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Cited by 679

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Platelet Function in Hyperlipoproteinemia

Carvalho, Angelina C. A., Colman, Robert W., Lees, Robert S.·1974·New England Journal of Medicine

Abstract

Platelet function was studied in 17 patients with Type II hyperlipoproteinemia. As compared with 26 normal subjects, platelets from patients with the Type II syndrome aggregated in response to 1/25 the mean concentration of epinephrine, one third the concentration of collagen, and one third the concentration of ADP. Total nucleotide release was increased from four to six fold with all aggregating agents. However, release of platelet factors 3 and 4, platelet adhesiveness and clot retraction were all normal in patients with Type II hyperlipoproteinemia. In contrast, platelets from 11 patients with Type IV hyperlipoproteinemia showed normal sensitivity to ADP and collagen, normal nucleotide release and normal release of 14C serotonin. The data suggest that heightened platelet function is associated with the thrombotic complications and accelerated atherogenesis of Type II hyperlipoproteinemia. (N Engl J Med 290:434–438, 1974)

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Metadata

Authors
Carvalho, A. C. A., Colman, R. W., & Lees, R. S.
Venue
New England Journal of Medicine
Published
1974-02-21
Volume
290
Issue
8
Pages
434-438
ISSN
  • 0028-4793 (ISSN-L)
  • 1533-4406
OpenAlex
W2319045997
Cited by
679
References
0
FWCI
19.89
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Platelet Function in Hyperlipoproteinemia. https://app.cochat.ai/papers/10.1056/nejm197402212900805
The paper
Carvalho, A. C. A., Colman, R. W., & Lees, R. S. (1974). Platelet Function in Hyperlipoproteinemia. New England Journal of Medicine. https://doi.org/10.1056/nejm197402212900805

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.