Younger H M, Hadoke P W, Dillon J F, Hayes P C
Department of Medicine, Royal Infirmary of Edinburgh, Scotland, UK.
Eur J Gastroenterol Hepatol. 1997 Oct;9(10):989-92. doi: 10.1097/00042737-199710000-00012.
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.
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.
Liver unit patients in a teaching hospital.
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.
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.
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.
