scholarly journals Vancomycin-dependent antibodies associated with thrombocytopenia and refractoriness to platelet transfusion in patients with leukemia

Blood ◽  
1990 ◽  
Vol 75 (2) ◽  
pp. 518-523 ◽  
Author(s):  
DJ Christie ◽  
N van Buren ◽  
SS Lennon ◽  
JL Putnam
Keyword(s):  
Platelet Transfusion ◽  
Protein A ◽  
Enzyme Linked Immunosorbent Assay ◽  
Severe Thrombocytopenia ◽  
Staphylococcal Protein A ◽  
Igg Antibodies ◽  
Patient Withdrawal ◽  
Life Threatening ◽  
Drug Dependent ◽  
Vancomycin Treatment

Two patients with leukemia experienced profound thrombocytopenia and refractoriness to platelet transfusion during vancomycin treatment. In one patient, withdrawal of drug and administration of platelet transfusions restored platelet counts to near normal levels (approximately 100 x 10(9)/L), however, subsequent challenge with vancomycin due to recurring infection again precipitated severe thrombocytopenia (platelets less than 10 x 10(9)/L) and life- threatening hemorrhagic symptoms. Potent vancomycin-dependent antiplatelet antibodies were detected in the serum of both patients during the refractory period using staphylococcal protein A rosette formation. Employing a monoclonal antibody-antigen capture enzyme- linked immunosorbent assay (ELISA), the patients were found to have vancomycin-dependent IgG antibodies that bound specifically to platelet glycoproteins (GP) IIb and/or IIIa. One of these antibodies failed to react with platelets deficient in GPIIb/IIIa obtained from an individual with Glanzmann's thrombasthenia. These findings provide the first major evidence for drug-dependent antibodies in association with severe thrombocytopenia and refractoriness to platelet transfusion in alloimmunized leukemia patients and, further, provide the first demonstration of vancomycin-dependent antibodies reactive with platelets.

scholarly journals Vancomycin-dependent antibodies associated with thrombocytopenia and refractoriness to platelet transfusion in patients with leukemia

Blood ◽  
1990 ◽  
Vol 75 (2) ◽  
pp. 518-523 ◽  
Author(s):  
DJ Christie ◽  
N van Buren ◽  
SS Lennon ◽  
JL Putnam
Keyword(s):  
Platelet Transfusion ◽  
Protein A ◽  
Enzyme Linked Immunosorbent Assay ◽  
Severe Thrombocytopenia ◽  
Staphylococcal Protein A ◽  
Igg Antibodies ◽  
Patient Withdrawal ◽  
Life Threatening ◽  
Drug Dependent ◽  
Vancomycin Treatment

Abstract Two patients with leukemia experienced profound thrombocytopenia and refractoriness to platelet transfusion during vancomycin treatment. In one patient, withdrawal of drug and administration of platelet transfusions restored platelet counts to near normal levels (approximately 100 x 10(9)/L), however, subsequent challenge with vancomycin due to recurring infection again precipitated severe thrombocytopenia (platelets less than 10 x 10(9)/L) and life- threatening hemorrhagic symptoms. Potent vancomycin-dependent antiplatelet antibodies were detected in the serum of both patients during the refractory period using staphylococcal protein A rosette formation. Employing a monoclonal antibody-antigen capture enzyme- linked immunosorbent assay (ELISA), the patients were found to have vancomycin-dependent IgG antibodies that bound specifically to platelet glycoproteins (GP) IIb and/or IIIa. One of these antibodies failed to react with platelets deficient in GPIIb/IIIa obtained from an individual with Glanzmann's thrombasthenia. These findings provide the first major evidence for drug-dependent antibodies in association with severe thrombocytopenia and refractoriness to platelet transfusion in alloimmunized leukemia patients and, further, provide the first demonstration of vancomycin-dependent antibodies reactive with platelets.

scholarly journals Identification of immunoreactive sites in bovine parathyroid cells to antibodies raised against the NH2-terminal sequence of parathyroid hormone.

1979 ◽  
Vol 27 (8) ◽  
pp. 1209-1214 ◽  
Author(s):  
W Limacher ◽  
P Wild ◽  
E Manser ◽  
H Lutz
Keyword(s):  
Parathyroid Hormone ◽  
Protein A ◽  
Electron Microscopic Level ◽  
Enzyme Linked Immunosorbent Assay ◽  
Staphylococcal Protein A ◽  
Terminal Sequence ◽  
Electron Microscopic ◽  
Secretion Granules ◽  
Parenchymal Cells ◽  
Bovine Parathyroid Hormone

The NH2-terminal sequence of bovine parathyroid hormone (1-84) was localized with different immunocytochemical methods on the light and electron microscopic level in bovine parathyroid glands and in isolated bovine parathyroid parenchymal cells. The peroxidase labeled staphylococcal protein A and the peroxidase anti-peroxidase method were found to be advantageous for light and electron microscopic localization, respectively. Reaction product was found light microscopically in the cytoplasma of the parenchymal cells and electron microscopically largely over the secretion granules of the parenchymal cells. The immunoreactive sites were subsequently identified to represent only intact parathyroid hormone (1-84) by gel electrophoresis derived enzyme linked immunosorbent assay.

scholarly journals Comparison of techniques for demonstrating antibodies to Rift Valley fever virus

1986 ◽  
Vol 97 (2) ◽  
pp. 317-329 ◽  
Author(s):  
R. Swanepoel ◽  
J. K. Struthers ◽  
M. J. Erasmus ◽  
S. P. Shepherd ◽  
G. M. McGillivray ◽  
...  
Keyword(s):  
Rift Valley ◽  
Rift Valley Fever ◽  
Rift Valley Fever Virus ◽  
Protein A ◽  
Haemagglutination Inhibition ◽  
Enzyme Linked Immunosorbent Assay ◽  
Staphylococcal Protein A ◽  
Valley Fever ◽  
Neutralization Techniques ◽  
Comparison Of Techniques

SummaryNine serological techniques were compared by monitoring the response to infection with Rift Valley fever (RVF) virus in three sheep. Antibodies were monitored daily for the first 14 days after infection, then weekly and later fortnightly up to week 24. The earliest antibody response was detected in one sheep on day 3 by a plaque reduction neutralization test, and by day 6 antibodies were demonstrable in all three sheep by haemagglutination-inhibition, reversed passive haemagglutination-inhibition, immunodiffusion, indirect immunofluorescence (IF), enzyme-linked immunosorbent assay and neutralization of cytopathic effect in cell cultures. Antibodies were demonstrable by complement fixation on day 8 at the earliest. IF and the two neutralization techniques produced the highest titres, but all tests could be used satisfactorily for the serological diagnosis of RVF. Inactivated antigen could be used for all except the neutralization tests. A radioimmunoassay technique using125I-labelIed staphylococcal protein A detected antibodies on day 8 at the earliest and produced lower mean titres than some of the other techniques. This was probably because sheep immunoglobulins bind protein A poorly.

Life-threatening reaction to staphylococcal protein A immunomodulation

1992 ◽  
Vol 7 (1) ◽  
pp. 4-5 ◽  
Author(s):  
Roy E. Smith ◽  
Jerome L. Gottschall ◽  
Anthony V. Pisciotta
Keyword(s):  
Protein A ◽  
Staphylococcal Protein A ◽  
Staphylococcal Protein ◽  
Life Threatening

scholarly journals A Novel αIIbβ3 Antagonist from Snake Venom Prevents Thrombosis without Causing Bleeding

Toxins ◽  
2019 ◽  
Vol 12 (1) ◽  
pp. 11 ◽  
Author(s):  
Yu-Ju Kuo ◽  
Ching-Hu Chung ◽  
Tzu-Yu Pan ◽  
Woei-Jer Chuang ◽  
Tur-Fu Huang
Keyword(s):  
Platelet Aggregation ◽  
Conformational Changes ◽  
Severe Thrombocytopenia ◽  
Rotational Thromboelastometry ◽  
Trimeresurus Flavoviridis ◽  
Structure Activity ◽  
Binding Epitope ◽  
Life Threatening ◽  
Drug Dependent ◽  
Hemostatic Effects

Life-threatening thrombocytopenia and bleeding, common side effects of clinically available αIIbβ3 antagonists, are associated with the induction of ligand-induced integrin conformational changes and exposure of ligand-induced binding sites (LIBSs). To address this issue, we examined intrinsic mechanisms and structure–activity relationships of purified disintegrins, from Protobothrops flavoviridis venom (i.e., Trimeresurus flavoviridis), TFV-1 and TFV-3 with distinctly different pro-hemorrhagic tendencies. TFV-1 with a different αIIbβ3 binding epitope from that of TFV-3 and chimeric 7E3 Fab, i.e., Abciximab, decelerates αIIbβ3 ligation without causing a conformational change in αIIbβ3, as determined with the LIBS antibody, AP5, and the mimetic, drug-dependent antibody (DDAb), AP2, an inhibitory monoclonal antibody raised against αIIbβ3. Consistent with their different binding epitopes, a combination of TFV-1 and AP2 did not induce FcγRIIa-mediated activation of the ITAM–Syk–PLCγ2 pathway and platelet aggregation, in contrast to the clinical antithrombotics, abciximab, eptifibatide, and disintegrin TFV-3. Furthermore, TFV-1 selectively inhibits Gα13-mediated platelet aggregation without affecting talin-driven clot firmness, which is responsible for physiological hemostatic processes. At equally efficacious antithrombotic dosages, TFV-1 caused neither severe thrombocytopenia nor bleeding in FcγRIIa-transgenic mice. Likewise, it did not induce hypocoagulation in human whole blood in the rotational thromboelastometry (ROTEM) assay used in perioperative situations. In contrast, TFV-3 and eptifibatide exhibited all of these hemostatic effects. Thus, the αIIbβ3 antagonist, TFV-1, efficaciously prevents arterial thrombosis without adversely affecting hemostasis.

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