Clinical Trial of a New Disposable Bleeding-Time Device

Toomey, K.; Kim, Hugh C.; Kosmin, Martin; Saidi, Parvin

doi:10.1093/ajcp/85.5.610

Cited by 6 publications

(3 citation statements)

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“…Platelets were also counted with a hemocytometer by optical microscopy. The bleeding time was measured with a fully automated incision-making device (Surgicutt, International Technidyne Corporation, Edison, NJ) using a modified Ivy method (14). In vitro platelet aggregation was studied in citrated platelet-rich plasma (PRP) by the method of Born as previously reported (15).…”

Section: Basic Hematological Analysismentioning

confidence: 99%

Effects of the R216Q mutation of GATA-1 on erythropoiesis and megakaryocytopoiesis

Balduini¹,

Pecci²,

Loffredo³

et al. 2004

Thromb Haemost

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The transcription factor GATA-1, together with its cofactor FOG-1, regulates erythropoiesis and megakaryocytopoiesis. Mutations in the DNA or FOG-1 binding sites of its N-terminal zinc finger result in different illnesses. Alterations of the FOG-1 face are responsible for dyserythropoietic anemia with thrombocytopenia while R216Q, the only mutation identified in the DNA face, induces X-linked thrombocytopenia with thalassemia (XLTT). The former disorder has been studied in detail whereas little is known about the latter since only one family has been investigated. We studied a second family with an R216Q, showing that XLTT and dyserythropoietic anemia with thrombocytopenia, even if different clinical entities, are closely related disorders. In both cases, patients present mild dyserythropoiesis, red cell hemolysis, severely defective maturation of megakaryocytes, macrothrombocytopenia with alpha-granule deficiency, and abnormalities of the cytoplasmic membrane system. However, a thalassemia minor phenotype has only been described in patients with XLTT whereas severe anemia and thrombocytopenia with evident defects of platelet composition and function may be observed only in dyserythropoietic anemia with thrombocytopenia.

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Section: Basic Hematological Analysismentioning

confidence: 99%

Effects of the R216Q mutation of GATA-1 on erythropoiesis and megakaryocytopoiesis

Balduini¹,

Pecci²,

Loffredo³

et al. 2004

Thromb Haemost

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“…Bleeding time wasmeasured with afullyautomated incisionmaking device (Surgicutt, InternationalT echnidyneC orporation, Edison,USA)according to amodified Ivy method (11). In vitro plateleta ggregation wass tudiedi nc itrated platelet-rich plasma usingthe Bornmethodaspreviouslyreported (12).Plateleta gonistsw ere fibrillar collagent ype I, 4a nd 20 µ g/ml (Chrono-LogC orporation, Havertown, USA), ADP 5a nd 20 mM and ristocetin 0.7 and 1.5 mg/ml(both from Sigma Chemi-calCo, St.Louis, USA).…”

Section: Basichematological Analysesmentioning

confidence: 99%

Autosomal dominant thrombocytopenias with reduced expression of glycoprotein Ia

Noris¹,

Guidetti²,

Conti³

et al. 2006

Thromb Haemost

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We have recently studied a case series of 46 unrelated patients with inherited thrombocytopenias and identified 18 cases that did not fit any known platelet disorder. In two unrelated families, a mild thrombocytopenia with normal platelet size was transmitted in an autosomal dominant fashion. Bleeding time was prolonged in 5 investigated patients. In all of them, flow cytometry and SDS-PAGE of platelet glycoproteins (GP) showed a reduced content of GPIa, a subunit of the GPIa-IIa complex (also known as integrin alpha 2 beta(1)) that is a major collagen receptor on platelets. All other membrane GPs were within the normal range. GPIa deficiency was associated with severely reduced in vitro platelet adhesion to molecules known to interact selectively with GPIa. In vitro platelet aggregation was normal in all subjects, except for a suboptimal platelet response to fibrillar collagen in two patients. A mild defect of alpha-granules was observed in all affected subjects. No mutation was identified in the genes encoding for GPIa or GPIIa. Since no other similar cases have been reported in the literature, we suggest that an autosomal dominant thrombocytopenia associated with GPIa deficiency and alpha-granule defect represents a new form of inherited thrombocytopenia.

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“…The bleeding time was measured by the method of Mielke et al (4), with a modification using Simplate template II device (General Diagnos tics, Morris Plains, NJ) and making two 5 mm horizontal incisions on the (5). Blood samples were collected by venipuncture through a 21 gauge butterfly needle.…”

Section: A S S a Y M E Th O D Smentioning

confidence: 99%

Patients With Prolonged Bleeding Time of Undefined Etiology, and Their Response to Desmopressin

et al. 1988

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SummaryBetween 1981 and 1986, we evaluated 59 patients who presented with isolated prolongation of bleeding time with normal platelet counts, platelet aggregation and coagulation parameters (including von Willebrand’s factor), and without evidence of liver or kidney disease, or exposure to anti-platelet agents. These patients, termed as vascular fragility syndrome (VFS), were analyzed to further characterize their bleeding patterns. The pattern of bleeding manifestations was similar to that of patients with platelet dysfunction, such as mucocutaneous bleeding or excessive post-operative bleeding. In 16 patients, desmopressin (l-desamino-8-d-arginine vasopressin, DDAVP) was infused to control active bleeding or as a part of pre-surgical evaluation. Bleeding time improved (pre-DDAVP bleeding time 15.3 ± 3.4 min, mean±S.D.; post-DDAVP bleeding time 10.7 ± 3.9 min; p<0.01) within 30 minutes following the DDAVP infusion with either satisfactory arrest of acute bleeding or good control of subsequent hemostasis with surgery. Side effects with DDAVP were transient and minor, i.e. facial flushing, or conjunctival erythema. These findings indicate that VFS with isolated prolongation of bleeding time is a frequently encountered bleeding disorder and that DDAVP is effective in achieving hemostasis for the management of acute bleeding and may be useful prior to surgical procedures.

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Clinical Trial of a New Disposable Bleeding-Time Device

Cited by 6 publications

References 0 publications

Effects of the R216Q mutation of GATA-1 on erythropoiesis and megakaryocytopoiesis

Effects of the R216Q mutation of GATA-1 on erythropoiesis and megakaryocytopoiesis

Autosomal dominant thrombocytopenias with reduced expression of glycoprotein Ia

Patients With Prolonged Bleeding Time of Undefined Etiology, and Their Response to Desmopressin

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