Platelet function in cirrhosis and the role of humoral factors

Hazel M. Younger, Patrick W. F. Hadoke, John F. Dillon, Peter C. Hayes

    Research output: Contribution to journalArticle

    12 Citations (Scopus)

    Abstract

    Background: Haemorrhagic complications are common in patients with cirrhosis of the liver and contribute to the morbidity and mortality seen in this condition. Several pathological processes are involved in these complications, including a delay and overall reduction in platelet aggregation.
    Objective: To determine whether impaired aggregation in cirrhosis is the result of an intrinsic abnormality in platelet function or is induced by a factor present in the blood of cirrhotic patients.
    Setting: Liver unit patients in a teaching hospital.
    Design: Blood was taken from 11 patients with cirrhosis (Child's B or C) and 11 healthy controls. Crossover experiments were carried out, suspending platelet pellets from patients in platelet-poor plasma from controls, and vice versa. Aggregation of both samples and also of platelet-rich plasma from patients and controls was measured.
    Results: Aggregation after 1 min was impaired significantly in patient, compared with control, platelets following incubation in either patient (P= 0.0012), or control (P= 0.0242), plasma. Correspondingly, maximum aggregation of patient platelets was also reduced significantly (P= 0.0036) after incubation in patient plasma. Aggregation after 1 min, and maximum aggregation, of control platelets was increased significantly (P= 0.034 and 0.013, respectively) following incubation in patient plasma. Furthermore, there was a trend (non-significant) towards reduced aggregation of patient platelets incubated in control plasma.
    Conclusion: These results confirm both an intrinsic platelet defect causing impaired aggregation and a circulating factor in the plasma of patients with cirrhosis which may compensate for this functional defect.
    Original languageEnglish
    Pages (from-to)989-992
    Number of pages4
    JournalEuropean Journal of Gastroenterology & Hepatology
    Volume9
    Issue number10
    Publication statusPublished - Oct 1997

    Fingerprint

    Fibrosis
    Blood Platelets
    Platelet Aggregation
    Platelet-Rich Plasma
    Pathologic Processes
    Teaching Hospitals
    Liver Cirrhosis
    Morbidity
    Mortality
    Liver

    Cite this

    Younger, Hazel M. ; Hadoke, Patrick W. F. ; Dillon, John F. ; Hayes, Peter C. / Platelet function in cirrhosis and the role of humoral factors. In: European Journal of Gastroenterology & Hepatology. 1997 ; Vol. 9, No. 10. pp. 989-992.
    @article{0c8c3bb3cf5545c4a01c5615be376a08,
    title = "Platelet function in cirrhosis and the role of humoral factors",
    abstract = "Background: Haemorrhagic complications are common in patients with cirrhosis of the liver and contribute to the morbidity and mortality seen in this condition. Several pathological processes are involved in these complications, including a delay and overall reduction in platelet aggregation. Objective: To determine whether impaired aggregation in cirrhosis is the result of an intrinsic abnormality in platelet function or is induced by a factor present in the blood of cirrhotic patients. Setting: Liver unit patients in a teaching hospital. Design: Blood was taken from 11 patients with cirrhosis (Child's B or C) and 11 healthy controls. Crossover experiments were carried out, suspending platelet pellets from patients in platelet-poor plasma from controls, and vice versa. Aggregation of both samples and also of platelet-rich plasma from patients and controls was measured. Results: Aggregation after 1 min was impaired significantly in patient, compared with control, platelets following incubation in either patient (P= 0.0012), or control (P= 0.0242), plasma. Correspondingly, maximum aggregation of patient platelets was also reduced significantly (P= 0.0036) after incubation in patient plasma. Aggregation after 1 min, and maximum aggregation, of control platelets was increased significantly (P= 0.034 and 0.013, respectively) following incubation in patient plasma. Furthermore, there was a trend (non-significant) towards reduced aggregation of patient platelets incubated in control plasma. Conclusion: These results confirm both an intrinsic platelet defect causing impaired aggregation and a circulating factor in the plasma of patients with cirrhosis which may compensate for this functional defect.",
    author = "Younger, {Hazel M.} and Hadoke, {Patrick W. F.} and Dillon, {John F.} and Hayes, {Peter C.}",
    note = "Times Cited: 9",
    year = "1997",
    month = "10",
    language = "English",
    volume = "9",
    pages = "989--992",
    journal = "European Journal of Gastroenterology & Hepatology",
    issn = "0954-691X",
    publisher = "Lippincott, Williams & Wilkins",
    number = "10",

    }

    Platelet function in cirrhosis and the role of humoral factors. / Younger, Hazel M.; Hadoke, Patrick W. F.; Dillon, John F.; Hayes, Peter C.

    In: European Journal of Gastroenterology & Hepatology, Vol. 9, No. 10, 10.1997, p. 989-992.

    Research output: Contribution to journalArticle

    TY - JOUR

    T1 - Platelet function in cirrhosis and the role of humoral factors

    AU - Younger, Hazel M.

    AU - Hadoke, Patrick W. F.

    AU - Dillon, John F.

    AU - Hayes, Peter C.

    N1 - Times Cited: 9

    PY - 1997/10

    Y1 - 1997/10

    N2 - Background: Haemorrhagic complications are common in patients with cirrhosis of the liver and contribute to the morbidity and mortality seen in this condition. Several pathological processes are involved in these complications, including a delay and overall reduction in platelet aggregation. Objective: To determine whether impaired aggregation in cirrhosis is the result of an intrinsic abnormality in platelet function or is induced by a factor present in the blood of cirrhotic patients. Setting: Liver unit patients in a teaching hospital. Design: Blood was taken from 11 patients with cirrhosis (Child's B or C) and 11 healthy controls. Crossover experiments were carried out, suspending platelet pellets from patients in platelet-poor plasma from controls, and vice versa. Aggregation of both samples and also of platelet-rich plasma from patients and controls was measured. Results: Aggregation after 1 min was impaired significantly in patient, compared with control, platelets following incubation in either patient (P= 0.0012), or control (P= 0.0242), plasma. Correspondingly, maximum aggregation of patient platelets was also reduced significantly (P= 0.0036) after incubation in patient plasma. Aggregation after 1 min, and maximum aggregation, of control platelets was increased significantly (P= 0.034 and 0.013, respectively) following incubation in patient plasma. Furthermore, there was a trend (non-significant) towards reduced aggregation of patient platelets incubated in control plasma. Conclusion: These results confirm both an intrinsic platelet defect causing impaired aggregation and a circulating factor in the plasma of patients with cirrhosis which may compensate for this functional defect.

    AB - Background: Haemorrhagic complications are common in patients with cirrhosis of the liver and contribute to the morbidity and mortality seen in this condition. Several pathological processes are involved in these complications, including a delay and overall reduction in platelet aggregation. Objective: To determine whether impaired aggregation in cirrhosis is the result of an intrinsic abnormality in platelet function or is induced by a factor present in the blood of cirrhotic patients. Setting: Liver unit patients in a teaching hospital. Design: Blood was taken from 11 patients with cirrhosis (Child's B or C) and 11 healthy controls. Crossover experiments were carried out, suspending platelet pellets from patients in platelet-poor plasma from controls, and vice versa. Aggregation of both samples and also of platelet-rich plasma from patients and controls was measured. Results: Aggregation after 1 min was impaired significantly in patient, compared with control, platelets following incubation in either patient (P= 0.0012), or control (P= 0.0242), plasma. Correspondingly, maximum aggregation of patient platelets was also reduced significantly (P= 0.0036) after incubation in patient plasma. Aggregation after 1 min, and maximum aggregation, of control platelets was increased significantly (P= 0.034 and 0.013, respectively) following incubation in patient plasma. Furthermore, there was a trend (non-significant) towards reduced aggregation of patient platelets incubated in control plasma. Conclusion: These results confirm both an intrinsic platelet defect causing impaired aggregation and a circulating factor in the plasma of patients with cirrhosis which may compensate for this functional defect.

    M3 - Article

    VL - 9

    SP - 989

    EP - 992

    JO - European Journal of Gastroenterology & Hepatology

    JF - European Journal of Gastroenterology & Hepatology

    SN - 0954-691X

    IS - 10

    ER -