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Abnormal Platelet Function and Ultrastructure in Fulminant Hepatic Failure
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1977
Year
PathologyPlatelet PathobiologyPlatelet AggregationCirrhosisThrombosisHematologyPlatelet ConcentratesHepatology FibrosisPlatelet AntagonistAbnormal Platelet FunctionHealth SciencesPlatelet BiologyLiver PhysiologyHistopathologyHepatology InflammationVascular BiologyVitro Platelet AggregationPharmacologyHepatologyBlood PlateletAcquired Platelet DefectHepatitisHemostasisAcute Liver FailureLiver DiseaseCoagulopathyMedicine
Evidence in favour of an acquired platelet defect in fulminant hepatic failure has been provided by studies of in vitro platelet aggregation with adenosine diphosphate (ADP). Platelets from six patients required a higher concentration (threshold concentration) of ADP to reach second phase aggregation than those from controls (12·3 compared with 2·2×10−6 M). Platelets from another six patients failed to show second phase aggregation at the highest concentration of ADP used (3·2×10−6 M). The degree of aggregation at a fixed concentration (3·2×−6 M) was significantly less than in controls (34·2 per cent compared with 57·5 per cent). Capillary bleeding times correlated positively with the abnormalities of platelet aggregation. In crossover studies, platelet poor plasma from these patients did not inhibit platelet aggregation in controls, nor did platelet poor plasma from controls enable patients' platelets to reach second phase aggregation suggesting that factors other than the plasma were responsible for this abnormal platelet function. Some relationship between the severity of hepatic necrosis and platelet dysfunction can be deduced as platelet function was normal in 16 patients with virus hepatitis or liver damage following paracetamol overdose who were ill enough to warrant hospital admission, but who did not develop fulminant hepatic failure. Electron microscopy of platelets from patients with fulminant hepatic failure showed many structural abnormalities including numerous pseudopods, vacuoles and blurred plasma membranes. Most striking were the numbers of platelets showing microtubules, and the increased microtubular content per platelet. As patients recovered from fulminant hepatic failure, platelet function improved and platelets with normal ultrastructure appeared amongst the abnormal ones. The abnormal-looking platelets may be responsible for the abnormalities of platelet function, but kinetic studies are required to elucidate their source and fate.