ristocetin has been researched along with Lymphoproliferative-Disorders* in 3 studies
2 review(s) available for ristocetin and Lymphoproliferative-Disorders
| Article | Year |
|---|---|
Von Willebrand's disease. Clinical picture, diagnosis, and treatment.
Recent developments regarding von Willebrand's disease, a complex disorder of hemostasis, have been helpful in understanding the clinical and laboratory manifestations of the disorder. This article discusses the pathogenesis and classification of the disorder, the role of von Willebrand factor in hemostasis, genetic counseling, and approaches to treatment. Topics: Adolescent; Adult; Autoimmune Diseases; Blood Platelets; Blood Transfusion; Blood Vessels; Child; Child, Preschool; Epitopes; Estrogens; Factor VIII; Genetic Counseling; Heterozygote; Homozygote; Humans; Lymphoproliferative Disorders; Ristocetin; von Willebrand Diseases; von Willebrand Factor | 1984 |
The von Willebrand syndrome.
Topics: Blood Platelets; Blood Vessels; Epitopes; Factor VIII; Genetic Variation; Humans; Lupus Erythematosus, Systemic; Lymphoproliferative Disorders; Platelet Adhesiveness; Platelet Aggregation; Ristocetin; von Willebrand Diseases; von Willebrand Factor | 1980 |
1 other study(ies) available for ristocetin and Lymphoproliferative-Disorders
| Article | Year |
|---|---|
Characterization of a new mode of defective ristocetin-induced platelet aggregation.
A patient with a reduced response to the platelet-aggregating agent ristocetin and a prolonged bleeding time was found to have an abnormally high level of vWf as measured by Laurell immunoelectrophoresis. Characterization of the patient's vWf by disc-gel electrophoresis and crossed immunoelectrophoresis showed it to be indistinguishable from vWf isolated from normal plasma. The specific activity of the purified vWf in supporting RIPA was the same for both patient and normal vWf. The diminished RIPA was therefore not due to decreased levels of vWf or the presence of a modified form of the vWf. The patient's platelet-poor plasma inhibited the ristocetin-induced platelet aggregating activity of normal PRP, indicating the presence of an inhibitor. Fractionation of the plasma by ion-exchange chromatography showed the inhibitory activity to be in the patient's gamma globulin fraction. The gamma globulin was not directed against either the patient's vWf or against the patient's platelets but appeared to interfere with RIPA by binding ristocetin. Topics: Aged; Female; Humans; Immunoglobulin G; Lymphoproliferative Disorders; Platelet Aggregation; Protein Binding; Ristocetin; von Willebrand Diseases | 1981 |