Reduced platelet activation and platelet aggregation in patients with alcoholic liver cirrhosis

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Resumé

Results from previous studies regarding platelet function in liver cirrhosis are discordant. The aim was to investigate platelet activation and platelet aggregation in patients with alcoholic liver cirrhosis. We included 27 patients with alcoholic liver cirrhosis and 22 healthy individuals. A recently established flow cytometric approach was used to measure platelet activation and platelet aggregation independent of sample platelet count. Platelet aggregation was further investigated using light transmission aggregometry (LTA) (for platelet count >100 × 10 9/L). Platelet agonists were adenosine diphosphate, thrombin receptor-activating peptide, arachidonic acid, collagen, and collagen-related peptide. Patients had lower median platelet count than healthy individuals, 125 × 10 9/L (interquartile range [IQR] 90˗185) versus 240 × 10 9 (IQR 204˗285), p < 0.001. Platelet activation levels in stimulated samples were lower in patients versus healthy individuals, e.g., after collagen-related peptide stimulation, the median percentage of platelets positive for activated glycoprotein IIb/IIIa was 85% (IQR 70–94) in patients versus 97% (IQR 94–99) in healthy individuals, p < 0.001; lower platelet activation capacity being associated with low platelet count and Child–Pugh class B/C cirrhosis. Flow cytometric platelet aggregation was reduced in patients for collagen-related peptide and for adenosine diphosphate, e.g., platelet aggregation (mean ± standard deviation) was 57% ± 4 in patients versus 70% ± 1 in healthy individuals for collagen-related peptide, p = 0.01. Light LTA showed reduced collagen-induced platelet aggregation in some patients compared with healthy individuals. In conclusion, platelet function was reduced in some patients with alcoholic liver cirrhosis and the severity was associated with platelet count and severity of liver cirrhosis.

OriginalsprogEngelsk
TidsskriftPlatelets
Vol/bind29
Udgave nummer5
Sider (fra-til)520-527
ISSN0953-7104
DOI
StatusUdgivet - 4. jul. 2018

Fingeraftryk

Alcoholic Liver Cirrhosis
Platelet Aggregation
Platelet Count
Liver Cirrhosis
Platelet Glycoprotein GPIIb-IIIa Complex
Arachidonic Acid

Citer dette

@article{53ec3e8e64fa4393ab495b54ac065913,
title = "Reduced platelet activation and platelet aggregation in patients with alcoholic liver cirrhosis",
abstract = "Results from previous studies regarding platelet function in liver cirrhosis are discordant. The aim was to investigate platelet activation and platelet aggregation in patients with alcoholic liver cirrhosis. We included 27 patients with alcoholic liver cirrhosis and 22 healthy individuals. A recently established flow cytometric approach was used to measure platelet activation and platelet aggregation independent of sample platelet count. Platelet aggregation was further investigated using light transmission aggregometry (LTA) (for platelet count >100 × 10 9/L). Platelet agonists were adenosine diphosphate, thrombin receptor-activating peptide, arachidonic acid, collagen, and collagen-related peptide. Patients had lower median platelet count than healthy individuals, 125 × 10 9/L (interquartile range [IQR] 90˗185) versus 240 × 10 9 (IQR 204˗285), p < 0.001. Platelet activation levels in stimulated samples were lower in patients versus healthy individuals, e.g., after collagen-related peptide stimulation, the median percentage of platelets positive for activated glycoprotein IIb/IIIa was 85{\%} (IQR 70–94) in patients versus 97{\%} (IQR 94–99) in healthy individuals, p < 0.001; lower platelet activation capacity being associated with low platelet count and Child–Pugh class B/C cirrhosis. Flow cytometric platelet aggregation was reduced in patients for collagen-related peptide and for adenosine diphosphate, e.g., platelet aggregation (mean ± standard deviation) was 57{\%} ± 4 in patients versus 70{\%} ± 1 in healthy individuals for collagen-related peptide, p = 0.01. Light LTA showed reduced collagen-induced platelet aggregation in some patients compared with healthy individuals. In conclusion, platelet function was reduced in some patients with alcoholic liver cirrhosis and the severity was associated with platelet count and severity of liver cirrhosis.",
keywords = "Journal Article, platelet count, Alcohol, platelet function, liver cirrhosis, Cross-Sectional Studies, Humans, Middle Aged, Male, Case-Control Studies, Platelet Aggregation/physiology, Flow Cytometry, Platelet Activation/physiology, Female, Aged, Liver Cirrhosis, Alcoholic/blood",
author = "Vinholt, {Pernille Just} and Anne-Mette Hvas and Christian Nielsen and S{\"o}derstr{\"o}m, {Anna Cecilia} and Ulrik Sprog{\o}e and Fialla, {Annette Dam} and Mads Nybo",
year = "2018",
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doi = "10.1080/09537104.2017.1349308",
language = "English",
volume = "29",
pages = "520--527",
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Reduced platelet activation and platelet aggregation in patients with alcoholic liver cirrhosis. / Vinholt, Pernille Just; Hvas, Anne-Mette; Nielsen, Christian; Söderström, Anna Cecilia; Sprogøe, Ulrik; Fialla, Annette Dam; Nybo, Mads.

I: Platelets, Bind 29, Nr. 5, 04.07.2018, s. 520-527.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

TY - JOUR

T1 - Reduced platelet activation and platelet aggregation in patients with alcoholic liver cirrhosis

AU - Vinholt, Pernille Just

AU - Hvas, Anne-Mette

AU - Nielsen, Christian

AU - Söderström, Anna Cecilia

AU - Sprogøe, Ulrik

AU - Fialla, Annette Dam

AU - Nybo, Mads

PY - 2018/7/4

Y1 - 2018/7/4

N2 - Results from previous studies regarding platelet function in liver cirrhosis are discordant. The aim was to investigate platelet activation and platelet aggregation in patients with alcoholic liver cirrhosis. We included 27 patients with alcoholic liver cirrhosis and 22 healthy individuals. A recently established flow cytometric approach was used to measure platelet activation and platelet aggregation independent of sample platelet count. Platelet aggregation was further investigated using light transmission aggregometry (LTA) (for platelet count >100 × 10 9/L). Platelet agonists were adenosine diphosphate, thrombin receptor-activating peptide, arachidonic acid, collagen, and collagen-related peptide. Patients had lower median platelet count than healthy individuals, 125 × 10 9/L (interquartile range [IQR] 90˗185) versus 240 × 10 9 (IQR 204˗285), p < 0.001. Platelet activation levels in stimulated samples were lower in patients versus healthy individuals, e.g., after collagen-related peptide stimulation, the median percentage of platelets positive for activated glycoprotein IIb/IIIa was 85% (IQR 70–94) in patients versus 97% (IQR 94–99) in healthy individuals, p < 0.001; lower platelet activation capacity being associated with low platelet count and Child–Pugh class B/C cirrhosis. Flow cytometric platelet aggregation was reduced in patients for collagen-related peptide and for adenosine diphosphate, e.g., platelet aggregation (mean ± standard deviation) was 57% ± 4 in patients versus 70% ± 1 in healthy individuals for collagen-related peptide, p = 0.01. Light LTA showed reduced collagen-induced platelet aggregation in some patients compared with healthy individuals. In conclusion, platelet function was reduced in some patients with alcoholic liver cirrhosis and the severity was associated with platelet count and severity of liver cirrhosis.

AB - Results from previous studies regarding platelet function in liver cirrhosis are discordant. The aim was to investigate platelet activation and platelet aggregation in patients with alcoholic liver cirrhosis. We included 27 patients with alcoholic liver cirrhosis and 22 healthy individuals. A recently established flow cytometric approach was used to measure platelet activation and platelet aggregation independent of sample platelet count. Platelet aggregation was further investigated using light transmission aggregometry (LTA) (for platelet count >100 × 10 9/L). Platelet agonists were adenosine diphosphate, thrombin receptor-activating peptide, arachidonic acid, collagen, and collagen-related peptide. Patients had lower median platelet count than healthy individuals, 125 × 10 9/L (interquartile range [IQR] 90˗185) versus 240 × 10 9 (IQR 204˗285), p < 0.001. Platelet activation levels in stimulated samples were lower in patients versus healthy individuals, e.g., after collagen-related peptide stimulation, the median percentage of platelets positive for activated glycoprotein IIb/IIIa was 85% (IQR 70–94) in patients versus 97% (IQR 94–99) in healthy individuals, p < 0.001; lower platelet activation capacity being associated with low platelet count and Child–Pugh class B/C cirrhosis. Flow cytometric platelet aggregation was reduced in patients for collagen-related peptide and for adenosine diphosphate, e.g., platelet aggregation (mean ± standard deviation) was 57% ± 4 in patients versus 70% ± 1 in healthy individuals for collagen-related peptide, p = 0.01. Light LTA showed reduced collagen-induced platelet aggregation in some patients compared with healthy individuals. In conclusion, platelet function was reduced in some patients with alcoholic liver cirrhosis and the severity was associated with platelet count and severity of liver cirrhosis.

KW - Journal Article

KW - platelet count

KW - Alcohol

KW - platelet function

KW - liver cirrhosis

KW - Cross-Sectional Studies

KW - Humans

KW - Middle Aged

KW - Male

KW - Case-Control Studies

KW - Platelet Aggregation/physiology

KW - Flow Cytometry

KW - Platelet Activation/physiology

KW - Female

KW - Aged

KW - Liver Cirrhosis, Alcoholic/blood

U2 - 10.1080/09537104.2017.1349308

DO - 10.1080/09537104.2017.1349308

M3 - Journal article

C2 - 28895774

VL - 29

SP - 520

EP - 527

JO - Platelets

JF - Platelets

SN - 0953-7104

IS - 5

ER -