ristocetin


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Translations

ris·to·ce·tin

n. ristocetina, antibiótico que se usa en el tratamiento de infecciones producidas por un estreptococo gram-positivo.
References in periodicals archive ?
There is absence of aggregation response with ristocetin on platelet aggregation studies with normal aggregation with other aggregating agents.8 BSS diagnosis is confirmed by Flow cytometric analysis of platelets showing defective binding with CD42a (GPIX), CD42b (GP Ib[alpha]), CD42c (GP Ib[beta]), and CD42d (GPV) antibodies.9 The defective fragments of GP Ib-IX-V complex after separating with sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) may be identified by immunobloating.10
However, but in line with this study, a defect in platelet aggregation indicated by a hyporeactivity of platelet after induction with ADP, ristocetin, and collagen was showed in major thalassemia children patients with an iron overload condition (12).
(39) No consistent in vitro platelet aggregation abnormalities to collagen, ADP, or ristocetin stimulation are observed.
Carbohydrate moiety of von willebrand factor is not necessary for maintaining multimeric structure and ristocetin cofactor activity but protects from proteolytic degradation.
Contract notice: provision of reagents and consumables for the determination of villebrand ristocetin cofactor-dependent activity with automaton provision
Laboratory evaluation typically reveals mild to moderate thrombocytopenia, unusually large platelets, and abnormal platelet function with absent or markedly reduced aggregation response to ristocetin. Flow cytometric analysis demonstrates absence of GPIb (CD 42) on the platelet surface.
The LTA evaluates shape change, lag phase, percent of aggregation, slope of aggregation, and deaggregation before and after the addition of an agonist (ADP, collagen, epinephrine, arachidonic acid, ristocetin, thrombin receptor-activating peptide, and thromboxane A2 mimetic).
[8], the sticky platelet syndrome is defined as a qualitative alteration of the platelet function and of autosomal dominant inheritance, characterized by platelet hyperaggregation in vitro with low concentrations of adenosine diphosphate (ADE) and/or epinephrine (EPI) but with normal aggregation in response to collagen, arachidonic acid, ristocetin, and thrombin [9].
The laboratory tests of the patient were as follows: quantitative hCG 117740 IU/ml, TSH 3,229 [mu]IU/ml, and free T3 and T4 were within normal ranges; hemoglobin 16,7 g/dl, hematocrit 47,6%, E2 >5000 pg/ml, PT, PTT, and fibrinogen were within normal limits; routine biochemical tests were normal (for example, total protein, albumin, creatinine, BUN, Na, K, AST, ALT, and LDH); interestingly CA-125 (564 IU/mL) was found higher, Inhibin A 861, Ristocetin cofactor (von Willebrand factor (VWF) activity) 100% (50-100%), and VWF antigen 150% (60-150%).
There is a normal aggregation response to ADP agonists, collagen, adrenaline and arachidonic acid, but aggregation is absent with the addition of ristocetin.
Further investigations such as luteinizing hormone/follicle-stimulating hormone (LH/ FSH), Von Willebrand factor activity, and Ristocetin cofactor assay were done in selected patients.
de Factor de Von Willebrand 93 % - Ristocetin Co-factor 113 % - Factor VW unido a colageno 94 % (diluciones) problema/testigo (correcciones)problema TTPa 92.2/30 seg.