% of the pregnancies that ended in losses and > or = 20 PL/mL in 5.4%; among pregnancies resulting in live-born infants, the percentages were 56.8% and 6.8%, respectively. Of the pregnancies that ended in a loss, 5.7% had anticardiolipin antibodies > or = 16 GPL/mL, compared with 5.2% of those ending in a live birth. CONCLUSION(S): This prospective study suggests that anticardiolipin antibodies and antiphospholipid antibodies are not associated with an increased risk for first-trimester pregnancy loss.

Abortion, Spontaneous↗
PubMed1992

Racial differences in coagulation studies in stroke.

Racial differences in stroke are known to exist with persons in the black race having a higher morbidity, mortality and incidence of stroke compared to whites. We evaluated coagulation factors in black and white stroke patients and compared the results between races. D-dimer was elevated more frequently in blacks than whites to a statistically significant degree. There were non-significant trends for blacks to have a positive lupus anticoagulant, low protein C and protein S, higher platelet factor 4, and hyporesponsive platelets to 10 microM epinephrine. The significance of these findings in understanding racial differences in stroke is discussed.

Aged↗
PubMed1990

A subchronic toxicity study of two inhaled aerosolized atropine sulfate formulations in rats and dogs.

The potential subchronic (21 days) toxicity of inhaled metered aerosol formulations (solution and suspension) of atropine sulfate was investigated in rats and dogs. The doses administered to rats were 0.78 and 2.5 mg/kg/day (solution) or 1.4 and 3.2 mg/kg/day (suspension). In the dog, the daily doses achieved were 0.5 and 1.3 mg/kg/day, regardless of formulation. In both species, sham control animals inhaled air only and vehicle control animals inhaled either placebo solution or placebo suspension. There was no mortality or other evidence of a toxic effect of atropine sulfate. The expected mydriatic effect of atropine sulfate was seen in both species and, similarly, the pupillary light reflex was impaired in rats and dogs receiving either formulation of atropine sulfate at both dose levels. Reduced salivation was also noted and ophthalmologic examinations in both species were unremarkable. In dogs, atropine sulfate (high-dose) caused tachycardia but there was no evidence of an adverse effect on the electrocardiogram or on systolic blood pressure. In both species, atropine sulfate did not alter body weight, food consumption or clinical pathology parameters. Necropsy observations and histopathological findings revealed no effect of atropine sulfate in either species although, in the rat, adrenal gland hypertrophy in both sexes followed inhalation of the suspension at both dose levels. With this possible exception, nothing but the expected pharmacological effects of atropine sulfate were seen in either rats or dogs.

Administration, Inhalation↗
PubMed1987

Delayed hemolytic transfusion reaction caused by anti-LebH antibody.

A major delayed hemolytic transfusion reaction produced by an antibody to Lewisb is reported. Delayed hemolysis following transfusion with Leb-positive red cells was not reported to the blood bank. Severe hemolysis recurred following a second transfusion with Leb-positive cells, but was avoided thereafter with Leb-negative red cells. This is the first reported case of a serious delayed hemolytic transfusion reaction caused by anti-Leb.

Aged↗
PubMed1985

Chronic allopurinol and adenine therapy in Duchenne muscular dystrophy: effects on muscle function, nucleotide degradation, and muscle ATP and ADP content.

Prompted by the controversy on the efficacy of allopurinol in Duchenne muscular dystrophy and by our observations of an abnormal adenine nucleotide turnover in this disease, we conducted an 18 month, double-blind clinical trial with allopurinol and adenine in 14 Duchenne boys paired according to age and functional activity. Detailed clinical evaluation was performed trimonthly. Muscle ATP and ADP content was measured before and after 1 year of treatment. The effect of therapy on adenine nucleotide turnover was determined. No significant difference was observed between the treated and placebo groups, but both showed a significant deterioration (p less than 0.05) in most clinical parameters. Muscle ATP was reduced in Duchenne dystrophy (p less than 0.02) but did not change with therapy, and no correction of the abnormal adenine nucleotide degradation was observed.

Adenine Nucleotides↗
PubMed1985

Coagulopathy induced by continuous infusion of high doses of human lymphoblastoid interferon.

Seven patients with myeloblastic leukemia were treated for 10 days with high-dose (15 or 30 million units/m2/day), human lymphoblastoid interferon (Wellferon) by continuous iv infusion. All patients developed prolonged activated partial thromboplastin time, and four developed prolonged prothrombin time. Factor assays demonstrated low levels of II, VII, IX, X, and XII. Coagulation abnormalities improved after discontinuation of interferon therapy.

Adolescent↗
PubMed1983

Relationship of clinical findings in systemic lupus erythematosus to seroreactivity.

We have characterized 52 consecutive patients fulfilling 4 or more of the American Rheumatism Association criteria for systemic lupus erythematosus in order to provide, for the first time, a homogeneous sample for statistical comparison of antinuclear antibody (ANA)-positive and ANA-negative groups. Ten patients (19%) were seronegative. There was no significant difference in age, disease activity, organ system involvement, erythrocyte sedimentation rate, immune complex levels, or C3 levels. The ANA-negative group showed a higher incidence of involvement for whites and men. Leukopenia, lower levels of antibody to DNA, and higher C4 levels were also characteristic of the ANA-negative group.

Adult↗
PubMed1983

Sequential changes in platelet function and coagulation in leukemic children treated with L-asparaginase, prednisone, and vincristine.

Coagulation and platelet function in 13 children with acute lymphoblastic leukemia were studied sequentially during a remission induction with L-asparaginase, prednisone, and vincristine. In the first weeks of therapy, which included four doses of L-asparaginase coagulation was characterized by significant decreases in plasma concentrations of plasminogen, antithrombin III alpha 2-macroglobulin, and fibrinogen. All measures gradually returned to normal after complication of L-asparaginase therapy. In the latter part of induction treatment, clotting times, especially partial Thromboplastin time, decreased significantly, while levels of factors V and VIII increased with recovery of platelet counts. At this time, 6 patients had an increased in vitro platelet aggregation response to adenosine diphosphate, and their partial thromboplastin times were significantly shorter than those of patients without increased aggregation. Concurrent abnormalities in coagulation and platelet function may account for the thrombotic complications that develop in some children receiving induction therapy with these agents.

Acute Disease↗
PubMed1983

Normal platelet function after therapy for acute lymphocytic leukemia.

The aggregation responses of platelets from 19 patients who had completed treatment of acute lymphocytic leukemia (ALL) and had remained in remission for two months to 4.8 years were studied both in vitro and in vivo. Responses to 0.5 micro M adenosine diphosphate (ADP), epinephrine, and collagen were all normal. One child had irreversible platelet aggregation to 0.1 micro M ADP, a concentration that only elicited a primary aggregation response from control platelets. The mean platelet-aggregate ratio was normal. We conclude that platelet defects, although a possible late effect of ALL or its chemotherapy, do not occur with any appreciable frequency in long-term survivors.

Adolescent↗
PubMed1974

Hemostatic defect due to acquired circulating inhibitors against lipid procoagulant and factor VIII.

An 85 year old woman was studied because of severe bleeding. Acquired inhibitors to factor VIII and to phospholipid procoagulants were demonstrated. Platelet factor 3 (Pf3) assay was prolonged with both kaolin and Russell's Viper Venom (Stypven-R). It was normal with patient's washed platelets and normal plasma, but abnormal when normal platelets were incubated with patient's plasma. The inhibitor also blocked the coagulant action of Bell and Alton thromboplastin, inosithin, phosphatidyl ethanolamine and phosphatidyl choline, but not that of tissue thromboplastin or cardiolipin. All other platelet functions were normal. The inhibitors were purified by Al (OH3) absorption, heating at 56degrees, precipitation by 50% ammonium sulfate, followed by dialysis and DEAE-cellulose chromatography. A partial separation of the two inhibitors was achieved. Cyclophosphamide treatment resulted in cessation of bleeding and dissappearance of the inhibitors. This seems to be the first instance of an acquired circulating inhibitor specifically directed against phospholipid procoagulants in a patient who also had an inhibitor to Factor VIII.

Aged↗