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.
| Originalsprog | Engelsk |
|---|---|
| Tidsskrift | Platelets |
| Vol/bind | 29 |
| Udgave nummer | 5 |
| Sider (fra-til) | 520-527 |
| ISSN | 0953-7104 |
| DOI | |
| Status | Udgivet - 4. jul. 2018 |
Fingeraftryk
Citer dette
}
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 tidsskrift › Tidsskriftartikel › Forskning › peer 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 -