Failure of two anti-platelet drugs (indobufen and dipyridamole) to improve thrombocytopenia in liver cirrhosis.

The hypothesis that thrombocytopenia in liver cirrhosis (LC) could be due to platelet activation was investigated. 18 patients with thrombocytopenia and LC have been studied. Circulating beta-thromboglobulin (beta TG) was normal, but appeared elevated when referred to platelet count. However, this may not accurately reflect alpha-granule release because of reduced liver cell function. Intraplatelet beta TG, on the contrary, should not be affected by liver cell function. It was markedly depressed, thus truly suggesting the existence of an exhausted state caused by platelet activation. Thromboxane B2 production was slightly increased. This could be due to a compensatory mechanism, or simply to platelet size, which was slightly increased, too. Anti-platelet therapy failed to improve thrombocytopenia. A platelet activation state seems therefore to be present in LC, but seems not to be the only cause of thrombocytopenia. Platelet factor 4 approximated zero, regardless of platelet count and therapy. This confirms that elevated values of such a protein represent only a laboratory artifact, due to platelet activation in vitro.