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Biomedical subjects

R L Bick

Publications and source records attributed to R L Bick.

At least 91 records · Page 5Linked to original sources
PubMed1984

Diagnostic efficacy of a simple radioimmunoassay test for fibrinogen/fibrin fragments containing the B beta 15-42 sequence.

A simple RIA method for B beta 15-42 RPs has been evaluated in our laboratory to investigate experimental and clinical fibrinolytic states. The assay utilizes bentonite precipitation to remove cross-reacting fibrinogen. Due to the heterogeneity in molecular weights of the B beta RPs, the results are expressed as nanograms per milliliter. The linear range of the assay is 2 to 40 ng/ml, with a capability of detecting up to 200 ng/ml. A special anticoagulant mixture (heparin or EDTA/aprotinin) is required for sample collection. Certain precautions in the care and handling of specimens are also necessary. Increased levels of B beta RPs were observed in the following conditions: malignancy (associated with increased release of tissue plasminogen activators), pancreatitis, liver diseases, pregnancy, and postexercise testing (associated with increased release of tissue plasminogen activators). Increased levels of B beta RPs were also found during thrombolytic therapy, anabolic steroid treatment, prothrombin complex concentrate therapy, blood component therapy, and low molecular weight heparin subcutaneous therapy (associated with an increase in tissue plasminogen activator release). Our studies suggest that B beta RPs are sensitive molecular markers of the endogenous activation of fibrinolytic system and may provide useful diagnostic information on a pathologic process that often remains undetectable by routine laboratory methods.

Evaluation Studies as Topic↗
PubMed1984

Clinical implications of molecular markers in hemostasis and thrombosis.

The general availability to all clinical laboratories of assays of molecular markers of the hemostasis system now offers the clinician the opportunity to screen selected high-risk patients and potentially to offer therapy that will ward off a significant and often catastrophic event. In addition, these molecular markers permit a rapid differential diagnosis of many disorders that are often confusing and often difficult, if not impossible, to differentiate using the more traditional global screening tests of hemostasis. This short review has served only to point out the importance of these newly developed molecular markers of the hemostatic system and only selected disorders have been highlighted with respect to the ability of these molecular markers to aid in a prethrombohemorrhagic event and to aid in a specific differential diagnosis in certain selected thrombohemorrhagic disorders. It is anticipated that more experience with these molecular markers with more patient populations will most likely greatly expand their usefulness in a wide variety of thrombohemorrhagic disorders, thus leading to enhanced medical care for patients.

Blood Coagulation Disorders↗
PubMed1984

Antithrombins and coronary artery disease.

The role of antithrombin-III with respect to atherogenesis and myocardial infarction remains unclear; however, it has been reported that antithrombin-III levels are decreased in many individuals with coronary artery disease and in those at high risk for coronary artery occlusion. However, the several reports available do not agree and remain inconclusive. Antithrombin-III levels were determined in 86 individuals undergoing coronary artery angiography. Results of these determinations reveal that the majority of patients with angiographically documented coronary artery disease have normal antithrombin-III levels. Additionally, there was found to be no correlation between antithrombin-III levels and severity or site of coronary artery involvement. The results of this study would suggest that plasma antithrombin-III determinations are of no particular significance in determining the presence, absence, or severity of coronary artery disease.

Antithrombin III↗
PubMed1983

Hydroxyethyl starch versus albumin in cardiopulmonary bypass prime solutions.

To compare hydroxyethyl starch (HES) with 25% albumin, 20 patients undergoing aortocoronary bypass were randomized into two groups: 10 received 1,000 ml of HES and 10 received 200 ml of 25% albumin in a bloodless priming solution for cardiopulmonary bypass (CPB). Platelet aggregation, antithrombin III, reptilase time, fibrinogen, plasminogen, fluid requirements, and hemodynamics were monitored. Platelet aggregation was abnormal in both groups, being relatively poorer in the albumin group. Both groups exhibited below normal antithrombin III and plasminogen levels, with significantly lower antithrombin III levels noted in the HES group postoperatively (41.9 +/- 11.8% versus 56.6 +/- 9.9%; p = 0.006). Compared with the albumin group, the HES group had slightly, but not significantly, elevated liver function test results, total volume replacement (9,173 +/- 2,046 ml versus 8,522 +/- 1,192 ml; p = 0.057), packed red blood cell usage (227 +/- 284 ml versus 75 +/- 168 ml; p = 0.066), and chest tube drainage (599 +/- 253 ml versus 454 +/- 174 ml; p = 0.144). In the HES group, 5% albumin requirement was greater (386 +/- 466 ml versus 50 +/- 158 ml; p = 0.002) and percent increase of body weight was higher (5.2 +/- 0.8% versus 2.3 +/- 0.6%; p = 0.05) postoperatively. Postoperative weight increase and colloid requirements plus trends toward larger blood loss and blood transfusions indicate possible further evaluation. However, results suggest that HES is a safe additive to priming solutions. Compared with albumin, HES has comparable changes in coagulation variables and slightly less severe derangements in platelet aggregation.

Aged↗
PubMed1983

Clinical hemostasis practice: the major impact of laboratory automation.

This article has reviewed basic disease states of hemostasis and thrombosis with an emphasis on laboratory technologic advances comparing manual and semiautomated techniques with new fully automated technology that is now available for both aiding in a diagnosis and monitoring efficacy of therapy. As these new automated methods become generally available, more and more information will be accumulated to determine exactly how precise many of these modalities will be for diagnosis and monitoring. Many of these newer modalities have already gained general acceptance as highly sophisticated tools that certainly belong in any clinical laboratory having to deal with patients with thrombohemorrhagic disorders.

Anticoagulants↗
PubMed1983

Impact of automation on the quantitation of low molecular weight markers of hemostatic defects.

Through in depth studies, the biochemical pathways of hemostasis-related systems have been elucidated in terms of well-defined molecular mechanisms. The interrelationships of coagulation, fibrinolytic, kallikrein-kinin, platelets, prostaglandins, blood vessel, and complement systems are now well understood. Methods are currently developed to quantitate the molecular markers of each of these systems and define the involvement of each in disease and drug-related aberrations. Molecular markers allow for very early detection of disease states well before clinical manifestations are seen or current coagulation methods are affected. Therefore prophylactic or therapeutic treatment can begin before a disease state causes damage. Platelet factor 4 and beta-thromboglobulin are low molecular weight proteins released from the light (alpha) granules of platelets and provide a reliable index of endogenous activation and consumption of platelets. Serotonin and ADP are released during activation from the beta-granules and can be measured by high-performance liquid chromatography. Fibrinopeptide A is a molecular marker of the activation of the coagulation process and provides a useful index of the action of thrombin on fibrinogen. Elevated levels of this peptide are found in patients with hypercoagulable states or a thrombotic tendency. B beta 15-42 peptides are released at the early stages of fibrinolysis and are a useful collective parameter for the measurement of the activation of fibrinolysis. In both the primary and secondary fibrinolytic disorders this peptide is elevated. Circulating kinins provide information on the activation of the kallikrein system and are useful in monitoring coagulation and shock related disorders. Arachidonic acid metabolites, such as thromboxanes and prostacyclins, are products of platelet and vascular endothelium interactions. Their measurement in peripheral blood provides a useful tool to measure the vascular and platelet-related thrombotic defects. Furthermore, antiplatelet therapy can be monitored using these parameters. Numerous other metabolites of arachidonic acid such as the leukotrienes and PAFs also are generated in various immunopathologic disorders associated with hemostatic activation. Unlike the other coagulant tests, the measurement of molecular markers in native blood or plasma samples provides a true picture of the endogenous physiology. Since no activator or additive is added to influence the test, these markers provide the most relevant information on the pathophysiologic condition. Since most of these markers are proteins or low molecular weight products, isotopic and nonisotopic immunoassays, high performance liquid chromatography and fluorometric methods can be used to analyze their levels. Furthermore, multiple panels can be developed to profile various pathologic states.(ABSTRACT TRUNCATED AT 400 WORDS)

Arachidonic Acid↗
PubMed1983

Molecular markers of hemostatic disorders: implications in the diagnosis and therapeutic management of thrombotic and bleeding disorders.

With current technological advances, it is now possible to measure in less than 50 microL of plasma picomolar amounts of circulating products of platelet activation, products of protease activation related to coagulation and fibrinolytic pathways, and prostaglandin metabolites formed during a physiologic or pathologic process. Most of these markers, which circulate in blood in nanogram or picogram amounts per milliliter during or after pathologic activation, provide pertinent information on the status of a patient in terms of specificity and early detection, and will be of crucial value in the diagnosis of hemostatic defects and the management of newer antithrombotic drugs that cannot be monitored by currently available assays. Currently, 125I- and 3H-based simple radioimmunoassays are available for platelet factor 4, beta-thromboglobulin, fibrinopeptide A, B beta 15-42 related peptides, thromboxane B2, and the prostaglandins 6-keto-PGF1 alpha and PGE2. Nonisotopic methods such as enzyme-linked immunosorbent assays and fluoroimmunoassays are being developed. Serotonin and ADP, products of platelet activation, are measurable by liquid-chromatographic, immunoenzymatic, and spectrophotofluorometric methods. Analytical methods for fibrin split products (fragments D and E) and serine protease inhibitor complexes such as thrombin-antithrombin-III, factor Xa-antithrombin-III, and kallikrein-C1-esterase are also being developed. We have evaluated all of these methods and found them to be very sensitive to those components of endogenous activation of the hemostatic system listed above.

Blood Coagulation Disorders↗
PubMed1982

Clinical relevance of antithrombin III.

Many unrelated clinical conditions that are associated with significant decreases in antithrombin III have been summarized. In addition, prospects for future therapy with antithrombin III concentrates have been discussed. The clinical indications for antithrombin III determinations, including the reasons for performing the assay and those specific patient populations subjected to antithrombin III assays in this author's clinical practice, have been outlined. It is to be anticipated that with the new general availability of simple reliable antithrombin III assay systems using synthetic substrates that more and more populations will be adequately studied and clinical indications for the use of antithrombin III determinations and concentrates may become more firm or may change.

Adolescent↗
PubMed1981

Disseminated intravascular coagulation: a clinical/laboratory study of 48 patients.

In summary, this series of 48 patients with acute and chronic DIC demonstrates the reliability of laboratory tests in both aiding a diagnosis of DIC and in offering reasonable predictability of efficacy of therapy, as noted by the correction of abnormalities after delivery of antiprocoagulant therapy for this syndrome. It appears that the diagnostic tests most likely to aid in diagnosis and to reliably inform the clinician when the intravascular clotting process has been stopped are those that determine the antithrombin-III level, the presence of soluble fibrin monomer, and the finding of elevated fibrin(ogen) degradation products, thrombocytopenia and a prolonged thrombin time in the face of the appropriate type of bleeding in the appropriate clinical setting. In addition, it would appear that mini-dose heparin therapy is highly effective in controlling the intravascular clotting process in acute DIC, whereas antiplatelet therapy utilizing two agents is effective in chronic DIC. In addition, in this population, patients with acute disease demonstrated a 74 percent survival rate and those with chronic disease had a 100 percent survival rate from the disseminated intravascular clotting process.

Acute Disease↗
PubMed1981

Hereditary hemorrhagic telangiectasia and disseminated intravascular coagulation: a new clinical syndrome.

In summary, 47 patients with documented HHT and a bleeding problem were referred to San Joaquin Hematology Oncology Medical Group over a 2-year period. Fifty-one percent of patients were noted to have an associated DIC syndrome and of these 24 patients, 19 had acute DIC episodes, six had chronic DIC, six presented with diffuse, recurrent deep venous thrombosis and of these six, three suffered pulmonary emboli. Other defects were also noted and were thought to be coincidental defects. This syndrome should be readily considered and searched for when seeing patients with HHT, especially if significant hemorrhage or thrombosis is present. It should further be appreciated that many patients with HHT and bleeding are candidates for the development of acute or chronic DIC and thus a "mini" Kasabach-Merritt syndrome. When patients with HHT present with undue bleeding, this syndrome should be appreciated, searched for from the clinical and laboratory standpoint and, when found, treated in the appropriate manner with supportive therapy, mini-heparin or antiplatelet therapy as the clinical situation dictates.

Acute Disease↗
PubMed1980

Antithrombin III patterns in disseminated intravascular coagulation.

Antithrombin III-heparin cofactor has now been recognized as a major inhibitor of thrombin and other serine proteases in the blood coagulation system. Since the reaction between antithrombin III and serine proteases is irreversible, one would expect antithrombin III consumption in the face of pathologic intravascular coagulation and attendant generation of thrombin, IXa, Xa, XIa, XIIa, and plasmin. Using a new assay system for antithrombin III that is unaffected by heparin or fibrino (geno) lytic degradation products, antithrombin III was monitored before and during therapy in 38 patients who had acute or chronic disseminated intravascular coagulation. It was found that early and significant decreases in anththrombin III occur in disseminated intravascular coagulation and thus may serve as a useful diagnostic tool. It was further found that monitoring antithrombin III during therapy reflected a cessation of antithrombin III consumption and, thus, served as an indicator of the efficacy of therapy in stopping the clotting process. Since the assay system is unaffected by fibrino(geno)lytic degradation products and heparin, it proved useful in monitoring the efficacy of heparin therapy for disseminated intravascular coagulation. In addition for this group of patients, it appeared that mini-heparin therapy and large doses of heparin were equally efficacious in correcting other laboratory abnormalities of disseminated intravascular coagulation, and in controlling clinical hemorrhage in disseminated intravascular coagulation.

Anticoagulants↗
PubMed1979

Vascular disorders associated with thrombohemorrhagic phenomena.

This paper has attempted to summarize the more common disease entities which may be accompanied by or may lead to a disorder of hemostasis and/or thrombosis. It is to be emphasized that the vascular component of hemostasis is often overlooked by clinicians caring for individuals with disorders in hemostasis and thrombosis. It is hoped that this brief summary will alert clinicians that the vasculature is equal in importance to the coagulation protein system and to platelets in leading to a hemorrhagic or thrombotic diathesis.

Amyloidosis↗
PubMed1979

Thrombotic thrombocytopenic purpura. An extended editorial.

A hypothesis for the pathogenesis of TTP is developed, centered on the views and findings of Kwaan (Fig. 8). By a series of deductions, inferences, and extensions, an attempt has been made to define considerably more restrictively than heretofore a TTP paradigm of clinical (Tables 1,2,3) and laboratory (Table 4) features. Revisions may be required in the future as increase of knowledge indicates. By similar methods rational, exigent therapeutic measures are selected (Table 5). The innovative therapeutic use of plasma transfusion, as proposed by Byrnes and Lian and their co-workers, is compatible with the paradigm in all respects. The paradigm discriminates for authentic cases of TTP among spurious if similar entities. Such sequestration will constitute a homogeneous universe of case material appropriate for study. The prospective use of the TTP paradigm defined in this papd therapeutic protocol, jointly developed, may accelerate our knowledge and improve our effectiveness in this lethal, if uncommon, disease [49,76,111,170].

Blood Platelets↗