摘要:

AbstractBone marrow examination (BME) has been used as a diagnostic test of last resort in HIV infected patients. Identifying factors that would increase the diagnostic yield of BME would be useful. A retrospective cohort study was done to determine the predictive value of BME for disseminated infection in 133 patients with HIV infection in a 4‐year period at an active HIV clinical center. Thirty‐two percent of the cases had evidence of a disseminated infection on BME but only 10% of cases had a diagnosis made exclusively by BME. Multivariate analysis demonstrated that a positive result was more likely in those patients with fewer than 50 CD4 cells/mm3and those with a hematocrit of less than 25% (P<0.01). BME can be a useful, low‐risk diagnostic procedure in selected patients with HIV infection who are ill with a low CD4 count and/or have a hematocrit less than 25%. A diagnosis can usually be made by other means, suggesting that this test should be limited to those in whom other diagnostic modalities have been exhausted. Am. J. Hematol. 56:1–4, 1997. © 1997 Wiley

ISSN:0361-8609    

DOI:10.1002/(SICI)1096-8652(199709)56:1<1::AID-AJH1>3.0.CO;2-U

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1997

数据来源: WILEY

摘要:

AbstractPolycythemia vera (PV) is associated with a high incidence of thrombosis. The association of apparent and secondary polycythemia with thrombosis is not clear. It was suggested that activation of the coagulation system contributes to thrombus formation in PV. However, the mechanism of activation is unknown. Monocytes generate a potent tissue factor (TF) upon stimulation with various substances, which is involved in thrombus formation in various disorders. Therefore, we studied the possibility that the factor is involved in the activation of coagulation and thrombus formation also in PV. Unstimulated peripheral blood mononuclear cells (PBMC) from each of the different types of polycythemia expressed weak TF activity (2 U) and antigen (41.4 to 52.9 pg/ml), which were similar to normal controls. Following stimulation with endotoxin, PBMC from normal controls and from apparent and secondary polycythemia showed a 3.9‐ to 4.5‐fold increase in TF, while cells from PV showed a 21‐fold increase (P<0.001). Similar levels were generated by PBMC after treatment of PV and at the spent phase. TF was generated by monocytes but not by lymphocytes. Plasma prothrombin fragment1+2(F1+2) levels, assayed at the same time, were significantly higher in PV (2.46 nm) compared to normals and apparent and secondary polycythemia (0.22 to 0.32 nm), and were in a significant correlation with monocyte TF activity and antigen levels (r = 0.77, 0.87). The high levels of F1+2confirm that the coagulation system is activated in PV. The increased capacity of monocytes to generate TF may be responsible for the activation of the coagulation system and thrombus formation. The hypercoagulability state that is induced by this mechanism suggests that long‐life oral anticoagulation should be considered once thrombosis has been developed in PV. Am. J. Hematol. 56:5–11, 1997 © 1997 Wiley

ISSN:0361-8609    

DOI:10.1002/(SICI)1096-8652(199709)56:1<5::AID-AJH2>3.0.CO;2-U

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1997

数据来源: WILEY

摘要:

AbstractHeparin‐induced thrombocytopenia with thrombosis (HITT) can lead to serious morbidity and may be potentially fatal. We reviewed our experience with this entity over a 4‐year period, to determine the following: 1) incidence and type of thrombosis in patients with heparin‐induced thrombocytopenia (HIT), 2) clinical consequences of thrombosis, i.e., amputation, cerebrovascular accidents and death, 3) risk factors associated with development of thrombosis, and 4) impact of therapy on clinical outcomes in patients with HITT. Between 1991–1994, 108 patients were diagnosed to have HIT by heparin‐induced platelet aggregation test. Thirty‐two (29%) of these developed thrombotic complications, of which 20 were venous, 8 arterial, and 4 both. Five of the 32 died, 3 underwent amputations, and 3 had cerebrovascular accidents. The patients who developed thrombotic complications, when compared to those with HIT alone, were older (68.7 ± 11.5 vs. 63.3 ± 16 years,P= .05), had more severe thrombocytopenia (platelet count 46,300 ± 30,400/mm3vs. 62,500 ± 34,400/mm3,P= .02), and developed it earlier (6.0 ± 2.9 vs. 7.4 ± 3.1 days,P= .03). Multivariate analysis showed that severity of thrombocytopenia and early fall in platelet count were independent risk factors for development of thrombotic complications. We did not find an association between development of thrombosis and clinical events (myocardial infarction, cardiac procedures or surgery, noncardiac surgery, and sepsis) that occurred immediately prior to onset of thrombocytopenia. Heparin was stopped in all 32 patients with HITT. Six received no additional therapy, and one received a single dose of aspirin. Three of these 7 died. The other 25 received anticoagulant or multiagent therapy, with 2 deaths. The death rate was lower in those who were treated with anticoagulant or multiagent therapy (P= .05). We conclude that: 1) Thrombotic complications occur in about 29% of hospitalized patients who develop HIT. 2) Early, severe fall in platelet count in elderly patients receiving heparin appears to be associated with development of thrombotic complications. 3) Our data do not show an association between development of thrombotic complications and clinical events immediately preceding the diagnosis of HIT. 4) In addition to discontinuation of heparin, anticoagulant or thrombolytic therapy should be considered in patients with HITT. Am. J. Hematol. 56:12–16, 1997. ©

ISSN:0361-8609    

DOI:10.1002/(SICI)1096-8652(199709)56:1<12::AID-AJH3>3.0.CO;2-5

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1997

数据来源: WILEY

摘要:

AbstractCurrent methods for studying platelet survival in vivo are limited by the use of radioisotopes, with their inherent safety and regulatory concerns, systemic drug administrations that produce biochemical modifications of platelet functions, or external labeling techniques, which may produce artifacts due to surface modifications. For these reasons, we sought to develop a simple, nonisotopic method for labeling platelets internally, thereby producing platelets more likely to have in vivo properties equivalent to native cells. Murine platelets in protein‐free buffer were fluorescently labeled internally by incubation with 2.5 μM 5‐chloromethyl fluorescein diacetate (CMFDA), and without washing, were injected into mice for platelet survival studies. CMFDA‐labeled platelets were unactivated, as shown by minimal P‐selectin expression. When tested in vitro for function by aggregometry, the response of CMFDA‐labeled platelets to collagen and thrombin was identical to that of unlabeled platelets. Flow cytometric analysis demonstrated that CMFDA platelets were an intensely stained, unimodal population that was completely separated from unlabeled platelets. The mean half‐life of labeled platelets in the murine circulation was 37.5 ± 4.5 hr (±1 SD), and the mean survival time was 3.1–3.3 days (n = 24), similar to results reported using51Cr and111In. No evidence of in vivo transfer of dye from labeled platelets to unlabeled cells was observed. CMFDA produces a population of platelets that are nonradioactively, internally labeled with a highly fluorescent, stable product. The labeled platelets function equivalently to native platelets, as demonstrated by immunocytometry and aggregometry, and importantly, in vivo, by normal platelet survival. Am. J. Hematol. 56:17–25, 1997. © 1

ISSN:0361-8609    

DOI:10.1002/(SICI)1096-8652(199709)56:1<17::AID-AJH4>3.0.CO;2-5

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1997

数据来源: WILEY

摘要:

AbstractA simple method to coat human red blood cells (RBC) with PEG is described. Using a reactive derivative, monomethoxy‐PEG (mPEG) was covalently attached to the surface of RBC in aqueous media under mild conditions. The PEG coating dramatically reduced aggregation and low shear viscosity of RBC resuspended in autologous plasma, and inhibited RBC agglutination by blood group‐specific antibodies. Morphology and deformability of the PEG‐treated cells were unaltered. The PEG coating of the RBC surface may be of significant benefit in the treatment of a variety of diseases characterized by vaso‐occlusion or impaired blood flow, e.g., myocardial infarction, sickle cell disease. Am. J. Hematol. 56:26–28, 1997. © 1997 Wiley

ISSN:0361-8609    

DOI:10.1002/(SICI)1096-8652(199709)56:1<26::AID-AJH5>3.0.CO;2-4

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1997

数据来源: WILEY

摘要:

AbstractTo study whether the circulating anticoagulant, activated protein C (APC), could be a regulator of thrombin activity in basal physiological conditions, fibrinopeptide A and activated protein C levels were determined in samples from 40 healthy individuals. There was a significant inverse correlation between the fibrinopeptide A and APC levels (Spearman rank correlation R = −0.487;P= 0.0023). Because of well‐known mechanisms by which decreasing APC levels could cause increased thrombin formation, we suggest that APC may downregulate thrombin activity in subjects with normal protein C levels. Regulation of thrombin formation in health is likely significant for maintaining vascular patency but its molecular mechanisms are poorly understood. The current data suggest that a single physiological anticoagulant, namely APC, may be a significant regulator of procoagulant thrombin activity. Am. J. Hematol. 56:29–31, 1997. © 1997 Wiley‐L

ISSN:0361-8609    

DOI:10.1002/(SICI)1096-8652(199709)56:1<29::AID-AJH6>3.0.CO;2-4

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1997

数据来源: WILEY

摘要:

AbstractAlthough excessive bleeding is widely recognized as a common complication of cardiac surgery, the recent success of antifibrinolytic drugs as prophylactic hemostatic agents has received little attention outside the surgical literature. The etiology of the coagulopathy following cardiac surgery is clearly multifactorial; however, the success of antifibrinolytic drugs as hemostatic agents suggests that fibrinolysis contributes to bleeding in this setting. Increasingly widespread administration of these drugs necessitates increased awareness of the risks and benefits posed by perioperative antifibrinolytic therapy. The objectives of this review are to understand the mechanisms of action of antifibrinolytic drugs in the context of the normal hemostatic response and to review evidence pertaining to the efficacy and safety of antifibrinolytic drugs as hemostatic agents during cardiac surgery. Am. J. Hematol. 56:32–36, 1997. © 1997 Wiley‐Liss,

ISSN:0361-8609    

DOI:10.1002/(SICI)1096-8652(199709)56:1<32::AID-AJH7>3.0.CO;2-3

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1997

数据来源: WILEY

摘要:

AbstractTen years of cumulative experience represented by 4,902 consecutive diagnostic bone‐marrow examinations at a tertiary care and referral center were reviewed to assess the value of specific components. While it has been shown previously that the information obtained from each component is generally complementary, the inclusion of some or all components may vary between institutions. The components studied included aspirate smears, clot sections, biopsy cores, and touch imprints of biopsy and clot sections. Three clinical presentations accounted for the majority of cases: staging for carcinoma or lymphoma, cytopenias, and acute leukemia. We conclude that bilateral aspirates with biopsies are required for diagnosis in staging of neoplasms and that a unilateral aspirate with biopsy is sufficient to assess patients with cytopenia or leukemia. Only rarely were touch imprints of biopsy cores necessary to establish a diagnosis; however, their early availability prior to examining sections of the clot and core did provide immediate information, when positive, in the staging of patients with carcinoma. In a small percentage of staging and leukemia cases the diagnosis rested with the clot section alone. The findings in this study address common assumptions associated with routine diagnostic hematology and oncology procedures, and are important to both clinicians and pathologists concerned with accuracy, quality assurance, turnaround time, and cost containment. Am. J. Hematol. 56:37–41, 1997. © 1997 Wiley‐Lis

ISSN:0361-8609    

DOI:10.1002/(SICI)1096-8652(199709)56:1<37::AID-AJH8>3.0.CO;2-3

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1997

数据来源: WILEY

摘要:

AbstractWe describe 3 patients with acute myeloblastic leukemia (AML), who received rhG‐CSF for infections such as pneumonia or for prophylaxis of infection, and who achieved complete remission. They had not received any antileukemic therapy before or during the administration of rhG‐CSF. These findings suggest the possibility that complete remission can be brought about by G‐CSF itself in some patients with AML. Am. J. Hematol. 56:42–44, 1997. © 1997 Wiley

ISSN:0361-8609    

DOI:10.1002/(SICI)1096-8652(199709)56:1<42::AID-AJH9>3.0.CO;2-2

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1997

数据来源: WILEY

摘要:

AbstractTherapy‐related acute myelogenous leukemia and myelodysplastic syndrome (t‐AML/MDS) are being reported with increasing frequency as a complication of ABMT for Hodgkin's disease and non‐Hodgkin's lymphoma. At present there is no method available to predict who is at risk or is destined to develop this nearly universally fatal disorder. We therefore investigated whether clonal growth of cells is predictive of the development of t‐AML/MDS. In a patient who developed secondary AML/MDS 18 months after ABMT, X‐linked clonality analysis at the human androgen receptor locus was performed on serial banked samples, and documented transition from polyclonal to clonal hematopoiesis. Clonal cells could be identified 6 months after transplant (1 year prior to the diagnosis of t‐AML/MDS), at a time when there was no morphologic or clinical evidence of disease. Clonality analysis can be predictive of the development of t‐AML/MDS after ABMT and may offer important insights into associated risk factors and strategies to minimize the risk of t‐AML/MDS. Am. J. Hematol. 56:45–51, 1997. © 19

ISSN:0361-8609    

DOI:10.1002/(SICI)1096-8652(199709)56:1<45::AID-AJH10>3.0.CO;2-1

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1997

数据来源: WILEY