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Biomedical subjects

R L Bick

Publications and source records attributed to R L Bick.

At least 55 records · Page 3Linked to original sources
PubMed1995

Blood protein defects associated with thrombosis. Laboratory assessment.

This review has stressed the common hereditary and acquired blood protein defects associated with thrombosis. The most common of the hereditary defects appear to be antithrombin, protein C, and protein S deficiency, and the most common acquired defects are anticardiolipin antibodies and the lupus anticoagulant. Therefore, these are the defects which should first be searched for in an individual with unexplained thrombosis. If these more common defects are not found, the rarer defects, including HC-II, plasminogen, or TPA deficiency, dysfibrinogenemia, elevated PAI-1, or heterozygous homocystinemia should be looked for. The incidence of activated protein C co-factor deficiency (APC resistance) is not yet clear but may also represent a common defect. PAI-1 defects may, with time, be shown to be common. Finding these defects has important implications for therapy for the individual patient and for the institution of family studies to identify, inform, and possibly treat others at risk. It is expected that as knowledge of hemostasis expands, more hereditary and acquired defects, such as elevated lipoprotein(a) or defects of extrinsic (tissue factor) pathway inhibitor (EPI, TFPI), may be associated with enhanced risks for thrombosis.

Blood Protein Disorders↗
PubMed1995

Molecular markers of hemostatic activation. Implications in the diagnosis of thrombosis, vascular, and cardiovascular disorders.

Until recently, the diagnosis of thromboembolic disorders remained difficult to establish before the occurrence of a pathologic event. Clearly, thrombosis is the result of a progressive alteration of the blood and vasculature. Various molecular markers of hemostatic alteration are found in increased or decreased amounts predisposing to thrombosis or in increased circulating amounts during the activation process.

Biomarkers↗
PubMed1995

The antiphospholipid and thrombosis (APL-T) syndromes. Clinical and laboratory correlates.

Anticardiolipin antibodies and the lupus anticoagulant are strongly associated with thrombosis and appear to be the most common of the acquired blood protein defects causing thrombosis. Although the precise mechanisms by which antiphospholipid antibodies alter hemostasis to induce a hypercoagulable state remain unclear, several theories have been advanced. The most common thrombotic events associated with anticardiolipin antibodies are deep venous thrombosis and pulmonary embolus (type I syndrome), coronary or peripheral artery thrombosis (type II syndrome), or cerebrovascular-retinal vessel thrombosis (type III syndrome); occasionally, patients present with mixtures (type IV syndrome). The relative frequency of anticardiolipin antibodies in association with arterial and venous thrombosis strongly suggests that these should be looked for in any individual with unexplained thrombosis; all three idiotypes (IgG, IgA, and IgM) should be measured. Also, the type of syndrome (I through V) should be defined, if possible, as this may dictate both the type and duration of both immediate and long-term anticoagulant therapy. Unlike patients with anticardiolipin antibodies, patients with primary lupus anticoagulant thrombosis syndrome usually sustain venous thrombosis. Because the aPTT is unreliable in patients with lupus anticoagulant (prolonged in approximately 40% to 50% of patients) and is seldom prolonged in patients with anticardiolipin antibodies, definitive tests (ELISA for anticardiolipin antibodies and the dRVVT for lupus anticoagulant) should be immediately ordered when antiphospholipid syndrome is suspected or when individuals present with otherwise unexplained thrombotic or thromboembolic events.

Antiphospholipid Syndrome↗
PubMed1995

Laboratory diagnosis of antiphospholipid syndromes.

The search for clinical outcomes associated with antiphospholipid antibodies (aPL) has been ongoing for a decade. This article focuses on the clinical use of tests for the detection of aPL. A review of the current thinking regarding the pathophysiology of antiphospholipid syndromes is relevant to the discussion of different aPL assays and methodologies. The value of aPL testing in specified patient populations is analyzed.

Antiphospholipid Syndrome↗
PubMed1994

Disseminated intravascular coagulation. Objective criteria for diagnosis and management.

Current concepts of the cause, pathophysiology, clinical and laboratory diagnosis, and management of fulminant and low-grade DIC have been presented. Considerable attention has been devoted to interrelationships within the hemostasis system. Only by clearly understanding these pathophysiological interrelationships can the clinician and laboratory scientist appreciate the divergent and wide spectrum of often confusing clinical and laboratory findings in patients with DIC. In this discussion, objective clinical and laboratory criteria for a diagnosis of DIC have been delineated, thus eradicating unnecessary confusion and empirical decisions regarding the diagnosis. Many therapeutic decisions to be made are controversial and will remain so until more is published about specific therapeutic modalities and survival patterns. Also, therapy must be highly individualized depending on the nature of DIC, age, cause of DIC, site and severity of hemorrhage or thrombosis, and hemodynamic and other clinical parameters. Also presented are clear criteria for severity of DIC and objective criteria for defining a response to therapy. Also, because it is often difficult for the individual physician to decide when to stop often extensive therapy, objective criteria whereby therapy may be stopped, as continuation is likely fruitless, have been presented as a guideline. Lastly, it should be appreciated that many syndromes that are often organ specific share common pathophysiology with DIC but are typically identified as an independent disease entity, such as hemolytic uremic syndrome, adult shock lung syndrome, eclampsia, and many other isolated organ-specific disorders.

Disseminated Intravascular Coagulation↗
PubMed1994

Platelet function defects associated with hemorrhage or thrombosis.

Platelet dysfunction, especially acquired forms, is a common cause of hemorrhage, especially when associated with trauma or surgery. Although the hereditary platelet function defects are generally quite rare, hereditary storage pool disease is common enough to be suspected in an individual, usually a child, with characteristic historical and clinical findings. The acquired platelet function defects, especially those resulting from drugs, are common and should promptly be suspected in patients developing easy and spontaneous bruising, mild-to-moderate mucosal membrane hemorrhage, or unexplained bleeding associated with trauma or surgery. The template bleeding time is generally useful as a screening test of platelet function, but a normal template bleeding time, in the face of a suggestive history, suggestive clinical findings, or in a patient frankly bleeding, is not reliable, and platelet aggregation or lumiaggregation should be done in appropriate clinical situations. Also, prolongation of the template bleeding time is an unreliable predictor of clinical bleeding propensity. The mainstay of therapy for almost all these defects, if bleeding is significant, is the liberal infusion of appropriate numbers of platelet concentrates. The acquired platelet function defects should also be managed by attempts to treat or control the underlying disease, if possible, and offending drugs or potentially offending drugs should immediately be stopped.

Blood Platelet Disorders↗
PubMed1994

Hypercoagulability and thrombosis.

This article has stressed the common hereditary and acquired blood protein defects associated with thrombosis. The commonest hereditary defects appear to be antithrombin, protein C, and protein S deficiency, and the commonest acquired defects are anticardiolipin antibodies and the lupus anticoagulant. Therefore these are the defects that should first be looked for in an individual with unexplained thrombosis. If these commoner defects are not found, the rarer defects, including HC-II, plasminogen or t-PA deficiency, dysfibrinogenemia, or elevated PAI-1, should next be sought. The incidence of activated protein C cofactor deficiency is not yet clear but may also represent a common defect. Likewise, PAI-1 defects may, with time, be shown to be quite common. The importance of finding these defects has significant implications for therapy of the individual patient and for institution of family studies to identify, inform, and possibly treat others at risk. It is expected that as knowledge of hemostasis expands, more hereditary and acquired defects, such as elevated lipoprotein (a) or defects of extrinsic (tissue factor) pathway inhibitor may be associated with enhanced risks of thrombosis.

Antithrombins↗
PubMed1994

The antiphospholipid and thrombosis syndromes.

Anticardiolipin antibodies and the lupus anticoagulant are strongly associated with thrombosis and appear to be the most common of the acquired blood protein defects causing thrombosis. Although the precise mechanism(s) whereby antiphospholipid antibodies alter hemostasis to induce a hypercoagulable state remain unclear, several theories have been advanced. The commonest thrombotic events associated with anticardiolipin antibodies are deep vein thrombosis and pulmonary embolus (type I syndrome), coronary or peripheral artery thrombosis (type II syndrome), or cerebrovascular/retinal vessel thrombosis (type III syndrome), and occasionally patients present with mixtures (type IV syndrome). The relative frequency of anticardiolipin antibodies in association with arterial and venous thrombosis strongly suggests that these should be looked for in any individual with unexplained thrombosis; all three idiotypes (IgG, IgA, and IgM) should be assessed. Also, the type of syndrome (I through IV) should be defined if possible because this may dictate both type and duration of immediate and long-term anticoagulant therapy. In contrast to those with anticardiolipin antibodies, patients with primary lupus anticoagulant thrombosis syndrome usually suffer venous thrombosis. Because the aPTT is unreliable in patients with lupus anticoagulant (prolonged in only about 40% to 50% of patients) and is not usually prolonged in patients with anticardiolipin antibodies, definitive tests (ELISA for anticardiolipin antibody and the dRVVT for lupus anticoagulant) should be immediately ordered when suspecting antiphospholipid syndrome or in individuals with otherwise unexplained thrombotic or thromboembolic events.

Antibodies, Anticardiolipin↗
PubMed1994

Deep vein thrombosis. Diagnosis and management.

In at least 50% of patients with suspected deep vein thrombosis, the diagnosis is not confirmed by objective testing. The addition of impedance plethysmography and real-time B-mode ultrasound with color-enhanced Doppler imaging to the available diagnostic modalities has altered the approach to clinical evaluation. Pharmacologic treatment has evolved to place emphasis on the use of subcutaneous heparins of greater efficacy and the reduction of hemorrhagic risk with the use of the INR system when warfarin is recommended for long-term therapy. Use of new approaches for diagnosis and management offers the potential of more prompt and accurate diagnosis, more effective therapy, and a reduction in the incidence of pulmonary thromboembolism.

Anticoagulants↗
PubMed1994

Current trends in the development of anticoagulant and antithrombotic drugs.

Developments in biotechnology, synthetic chemistry, and extraction methods have contributed significantly to provide many newer antithrombotic and anticoagulant drugs. Many of these drugs exhibit mechanisms of actions distinct from heparin and oral anticoagulants. The depolymerization of heparin has resulted in the development of LMWHs. These drugs have now attained the agent of choice status for the prophylaxis of postsurgical and medical thrombotic disorders. LMWHs are now being clinically evaluated for the treatment of established thrombosis and prevention of post-acute angioplasty occlusion and reocclusion. Many newer applications of these agents will be proposed in coming years. Synthetic and recombinant antithrombin agents, such as hirudin and hirulog, have been claimed to exhibit effective anticoagulant and antithrombotic actions. The clinical data, however, are rather limited, and additional validation studies are needed. These agents, however, provide an alternate anticoagulation approach in patients who are refractory to the actions of heparin or who developed heparin-induced thrombocytopenia. Both hirudin and peptide conjugates are undergoing extensive clinical trials throughout the world in various indications. Once validated, their optimized use will provide physicians and surgeons an alternate anticoagulant approach for heparin-compromised patients. Glycosaminoglycans, such as dermatan sulfate, heparan sulfate, and other mixtures, have been developed for various indications. These drugs, however, are relatively inferior to LMWHs for the prophylaxis of thromboembolism. Although these agents have been used for phlebitis and other indications, well-designed objective clinical trials are not available at this time. Because these agents exhibit other effects, such as the effect on smooth muscle cell proliferation, these may be of some value in the control of post-percutaneous transluminal coronary angioplasty restenosis. Several synthetic analogs of heparin and related glycosaminoglycans have also been developed. One of these agents is a synthetic pentasaccharide that represents the AT-III binding site in the heparin molecule. This agent produces a strong anti-Xa effect and is devoid of any antithrombin actions. This agent is currently being developed for the prophylaxis of thromboembolism. The synthetic pentasaccharide is devoid of any effects on platelets and thus does not produce any thrombocytopenic effects. Thus it may be useful in those patients who develop thrombocytopenia and white clot syndrome. A hypersulfated lactobionic acid analog has also been developed as an antithrombotic agent. This agent was initially found to produce its antithrombotic action via HC-II. More recent data, however, show that it also releases TFPI from endogenous sites.(ABSTRACT TRUNCATED AT 400 WORDS)

Anticoagulants↗
PubMed1994

Antiphospholipid and thrombosis syndromes.

ACAs and the lupus anticoagulant are strongly associated with thrombosis and appear to be the most common of the acquired blood protein defects causing thrombosis. Although the precise mechanism or mechanisms whereby antiphospholipid antibodies alter hemostasis to induce a hypercoagulable state remain unclear, several theories, as previously discussed, have been advanced. The most common thrombotic events associated with ACAs are DVT and PE (type I syndrome), coronary or peripheral artery thrombosis (type II syndrome), cerebrovascular or retinal vessel thrombosis (type III syndrome), and occasionally patients present with mixtures (type IV syndrome). The relative frequency of ACAs in association with arterial and venous thrombosis strongly suggests that these should be looked for in any patient with unexplained thrombosis; all three idiotypes (IgG, IgA, and IgM) should be assessed. Also, the type of syndrome (I through IV) should be defined, if possible, because this may dictate both type and duration of both immediate and long-term anticoagulant therapy. Unlike those with ACAs, patients with primary lupus anticoagulant thrombosis syndrome usually have venous thrombosis. Since the aPTT is unreliable in patients with lupus anticoagulant and is not usually prolonged in patients with ACAs, definitive tests (ELISA for ACA and the dRVVT for lupus anticoagulant) should be immediately ordered when suspecting antiphospholipid syndrome or in patients with otherwise unexplained thrombotic or thromboembolic events.

Antibodies, Anticardiolipin↗
PubMed1994

Antiphospholipid antibodies in coronary artery disease: a review.

APAs present a clinical problem that is now recognized to be a significant causative factor of both fatal and nonfatal myocardial infarction as well as other coronary syndromes. Similar to the thrombotic complications of APAs in the cerebrovascular system, the result can be life-threatening or fatal. Correct diagnosis requires a high index of suspicion, especially in patients with known prior thrombotic events and in those who present with myocardial ischemia or infarction without underlying risk factors and at a young age. In these patients an aggressive laboratory evaluation must be performed, including testing for APAs. The treatment of the coronary syndrome must progress along currently accepted approaches, including the aggressive and early use of thrombolytic therapy followed by anticoagulation with heparin, porcine heparin, or possibly low molecular weight heparin. Intermediate and long-term therapy with some form of heparin or high-intensity warfarin anticoagulation is essential to have any chance of preventing coronary reocclusion and recurrent myocardial infarction as well as other thrombotic events. Although the precise incidence of APAs in the general and coronary artery disease population is not known and although in the individual patient early disease may be difficult to detect, an enhanced awareness of the possibility of the association of APAs with coronary artery disease may allow earlier diagnosis and may save lives. Studies of larger numbers of patients over extended time periods with various pharmacological approaches to anticoagulation are needed to define more clearly optimal management.

Amino Acid Sequence↗
PubMed1994

Syndromes of hypercoagulability and thrombosis: a review.

This review has stressed the common hereditary and acquired blood protein defects associated with thrombosis. The most common of the hereditary defects appear to be antithrombin, protein C, and protein S deficiency and the most common acquired defects are anticardiolipin antibodies and the lupus anticoagulant. Therefore these are the defects that should first be looked for in an individual with unexplained thrombosis. If these more common defects are not found, then the rarer defects, including heparin cofactor II, plasminogen or tissue plasminogen activator deficiency, dysfibrinogenemia, or elevated PAI-1 should next be sought. The importance of finding these defects has significant implications for therapy of the individual patient and for institution of family studies to identify, inform, and possibly treat others at risk. It is expected that as knowledge of hemostasis expands, more hereditary and acquired defects, such as elevated lipoprotein(a) or defects of extrinsic (tissue factor) pathway inhibitor may be associated with enhanced risks of thrombosis.

Antithrombins↗
PubMed1994

Physiology of hemostasis.

The consequences of acute insults to the hemostatic system, whether congenital or acquired, frequently present a considerable challenge in diagnosis and therapy. Logical and effective management depends upon the proper identification of the hemostatic compartments involved; an appreciation for the considerably complex, delicately modulated interplays of various enzyme/inhibitor systems; and knowledge of the mechanism by which a variety of apparently unrelated disease processes precipitate sometimes catastrophic events--thrombosis/embolism/hemorrhage. We have attempted a logical review of basic mechanisms of hemostasis. The text is obligatorily brief, focusing on key elements of the biochemistry and physiology of the vessel wall, the platelet, and pertinent plasma factors. The section on plasma proteins pays particular attention to biocybernetic principles (positive/negative feedback loops) and to the interrelationship of enzyme systems involved in coagulation, fibrinolysis, kinin generation, and complement activation. No attempt was made to be encyclopedic. In the interest of brevity and clarity, the text has been limited to current concepts, with the reference material selected, whenever possible, in the form of review articles, volumes and monographs. We apologize for omissions. It is our belief that a working knowledge of basic mechanisms provides not only advantages in diagnostic/therapeutic management but also serves as a firm foundation for the development of novel diagnostic and therapeutic modalities.

Animals↗
PubMed1994

Disseminated intravascular coagulation. Objective laboratory diagnostic criteria and guidelines for management.

Current concepts of the etiology, pathophysiology, clinical and laboratory diagnosis, and management of fulminant and low-grade DIC have been presented. Considerable attention has been devoted to interrelationships within the hemostasis system. Only by clearly understanding these pathophysiological interrelationships can the clinician and laboratory scientist appreciate the divergent and wide spectrum of often confusing clinical and laboratory findings in patients with DIC. In this discussion, objective clinical and laboratory criteria for the diagnosis of DIC have been delineated, thus eradicating needless confusion and empirical decisions regarding the diagnosis. Many therapeutic decisions to be made are controversial and will remain so until more is published about specific therapeutic modalities and survival patterns. Also, therapy must be highly individualized depending on the nature of DIC, age, etiology of DIC, site and severity of hemorrhage or thrombosis, and hemodynamic and other clinical parameters. Also presented are clear criteria for the severity of DIC and objective criteria for defining a response to therapy. Because it frequently is difficult for the individual physician to decide when to stop often extensive and expensive therapy, objective criteria whereby therapy may be stopped, as it is deemed that continuation is most likely fruitless, have been presented as a guideline. Many syndromes, which frequently are organ-specific, share common pathophysiology with DIC but are typically identified as an independent disease entity, for example, hemolytic uremic syndrome, adult shock-lung syndrome, eclampsia, and many other isolated organ-specific disorders.

Blood Coagulation Tests↗
PubMed1993

The antiphospholipid-thrombosis syndromes. Fact, fiction, confusion, and controversy.

Anticardiolipin antibodies and the lupus anticoagulant are strongly associated with thrombosis and appear to be the most common of the acquired blood protein defects causing thrombosis. Although the precise mechanism(s) whereby antiphospholipid antibodies alter hemostasis to induce a hypercoagulable state remain unclear, several theories have been advanced. Because the aPTT is unreliable in patients with lupus anticoagulant and is not usually prolonged in patients with anticardiolipin antibodies, definitive tests, such as ELISA for IgG, IgA, and IgM anticardiolipin antibodies and the dRVVT (followed by cephalin correction for confirmation) for lupus anticoagulant, should be immediately ordered when suspecting antiphospholipid syndrome in persons with otherwise unexplained thrombotic or thromboembolic events or fetal wastage syndrome. The laboratory diagnosis of APL-T syndrome is summarized in Figure 1.

Antibodies, Anticardiolipin↗