Acquired dysfunction due to the circulation of 'exhausted' platelets

F. I. Pareti, A. Capitanio, L. Mannucci, C. Ponticelli, P. M. Mannucci

Research output: Contribution to journalArticle

113 Citations (Scopus)

Abstract

An acquired platelet functional defect was found to be present in eight patients who presented with various clinical conditions- three with renal allograft rejection, three with the hemolytic uremic syndrome or thrombotic thrombocytopenic purpura, one with acute consumption coagulopathy due to an incompatible transfusion and one with systemic lupus erythematosus. They showed defective platelet aggregation and reduced levels of adenine nucleotides and serotonin with abnormal uptake and storage of the amine. The bleeding time was more prolonged than predicted from the platelet count. These abnormalities were strikingly similar to those occurring in patients with congenital storage pool deficiency. The acquired defect is thought to be related to the presence in the circulation of 'exhausted' platelets following their in vivo exposure to inducers of the release reaction such as damaged endothelium, thrombin and immune complexes. The bleeding tendency of the underlying diseases might be aggravated by the impairment of platelet function.

Original languageEnglish
Pages (from-to)235-240
Number of pages6
JournalAmerican Journal of Medicine
Volume69
Issue number2
DOIs
Publication statusPublished - 1980

Fingerprint

Blood Platelets
Platelet Storage Pool Deficiency
Thrombotic Thrombocytopenic Purpura
Hemolytic-Uremic Syndrome
Bleeding Time
Adenine Nucleotides
Disseminated Intravascular Coagulation
Antigen-Antibody Complex
Platelet Count
Platelet Aggregation
Thrombin
Systemic Lupus Erythematosus
Endothelium
Amines
Allografts
Serotonin
Hemorrhage
Kidney

ASJC Scopus subject areas

  • Nursing(all)

Cite this

Acquired dysfunction due to the circulation of 'exhausted' platelets. / Pareti, F. I.; Capitanio, A.; Mannucci, L.; Ponticelli, C.; Mannucci, P. M.

In: American Journal of Medicine, Vol. 69, No. 2, 1980, p. 235-240.

Research output: Contribution to journalArticle

Pareti, F. I. ; Capitanio, A. ; Mannucci, L. ; Ponticelli, C. ; Mannucci, P. M. / Acquired dysfunction due to the circulation of 'exhausted' platelets. In: American Journal of Medicine. 1980 ; Vol. 69, No. 2. pp. 235-240.
@article{b251a0f8f40a4832a5477198d1a22c04,
title = "Acquired dysfunction due to the circulation of 'exhausted' platelets",
abstract = "An acquired platelet functional defect was found to be present in eight patients who presented with various clinical conditions- three with renal allograft rejection, three with the hemolytic uremic syndrome or thrombotic thrombocytopenic purpura, one with acute consumption coagulopathy due to an incompatible transfusion and one with systemic lupus erythematosus. They showed defective platelet aggregation and reduced levels of adenine nucleotides and serotonin with abnormal uptake and storage of the amine. The bleeding time was more prolonged than predicted from the platelet count. These abnormalities were strikingly similar to those occurring in patients with congenital storage pool deficiency. The acquired defect is thought to be related to the presence in the circulation of 'exhausted' platelets following their in vivo exposure to inducers of the release reaction such as damaged endothelium, thrombin and immune complexes. The bleeding tendency of the underlying diseases might be aggravated by the impairment of platelet function.",
author = "Pareti, {F. I.} and A. Capitanio and L. Mannucci and C. Ponticelli and Mannucci, {P. M.}",
year = "1980",
doi = "10.1016/0002-9343(80)90383-6",
language = "English",
volume = "69",
pages = "235--240",
journal = "American Journal of Medicine",
issn = "0002-9343",
publisher = "Elsevier Inc.",
number = "2",

}

TY - JOUR

T1 - Acquired dysfunction due to the circulation of 'exhausted' platelets

AU - Pareti, F. I.

AU - Capitanio, A.

AU - Mannucci, L.

AU - Ponticelli, C.

AU - Mannucci, P. M.

PY - 1980

Y1 - 1980

N2 - An acquired platelet functional defect was found to be present in eight patients who presented with various clinical conditions- three with renal allograft rejection, three with the hemolytic uremic syndrome or thrombotic thrombocytopenic purpura, one with acute consumption coagulopathy due to an incompatible transfusion and one with systemic lupus erythematosus. They showed defective platelet aggregation and reduced levels of adenine nucleotides and serotonin with abnormal uptake and storage of the amine. The bleeding time was more prolonged than predicted from the platelet count. These abnormalities were strikingly similar to those occurring in patients with congenital storage pool deficiency. The acquired defect is thought to be related to the presence in the circulation of 'exhausted' platelets following their in vivo exposure to inducers of the release reaction such as damaged endothelium, thrombin and immune complexes. The bleeding tendency of the underlying diseases might be aggravated by the impairment of platelet function.

AB - An acquired platelet functional defect was found to be present in eight patients who presented with various clinical conditions- three with renal allograft rejection, three with the hemolytic uremic syndrome or thrombotic thrombocytopenic purpura, one with acute consumption coagulopathy due to an incompatible transfusion and one with systemic lupus erythematosus. They showed defective platelet aggregation and reduced levels of adenine nucleotides and serotonin with abnormal uptake and storage of the amine. The bleeding time was more prolonged than predicted from the platelet count. These abnormalities were strikingly similar to those occurring in patients with congenital storage pool deficiency. The acquired defect is thought to be related to the presence in the circulation of 'exhausted' platelets following their in vivo exposure to inducers of the release reaction such as damaged endothelium, thrombin and immune complexes. The bleeding tendency of the underlying diseases might be aggravated by the impairment of platelet function.

UR - http://www.scopus.com/inward/record.url?scp=0018957893&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0018957893&partnerID=8YFLogxK

U2 - 10.1016/0002-9343(80)90383-6

DO - 10.1016/0002-9343(80)90383-6

M3 - Article

C2 - 7405945

AN - SCOPUS:0018957893

VL - 69

SP - 235

EP - 240

JO - American Journal of Medicine

JF - American Journal of Medicine

SN - 0002-9343

IS - 2

ER -