What is the clinical evidence from this study?

Study design: Observational. Population: Healthy blood donors deficient in GPIIIb (n=3). Intervention: GPIIIb deficiency vs. Control platelets. Primary outcome: Platelet aggregation and secretion in response to collagens type I, III, and V.

December 1, 1993Blood

Platelets deficient in glycoprotein IIIb aggregate normally to collagens type I and III but not to collagen type V

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Key result

Platelets deficient in GPIIIb aggregated normally to type I and III collagens but showed no aggregation and impaired secretion in response to type V collagen compared to control platelets.

Population

Platelets from 3 healthy blood donors deficient in glycoprotein IIIb (GPIIIb)

Comparison

Exposure to collagens type I, III, and V vs Control platelets

Design

Preclinical

Authors

BKBeate E. Kehrel AKA Kronenberg JRJ. Rauterberg

Discussion

Member takes

Overview

May inform selective antiplatelet targeting without broad hemostatic risk; leaves open human translation from animal data.

Study Design

Type

Observational (n=3)

Structured PICO

Population

3 healthy blood donors with platelets deficient in GPIIIb.

Exposure

Exposure to collagens type I, III, and V

Comparator

Control platelets

Outcome

Platelet aggregation and secretion of platelet factor 4, beta-thromboglobulin, and ATPsurrogate

GPIIIb is essential for platelet aggregation induced by type V collagen, but not for types I and III, explaining the lack of hemostatic problems in GPIIIb-deficient individuals.

Cite This Study

Kehrel et al. (1993) conducted an observational in Healthy blood donors deficient in GPIIIb (n=3). GPIIIb deficiency vs. Control platelets was evaluated on Platelet aggregation and secretion in response to collagens type I, III, and V. Platelets deficient in GPIIIb aggregated normally to type I and III collagens but showed no aggregation and impaired secretion in response to type V collagen compared to control platelets.

synapsesocial.com/papers/6a9448e578fe3e71bd43eafd https://doi.org/10.1182/blood.v82.11.3364.3364

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December 1, 1993Blood

Platelets deficient in glycoprotein IIIb aggregate normally to collagens type I and III but not to collagen type V

View Full Paper

Ask AI

Bookmark

Key result

Platelets deficient in GPIIIb aggregated normally to type I and III collagens but showed no aggregation and impaired secretion in response to type V collagen compared to control platelets.

Population

Platelets from 3 healthy blood donors deficient in glycoprotein IIIb (GPIIIb)

Comparison

Exposure to collagens type I, III, and V vs Control platelets

Design

Preclinical

Authors

BKBeate E. Kehrel AKA Kronenberg JRJ. Rauterberg

Discussion

Member takes

Overview

May inform selective antiplatelet targeting without broad hemostatic risk; leaves open human translation from animal data.

Study Design

Type

Observational (n=3)

Structured PICO

Population

3 healthy blood donors with platelets deficient in GPIIIb.

Exposure

Exposure to collagens type I, III, and V

Comparator

Control platelets

Outcome

Platelet aggregation and secretion of platelet factor 4, beta-thromboglobulin, and ATPsurrogate

GPIIIb is essential for platelet aggregation induced by type V collagen, but not for types I and III, explaining the lack of hemostatic problems in GPIIIb-deficient individuals.

Cite This Study

synapsesocial.com/papers/6a9448e578fe3e71bd43eafd https://doi.org/10.1182/blood.v82.11.3364.3364

Also Consider

Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context:

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