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Biomedical subjects

D Deykin

Publications and source records attributed to D Deykin.

At least 109 records · Page 6Linked to original sources
PubMed1977

The spectrum of vitamin K deficiency.

The coagulopathy induced by vitamin K deficiency commonly results from our lack of awareness of the clinical setting associated with vitamin K deficiency. Thirteen cases are reviewed to illustrate the clinical correlates most frequently observed. Dietary deficiency was always present, but concomitant antibiotic therapy was not an absolute requirement. The postoperative patient is at high risk, as is the patient with cancer or renal failure. Abnormal bleeding was common, but significant hemorrhage occurred only in postoperative patients. Factor assays were helpful and occasionally necessary to make the diagnosis, but a therapeutic trial with parenteral vitamin K was often enough to provide the right diagnosis. Greater awareness of this deficiency syndrome is necessary to avoid the serious morbidity that often results.

Adult↗
PubMed1977

A chlorpromazine-induced inhibitor of blood coagulation.

An inhibitor of blood coagulation was detected in the plasma of four schizophrenic patients receiving long-term chlorpromazine therapy. The partial thromboplastin time (PTT) was prolonged in all four patients and the prothrombin time (tpt) was prolonged in one. The inhibitor which resembled in many respects that seen in patients with systemic lupus erythematosus (SLE), was shown to be associated with the tigM-rich fractions of the serum. None of the patients manifested a clinical bleeding tendency and in two, discontinuation of the chlorpromazine was followed by a decrease in the activity of the anticoagulant. While three of the patients had a positive antinuclear antibody test (ANA) and the fourth a false positive serology for syphilis, no further evidence for SLE was found.

Adult↗
PubMed1977

The mobilization of arachidonic acid in platelets exposed to thrombin or ionophore A23187. Effects of adenosine triphosphate deprivation.

In studies conducted with human gel-filtered platelets, we have found: (a) that the release of serotonin and transfer of [3H]arachidonic acid from phosphatidylcholine and phosphatidylinositol to plasmalogen phosphatidylethanolamine which are associated with the activation of platelets by thrombin are both strongly dependent upon the presence of metabolic ATP; (b) that serotonin release and arachidonic acid mobilization in labeled phosphatides are promoted by the calcium ionophore A-23187 in media free of calcium ions; (c) that inhibitors of ATP synthesis, while leading to impairment of the release reaction induced by ionophore, do not inhibit ionophore-stimulated mobilization of arachidonic acid. We conclude that the activation of phospholipase A2 responsible for freeing arachidonic acid from platelet phosphatides is solely dependent upon the increased cytoplasmic levels of calcium ions promoted by either ionophore or, in an energy-dependent fashion by thrombin. Phospholipase activation is not a function of latent hydrolytic activity made available by the release reaction.

Adenosine Triphosphate↗
PubMed1977

Heparin Therapy: regimens and management.

Heparin remains the most effective antithrombotic drug. It acts by combining with plasma antithrombin, thereby accelerating the neurtalisation of thrombin and other acitvated coagulation factors. Full-dose intravenous heparin is indicated in all cases of pulmonary embolism and established deep venous thrombosis, unless there exist compelling contraindications. Continuous intravenous infusion of heparin appears to be safer than intermittent injection. Low-dose subcutaneous heparin is effective in preventing the initial occurrence of thigh vein thrombi and in reducing the incidence of fatal pulmonary embolism in general surgical patients over the age of 40. The efficacy of low-dose heparin in preventing pulmonary emboli following hip surgery has not been established. The incidence of severe heparin-induced thrombocytopenia appears to be rising. Platelet counts should be performed in all patients receiving heparin by any mode of administration.

Heparin↗
PubMed1977

Circulating anticoagulant in a family with prolonged bleeding time and factor VIII deficiency.

A circulating anticoagulant against factor VIII activity was demonstrated in the plasma of a boy from a family with both factor VIII deficiency and prolonged bleeding time. However, the factor VIII-related antigen, ristocetin-induced platelet aggregation activity, platelet retention in glass bead columns, platelet aggregation with adenosine 5'-diphosphate, collagen and epinephrine, and clot retraction among affected members were normal. The electrophoretic mobility of factor VIII-related antigen on crossed immunoelectrophoresis was normal. The inactivation of factor VIII activity by the inhibitor was time dependent and was nonlinear as the concentration of the inhibitor was increased. Immunotyping showed that the inhibitor was IgG with k light chains.

Anticoagulants↗
PubMed1976

Isolation of membranes from normal and thrombin-treated gel-filtered platelets using a lectin marker.

We report a technique for the isolation of plasma membranes from gel-filtered platelets exposed to thrombin, using 125I-labeled lentil lectin as an external marker. Labeled cells not exposed to thrombin could be lysed on a gradient of glycerol. Those cells incubated with thrombin (without external Ca2+) were made more susceptible to breakage on a gradient of glycerol-EDTA, and homogenized with a zero-clearance homogenizer. Lysates were spun on gradients of sodium diatrizoate. The membranes obtained from such gradients have been examined by electron microscopy and by assays for enzymes and 125I label. Membranes from platelets incubated without and with thrombin were found to be enriched as follows: lectin marker, 8- and 9-fold, respectively; phosphodiesterase, 9- and 12-fold; acid phosphatase, 2.5 and 2-fold. There is thus a particularly close correlation of lectin marker with phosphodiesterase, an enzyme characteristic of normal purified membranes. Monitoring for 125I-labeled lentil lectin appears to be a useful procedure for following platelet membranes during isolations from relatively small quantities of blood.

Binding Sites↗
PubMed1976

The effect of thrombin on the uptake and transformation of arachidonic acid by human platelets.

Washed human platelets take up arachidonic acid from plasma and incorporate the fatty acid into the major classes of complex lipids. Thrombin impairs net incorporation. It activates endogenous phospholipases which liberate arachidonic acid from phospholipids. As a consequence of thrombin induced aggregation platelets release arachidonic acid intermediates formed by the action of platelet fatty acid cyclooxygenase and by platelet fatty acid lipoxygenase. Cyclooxygenase, but not lipoxygenase, is inhibited by aspirin and indomethicin. Analysis of the pathways of arachidonic acid metabolism may furnish new insight into platelet function and into disorders of primary hemostasis.

Arachidonic Acids↗
PubMed1976

In vivo dissociation of factor VII (AHF) activity and factor VII-related antigen in von Willebrand's disease.

Using monospecific rabbit antihuman factor VIII antiserum, we have examined the amounts of factor VIII-related antigen and compared these to the levels of factor VIII procoagulant activity in normal subjects and patients with von Willebrand's disease. We have observed that even without transfusion all nine probands with von Willebrand's disease and 20 of their 34 relatives possessed a significantly elevated factor VIII activity/factor VIII-related antigen ratio when compared to that of 55 normal subjects. It is suggested that an elevated factor VIII activity/factor VIII-related antigen ratio may be used for detection of the carriers of von Willebrand's disease.

Animals↗
PubMed1976

Combined deficiencies of Factor VIII (AHF) and Factor XI (PTA).

Combined deficiencies of Factor VIII and Factor XI associated with moderate degree of bleeding symptoms were found in 3 brothers. Examination of Factor VIII activity and Factor VIII-related antigen revealed that the Factor VIII activity/Factor VIII-related antigen ratio was significantly decreased in their mother and maternal grandmother consistent with the carrier state of hemophilia. Factor XI deficiency was found in 2 siblings, the father, and 2 of his sisters. The paternal grandmother was thought to carry the abnormal Factor X I gene, although her Factor XI level was normal, because of a significant bleeding history. It was concluded that the combined Factor VIII and XI deficiencies in the 3 brothers represent the coincidental inheritance of 2 separate and independent abnormal genes.

Adolescent↗
PubMed1976

Diagnosis of von Willebrand's disease. A comparative study of diagnostic tests on nine families with von Willebrand's disease and its differential diagnosis from hemophilia and thrombocytopathy.

Nine probands with von Willebrand's disease, and their family members, totalling 43 people, were examined. Twenty-seven had a history of bleeding; 29 had an increased factor VIII activity:factor VIII related antigen ratio; 24 had a decreased factor VIII related antigen; 23 had a prolonged bleeding time; 19 had a reduced platelet adhesiveness; 16 had a decreased factor VIII activity; and 14 had an abnormal ristocetin-induced platelet aggregation. Eight members with both normal beleeding time and normal factor VIII activity were found to have other abnormal tests: elevated ratio of factor VIII activity to factor VIII related antigen in seven; decreased factor VIII related antigen in four; and reduced platelet adhesiveness in one. Therefore, ratio of factor VIII activity to factor VIII related antigen and factor VIII related antigen are more sensitive and may be used for the detection of heterozygous carriers of von Willebrand's disease. Although patients with thrombocytopathy may have a prolonged bleeding time, decreased platelet adhesiveness and reduced platelet aggregation by ristocetin, their factor VIII activity, factor VIII related antigen and ratio of factor VIII activity to factor VIII related antigen are normal and their abnormal ristocetin test cannot be corrected by the addition of factor VIII concentrate. Hemophilic subjects and hemophilic carriers, who are deficient in factor VIII activity, usually have a normal bleeding time, normal platelet adhesiveness, and normal ristocetin test. In contrast to patients with von Willebrand's disease, their factor VIII related antigen is normal or slightly increased and their ratio of factor VIII activity to factor VIII related antigen is significantly reduced. We conclude that ratio of factor VIII activity to factor VIII related antigen and factor VIII related antigen are not only more sensitive but also more specific for the diagnosis of von Willebrand's disease.

Antigens↗
PubMed1976

Quantitative determination of factor-VIII protein by two-stage gel electrophoresis.

A new method for the quantification of factor-VIII protein in plasma is described which utilizes only commercially available equipment and material. The procedure involves separation of factor VII from other plasma proteins by a two-stage sodium dodecyl sulphate gel electrophoretic technique and quantification of the protein by scanning densitometry. The plasma from normal individuals, haemophiliacs, obligate carriers of haemophilia and patients with von Willebrand's disease have been examined by this technique. In general, the data support the earlier findings obtained by quantitative immunoelectrophoresis. In addition, some abnormalities not detected by immunoelectrophoresis are observed by the gel electrophoresis technique.

Electrophoresis, Agar Gel↗
PubMed1975

Management of heparin therapy: Controlled prospective trial.

Among 100 consecutive patients receiving heparin in therapeutic dosage, major bleeding occurred in 21, and minor bleeding in 16. Two patients died from bleeding, and two had recurrent pulmonary embolism. Major bleeding occurred in 21% when therapy was regulated with whole-blood clotting time and in 20% when heparin was given without clotting tests. In a subsequent prospective trial patients received heparin by intermittent intravenous injection with or without laboratory control according to the partial thromboplastin time or continuously by intravenous infusion. Recurrent thromboembolism occurred once in each group. Major bleeding was seven times more frequent with intermittent injection than with continuous infusion. Control with the partial thromboplastin time did not prevent major bleeding in patients receiving intermittent injections. With continuous infusion, one-fourth less heparin was required than with intermittent injections. Administration of heparin by continuous infusion appears safer than intermittent injection with or without laboratory control and is no less effective for prevention of thromboembolism.

Administration, Oral↗