J N George

University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States

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Publications (35)243.76 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: The Oklahoma Thrombotic Thrombocytopenic Purpura-Haemolytic Uraemic Syndrome (TTP-HUS) Registry has a 24 year record of success for collaborative clinical research, education, and patient care. This article tells the story of how the Registry began and it describes the Registry's structure and function. The Registry provides a model for using a cohort of consecutive patients to investigate a rare disorder. Collaboration between Oklahoma, United States and Bern, Switzerland has been the basis for successful interpretation of Registry data.Registry data have provided new insights into the evaluation and management of TTP. Because recovery from acute episodes of TTP has been assumed to be complete, the increased prevalence of hypertension, diabetes, depression, and death documented by long-term follow-up was unexpected. Registry data have provided opportunities for projects for students and trainees, education of physicians and nurses, and also for patients themselves. During our follow-up, patients have also educated Registry investigators about problems that persist after recovery from an acute episode of TTP. Most important, Registry data have resulted in important improvements for patient care.
    Hamostaseologie 01/2013; 33(2). · 1.59 Impact Factor
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    A T Nurden, D R Phillips, J N George
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    ABSTRACT: The function of blood platelets to prevent blood loss at injured sites in the vasculature depends largely on their capacity to adhere, aggregate, promote coagulation and secrete factors that induce vasoconstriction and recruit inflammatory cells. Produced in large numbers from megakaryocytes, platelets enter the circulation for 7-10 days primed to fulfill their hemostatic function. By 1970, thoughts were becoming well formulated concerning the involvement of platelets not only in hemostasis, but also in the pathogenesis of arterial thrombosis. By this timeframe, pioneering studies had also established many of the basic concepts of platelet biology. Physiologic agonists of platelet aggregation such as ADP, collagen and thrombin had already been identified. Protein cofactors including von Willebrand factor (VWF) and fibrinogen were known to be involved in platelet aggregation (1). However, in the background of these basic studies, the elegant morpholo- gical characterizations of platelets by investigators such as Jim White and Dorothea Zucker-Franklin were teaching us that that the two primary activities of platelets in thrombosis and hemostasis, that is adhesion and aggregation, were dependent upon as yet undescribed elements on the platelet membrane surface. It was also clear that this surface had procoagulant activity. While important studies had been initiated to study platelet membrane proteins, for example, the work in Graham Jamieson's laboratory to characterize peptide fragments of membrane proteins released by proteases (2-5), and the contri- butions of Ralph Nachman's laboratory on platelet membrane protein content (6,7), further progress in our understanding of thrombosis and hemostasis required defining the protein content of the platelet membrane surface and identifying specific proteins that were involved in platelet function. What follows is a story of collaborative research that began 30 years ago and has lasted across our careers. The ability to label platelet surface glycoproteins with radioisotopes and to solubilize them in sodium dodecyl sulfate (SDS) and separate them by polyacrylamide gel electrophoresis (PAGE) was an important advance that provided the basis for each of our projects. Using these techniques, each of us began with different perspectives and different goals. Our ideas all came together in 1975 at the meeting of the International Society for Thrombosis and Haemostasis (ISTH) in Paris. By that time we appreciated the complexity of the platelet membrane glyco- proteins and understood that they had important roles in platelet function, documented by their abnormalities in the congenital disorders, Glanzmann thrombasthenia and Bernard-Soulier syndrome. Many of the other early investiga- tors in this field are to be found in Fig. 1, a group photograph taken at am eeting held in San Antonio, Texas in 1983 to develop our book, Platelet Membrane Glycoproteins (Fig. 2) (8). But to tell the story of how the three of us arrived at this point requires that we begin again, each of us on our own.
    Journal of Thrombosis and Haemostasis 02/2006; 4(1):3-9. · 6.08 Impact Factor
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    ABSTRACT: Accurate estimates of the incidence of thrombotic thrombocytopenic purpura (TTP) are important to assess the resources required for current treatments as well as to anticipate the need to develop new treatments. Previous estimates have been indirect and have not reported data on patients with ADAMTS-13 deficiency. To determine the incidence of patients with TTP-hemolytic uremic syndrome (HUS) in three categories: all patients with clinically suspected TTP-HUS, patients with idiopathic TTP-HUS, and patients with severe ADAMTS-13 deficiency. Incidence rates were estimated from the Oklahoma TTP-HUS Registry, analyzing all 206 consecutive patients from January 1, 1996 to June 30, 2004 who were treated with plasma exchange for their initial episode of clinically suspected TTP-HUS. ADAMTS-13 activity was measured in 186 (90%) of the 206 patients. The age-sex-race standardized annual incidence rates were 11.29 x 10(6) (95% CI: 9.70-12.88) for all patients with clinically suspected TTP-HUS; 4.46 x 10(6) (95% CI: 3.43-5.50) for patients with idiopathic TTP-HUS; and 1.74 x 10(6) (95% CI: 1.06-2.41) for patients with severe ADAMTS-13 deficiency (<5% activity). In all three categories, the incidence rates were greater for women and for blacks. For patients with severe ADAMTS-13 deficiency, the age-sex standardized incidence rate ratio of blacks to non-blacks was 9.29 (95% CI: 4.33-19.93). Accurate incidence rate estimates for all patients with clinically suspected TTP-HUS, idiopathic TTP-HUS, and TTP associated with severe ADAMTS-13 deficiency have been determined. The greater incidence among women and blacks is comparable with their increased risk for other autoimmune disorders.
    Journal of Thrombosis and Haemostasis 07/2005; 3(7):1432-6. · 6.08 Impact Factor
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    J. N. George, S. K. Vesely
    Journal of Thrombosis and Haemostasis 09/2003; 1(9). · 6.08 Impact Factor
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    ABSTRACT: BACKGROUND: With the increased frequency of diagnosis and improved survival of thrombotic thrombocytopenic purpura-hemolytic-uremic syndrome (TTP-HUS), the morbidity of plasma exchange (PE) treatment has become more important.STUDY DESIGN AND METHODS: Data were prospectively collected on 71 consecutive patients referred to the Oklahoma Blood Institute (OBI) for PE treatment for clinically suspected TTP-HUS from mid-1996 to mid-1999. Complications were defined as major or minor, and distinguished between those related to central venous catheter access or to the plasma.RESULTS: Twenty-one patients (30%) had 27 major complications, which caused two deaths. The major complications included 2 episodes of hemorrhage after subclavian line insertion (1 death), 1 pneumothorax requiring a chest tube, 12 systemic infections (1 death), 7 episodes of catheter thrombosis requiring removal of the central venous catheter, 2 episodes of venous thrombosis requiring anticoagulant treatment, 2 episodes of hypoxemia and hypotension, and 1 episode of serum sickness. Minor complications occurred in 22 additional patients (31%). Twenty-eight patients (39%) had no complications.CONCLUSIONS: The morbidity and mortality of catheter placement and PE are important considerations when PE treatment for clinically suspected TTP-HUS is anticipated.
    Transfusion 04/2002; 40(8):896 - 901. · 3.53 Impact Factor
  • J N George
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    ABSTRACT: Since idiopathic (immune) thrombocytopenic purpura (ITP) in adults is usually a chronic condition with few spontaneous remissions, the goal of treatment is not cure, but to maintain a hemostatically safe platelet level. The indication for treatment should be based not merely on platelet counts, but also clinical indices of bleeding. Although most patients show good initial response to prednisone, the side effects of steroids limit this treatment. Currently, long-term management usually involves splenectomy. Since splenectomy has surgical risks and may also predispose the patient to sepsis, a clinical trial using anti-D (WinRho-SDR) has been performed to determine whether this treatment can safely delay or avoid the need for surgery. The use of WinRho may also reveal the occurrence of spontaneous remissions, a previously unrecognized subgroup of adults with chronic ITP.
    Blood Reviews 04/2002; 16(1):37-8. · 6.00 Impact Factor
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    K Kojouri, S K Vesely, J N George
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    ABSTRACT: Quinine-associated thrombotic thrombocytopenic purpura-hemolytic uremic syndrome (TTP-HUS) is thought to be uncommon and to have a good prognosis. To describe the frequency, clinical features, and long-term outcomes of quinine-associated TTP-HUS. Case series. Hospitals in central-western Oklahoma. 225 consecutive patients with TTP-HUS, 1989-2000. Presenting features and clinical outcomes. Thrombotic thrombocytopenic purpura-hemolytic uremic syndrome was associated with quinine in 17 patients. Four patients died, and 7 survivors currently have chronic renal failure. Since 1 July 1995, 132 patients with clinically suspected TTP-HUS were explicitly asked about drug exposure. Fourteen (11%) had taken quinine, and 7 had taken other drugs associated with TTP-HUS. Neurologic abnormalities were as severe in patients with quinine-associated TTP-HUS as in the 118 patients who had not taken quinine. Quinine is a common cause of drug-associated TTP-HUS and can cause death and chronic renal failure. When the disorder is described as TTP-HUS rather than only as HUS, the severity of neurologic abnormalities and the occasional absence of renal failure are emphasized. If recurrent disease is to be prevented, clinicians must recognize quinine as a possible cause.
    Annals of internal medicine 01/2002; 135(12):1047-51. · 13.98 Impact Factor
  • J N George, S K Vesely
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    ABSTRACT: Prompt recognition of thrombotic thrombocytopenic purpura-hemolytic uremic syndrome (TTP-HUS) and initiation of plasma exchange treatment is critical as it substantially decreases mortality. Nevertheless, death and long-term complications remain common. The recent relaxation of diagnostic criteria has dramatically increased the number of patients treated for clinically suspected TTP-HUS.
    Cleveland Clinic Journal of Medicine 11/2001; 68(10):857-8, 860, 863-4 passim. · 3.40 Impact Factor
  • P J Medina, J M Sipols, J N George
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    ABSTRACT: Thrombotic thrombocytopenic purpura-hemolytic uremic syndrome (TTP-HUS) is an inclusive term describing diverse syndromes of multiple etiologies with the common features of thrombocytopenia and microangiopathic hemolytic anemia. Other organ involvement, including renal failure, neurologic abnormalities, and gastrointestinal symptoms, is common. Adverse reactions to drugs increasingly are reported as a potential cause of TTP-HUS. More than 50 drugs and other substances have been associated with the development of TTP-HUS, but many case reports are difficult to interpret because there is uncertainty regarding the diagnosis of TTP-HUS and because there is uncertainty regarding the relation of drug exposure to the onset of TTP-HUS. A systematic analysis of reports of drug-associated TTP-HUS will be required to better understand the strength of clinical evidence linking drugs to the etiology of TTP-HUS. In this review, five drugs that have been the subject of the most and the most recent reports of drug-associated TTP-HUS are discussed: mitomycin C, cyclosporine, quinine, ticlopidine, and clopidogrel. The clinical features of TTP-HUS associated with these drugs are different, suggesting two principal mechanisms by which drugs may cause TTP-HUS: dose-related toxicity (mitomycin C, cyclosporine), and immune-mediated reaction (quinine, ticlopidine, clopidogrel). The role of plasma exchange is uncertain, but this treatment is appropriate because of the high mortality and morbidity of drug-associated TTP-HUS. Recognition of a drug-associated etiology in a patient with TTP-HUS is critical to avoid re-exposure and recurrent illness.
    Current Opinion in Hematology 10/2001; 8(5):286-93. · 4.11 Impact Factor
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    V Roy, M A Rizvi, S K Vesely, J N George
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    ABSTRACT: The diagnosis and treatment of thrombotic thrombocytopenic purpura (TTP) in patients following BMT are often uncertain and unsuccessful. To better understand the evaluation and management of these patients, we describe 17 patients treated with plasma exchange for a presumptive diagnosis of TTP following BMT during a 10 year period, 1989-1998. Because of the uncertainty of the diagnosis, these patients are described as having a 'TTP-like syndrome'. All 17 patients had received an allogeneic BMT. Comparison with the other 245 patients who had an allogeneic BMT during the same period demonstrated that patients with a TTP-like syndrome more frequently had unrelated and/or HLA-mismatched donors, and had also experienced more serious complications: grade III-IV acute GVHD and systemic bacterial, fungal, and viral infections. Three months after the diagnosis of the TTP-like syndrome, only four of 17 patients (24%) were alive; currently only one patient survives. These data emphasize: (1) the diagnosis of TTP following BMT is uncertain because of the presence of multiple BMT-associated complications. (2) The outcome of patients with TTP-like syndromes following BMT is poor. (3) Urgent intervention with plasma exchange when TTP is suspected following BMT may not always be appropriate. Alternative explanations for the signs and symptoms should be considered and treated aggressively.
    Bone Marrow Transplantation 04/2001; 27(6):641-6. · 3.54 Impact Factor
  • M A Rizvi, K Kojouri, J N George
    Annals of internal medicine 03/2001; 134(4):346. · 13.98 Impact Factor
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    J R McMinn, J N George
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    ABSTRACT: Thrombotic thrombocytopenic purpura-hemolytic uremic syndrome (TTP-HUS) is more common in women, and commonly occurs during pregnancy and the immediate postpartum period. An important clinical issue is the distinction of TTP-HUS from the more common obstetric complications, preeclampsia and HELLP syndrome (hemolysis, elevated liver function tests, low platelets). Clinical suspicion of TTP-HUS requires urgent intervention with plasma exchange treatment, a procedure with substantial risk, while preeclampsia and HELLP syndrome typically resolve spontaneously following delivery. Since clinical features of these syndromes can be similar, especially if preeclampsia becomes severe or if seizures (defining eclampsia) occur, the differential diagnosis may be arbitrary. This review addresses the evaluation and management of these syndromes and describes a clinical approach for determining when plasma exchange is appropriate.
    Journal of Clinical Apheresis 02/2001; 16(4):202-9. · 2.27 Impact Factor
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    ABSTRACT: Therapeutic plasmapheresis may remove platelets as well as plasma. Unintentional platelet loss, if not recognized, may lead to inappropriate patient assessment and treatment. A patient with thrombotic thrombocytopenic purpura-hemolytic uremic syndrome (TTP-HUS) is reported in whom persistent thrombocytopenia was interpreted as continuing active disease; thrombocytopenia resolved only after plasma exchange treatments were stopped. This observation prompted a systematic study of platelet loss with plasmapheresis. Data are reported on platelet loss during 432 apheresis procedures in 71 patients with six disease categories using three different instruments. Comparing the first procedure recorded for each patient, there was a significant difference among instrument types (P<0.001); platelet loss was greater with the Fresenius AS 104 (17.5%, N = 21) than with the COBE Spectra (1.6%, N = 26) or the Haemonetics LN9000 (2.6%, N = 24). With all procedures, platelet loss ranged from 0 to 71%. Among disease categories, platelet loss was greater in patients with dysproteinemias who were treated for hyperviscosity symptoms. Absolute platelet loss with the first recorded apheresis procedure, in the 34 patients who had a normal platelet count before the procedure, was also greater with the AS 104 (2.23 x 10(11) platelets) than with the Spectra (0.29 x 10(11) platelets) or the LN9000 (0.37 x 10(11) platelets). In 39 patients in whom data were collected on consecutive days, platelet removal by plasmapheresis correlated with a decreased patient platelet count (r = 0.40, P = 0.011). In these 39 patients, the platelet counts were significantly decreased at 24 hours (P = 0.002).
    Journal of Clinical Apheresis 02/2001; 16(2):55-60. · 2.27 Impact Factor
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    ABSTRACT: Quinine is universally used for the very common symptom of night leg cramps. Patients may not mention it among their medicines, since it is so commonly used and they regulate it themselves. A 68-year-old man suddenly developed extensive bleeding due to severe thrombocytopenia. The diagnosis was initially thought to be a recurrence of idiopathic thrombocytopenic purpura (ITP) that had initially occurred in 1992 and had required splenectomy. Drug-induced thrombocytopenia was also considered, and he was told to stop all of his medicines. Only after three subsequent episodes of severe, symptomatic thrombocytopenia over the next four weeks did he say, upon repeat questioning, that he had continued to take quinine for night leg cramps. Even after a strict warning, he took another quinine tablet that evening, which triggered his fifth episode of severe thrombocytopenia, and confirmed the etiology of quinine-induced thrombocytopenia. The diagnosis thrombocytopenia caused by common drugs can be difficult, requiring persistent, explicit questions.
    The Journal of the Oklahoma State Medical Association 12/2000; 93(11):519-21.
  • S H Woolf, J N George
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    ABSTRACT: The ascendancy of EBM has been accompanied by a greater awareness of its shortcomings. It is increasingly evident from the cost, length, and difficulty of performing RCTs that studies cannot be launched to address every question in medicine. Good evidence is often lacking in medicine. Epistomologists question the very notions of evidence and the suitability of current study designs and measurement tools to research the salient issues of concern to patients and others concerned with quality. Lack of evidence of effectiveness does not prove ineffectiveness, yet, in reaction to EBM, insurance companies and government often make this inference to justify decisions to withhold coverage or research support. The unbridled enthusiasm for the evidence-based practice guideline of the early 1990s has been tempered by a more mature understanding of its limitations. Not many practice guidelines are developed well, and the implementation of flawed guidelines can cause harm. The seven-step process outlined earlier is slow, laborious, and expensive (sometimes costing hundreds of thousands of dollars). Moreover, there is little evidence that either the rigor of the methods or the guidelines themselves have a meaningful effect on practice behavior or patient outcomes. To the most cynical observers, the only consistent beneficiaries of guidelines are payers, who use guidelines with considerable success in reducing costs, lengths of stay, and utilization rates. Even ardent advocates of guidelines acknowledge the evidence that disseminating reviews and recommendations, by itself, fails to motivate clinicians to increase delivery of effective interventions and to abandon ineffective ones. This absence of response has stimulated a closer look at the barriers to behavior change and the design of thoughtful implementation strategies that begin with, but reach beyond, simple guidelines. Tools such as reminder systems, standing orders, academic detailing, peer review and audit, feedback, and health system changes recognize that knowing what to do is only one piece of an increasingly complex puzzle. The competitive marketplace of managed health care has added new economic influences on clinician behavior but is also fueling private-sector interest in good research. Patients, clinicians, and policy makers will continue to seek better data concerning what works in medicine and what does not.
    Hematology/Oncology Clinics of North America 09/2000; 14(4):761-84. · 2.08 Impact Factor
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    J N George
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    ABSTRACT: Thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS) are, in adults, clinically and pathologically indistinguishable except for the severity of renal failure. They are best described as a single disorder, TTP-HUS, because the diagnostic evaluation and initial management are the same. Treatment with plasma exchange, available for more than 20 years, has dramatically altered the course of disease in adults with TTP-HUS. Plasma exchange has improved survival rates from 10% to between 75% and 92%, creating urgency for the initiation of treatment. This has resulted in decreased stringency of diagnostic criteria, which in turn has resulted in a broader spectrum of disorders for which the diagnosis of TTP-HUS is considered. Long-term follow-up has revealed increasing frequencies of relapse and of chronic renal failure. Although the increased survival rate is dramatic and recent advances in understanding the pathogenesis of these syndromes are remarkable, clinical decisions remain empirical. Therefore, the management decisions for patients with suspected TTP-HUS rely on individual experience and opinion, resulting in many different practice patterns. Multipractice clinical trials are required to define optimal management. (Blood. 2000;96:1223-1229)
    Blood 09/2000; 96(4):1223-9. · 9.78 Impact Factor
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    ABSTRACT: With the increased frequency of diagnosis and improved survival of thrombotic thrombocytopenic purpura-hemolytic-uremic syndrome (TTP-HUS), the morbidity of plasma exchange (PE) treatment has become more important. Data were prospectively collected on 71 consecutive patients referred to the Oklahoma Blood Institute (OBI) for PE treatment for clinically suspected TTP-HUS from mid-1996 to mid-1999. Complications were defined as major or minor, and distinguished between those related to central venous catheter access or to the plasma. Twenty-one patients (30%) had 27 major complications, which caused two deaths. The major complications included 2 episodes of hemorrhage after subclavian line insertion (1 death), 1 pneumothorax requiring a chest tube, 12 systemic infections (1 death), 7 episodes of catheter thrombosis requiring removal of the central venous catheter, 2 episodes of venous thrombosis requiring anticoagulant treatment, 2 episodes of hypoxemia and hypotension, and 1 episode of serum sickness. Minor complications occurred in 22 additional patients (31%). Twenty-eight patients (39%) had no complications. The morbidity and mortality of catheter placement and PE are important considerations when PE treatment for clinically suspected TTP-HUS is anticipated.
    Transfusion 09/2000; 40(8):896-901. · 3.53 Impact Factor
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    ABSTRACT: Chronic refractory idiopathic thrombocytopenic purpura (ITP) is defined as ITP with persistent thrombocytopenia despite conventional initial management with prednisone and splenectomy. Rare in children, It may occur in as many as one third of adults with ITP. The goal of treatment is not cure of the ITP, but only to achieve a safe platelet count, which is arbitrarily assumed to be greater than 30,000 to 50,000/microL. The risk for major bleeding seems great only when the platelet count is less than 10,000/microL. Treatment of patients with moderate thrombocytopenia and no clinically important bleeding symptoms should be avoided. There is no accepted algorithm for management of patients with chronic refractory ITP. Observation without specific treatment must be considered a cornerstone of management. Combination regimens of Immunosuppressive agents may be required for patients with severe and symptomatic thrombocytopenia. Additional supportive care measures are also important.
    Seminars in Hematology 08/2000; 37(3):290-8. · 3.36 Impact Factor
  • J N George
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    ABSTRACT: The goal of treatment for idiopathic (immune) thrombocytopenic purpura (ITP) is to prevent serious bleeding. Traditionally, corticosteroids have been used as first-line therapy followed by splenectomy. Experience with splenectomy over 60 years shows that approximately two thirds of patients achieve normal platelet counts during the initial observation, but that thrombocytopenia often recurs with longer follow-up. We know that long-term use of corticosteroids can lead to significant morbidities; there is no consensus regarding the appropriate timing or indications for splenectomy. To address the Issue of appropriate use of splenectomy, we designed a multicenter clinical trial that will randomize patients to either standard care, involving prednisone followed by splenectomy, or to a novel regimen of limited prednisone treatment followed by WinRho SDF (Nabi, Boca Raton, FL) (anti-D) therapy to maintain the platelet count in a safe range for 1 year. Anti-D can be administered easily in an outpatient setting with few side effects and can provide predictable, transient increases in platelet count. The hypothesis is that prolonged maintenance therapy with a nontoxic regimen may increase the percentage of patients who will experience a spontaneous remission from thrombocytopenia, thereby avoiding an invasive and permanent surgical procedure, splenectomy, and its potentially life-threatening sequelae.
    Seminars in Hematology 02/2000; 37(1 Suppl 1):31-4. · 3.36 Impact Factor
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    ABSTRACT: Compression ultrasonography has a high negative predictive value for deep vein thrombosis in symptomatic outpatients. Limited data are available on factors influencing positive predictive value. The objective of this study was to evaluate the positive predictive value of compression ultrasonography according to the anatomic site of vein noncompressibility. We performed a prospective cohort study of 756 consecutive outpatients with suspected first-episode deep vein thrombosis. Compression ultrasonography was performed at the initial visit: results were abnormal if a noncompressible segment was identified or normal if all segments were fully compressible. Venography was performed in patients with abnormal compression ultrasonography results. Positive predictive value was determined according to the site of noncompressibility: common femoral vein only, popliteal vein only, or both sites. Venography was the reference standard for the presence of deep vein thrombosis. Positive predictive value was 16.7% (95% confidence interval, 0.4%-64.1%) for noncompressibility isolated to the common femoral vein compared with 91.3% (95% confidence interval, 72.0%-98.9%) for the popliteal vein only and 94.4% (95% confidence interval, 72.7%-99.9%) for both sites (P<.001). Of 15 patients with isolated noncompressibility of the common femoral vein, 8 (53%) had pelvic neoplasm or abscess compared with 2 (5%) of 42 with noncompressibility of the popliteal vein only and 6 (13%) of 47 with noncompressibility of both sites (P<.001). The positive predictive value of noncompressibility isolated to the common femoral vein is too low to be used alone as the diagnostic end point for giving anticoagulant therapy. Noncompressibility isolated to the common femoral vein is a diagnostic marker for pelvic disease.
    Archives of Internal Medicine 02/2000; 160(3):309-13. · 11.46 Impact Factor

Publication Stats

2k Citations
243.76 Total Impact Points

Institutions

  • 1994–2013
    • University of Oklahoma Health Sciences Center
      • • Section of Hematology/Oncology
      • • College of Medicine
      • • Department of Biostatistics and Epidemiology
      • • College of Public Health
      Oklahoma City, OK, United States
  • 2002
    • Oklahoma Blood Institute
      Oklahoma City, Oklahoma, United States
  • 2000
    • Virginia Commonwealth University
      • Department of Family Practice
      Richmond, VA, United States