[Frequency and pathogenis of thrombocytopenia in cardiac failure]. / Häufigkeit und Pathogenese einer Thrombozytopenie bei Herzinsuffizienz

In 395 consecutively investigated patients with cardiac failure of varying aetiologythe platelet ocurt in venous blood was less than 100 000/mm(3) in 5.3% and below the 2s devaition (less than 136 000/mm (3)) in 19.2. The average platelet count of the whole group was 197 500 +/- 70 800/mm (3) which was significantly lower (P less than 0.001) than in normal controls (n = 128). In 6 patients a (51)Cr study of platelet kinetics was performed; the results support the conclusion that the faculatative thrombocytopenia in cardiac failure is mainly,but not exclusively, due to an increased uptake of platelets in the congested spleen.

[Production and splenic storage of platelets in autoimmune thrombocytopenia (author's transl)]. / Plättchenproduktion und lienale Plättchenspeicherung bei Autoimmun-Thrombozytopenien

Platelet kinectics (using 51Cr labelling) was measured in 66 tests on 59 patients with autoimmune thrombocytopenia (the majority with chronic Werlhof's disease plus cases of acute Werlhof's disease, Evans' syndrome and visceral lupus), measuring platelet survival time, platelet production, and splenic storage rate of platelets. Dependent on the severity of the disease, the elimination curve showed an abnormal course during the initial phase which - in comparison with the normal - indicated approximately a difference of the spleen-dependent part of the disappearance rate from the antibody-dependent destruction. Accordingly, platelet storage in the spleen was slightly supernormal in the studied diseases. On average, platelet destruction was increased to more than twice normal. In 36% of cases platelet production remained within normal range. On average, the least increase in platelet production occurred in the acute form of Werlhof's disease. Maximal storage capacity, which can be six times normal and above, was reached in only a few cases.