Thrombocytopenia of chronic liver disease corrected by erythropoietin treatment

To investigate the possibility of correcting thrombocytopenia of chronic liver disease, 19 patients (6 male and 13 female) with long-term chronic liver disease and platelet count ≤85 000/μl were studied. Either a short-term course (7-20 days) of recombinant human erythropoietin, 4000 U daily SQ (12 patients) or placebo (7 patients) was administered. Treatment was interrupted if the platelets rose to ≥100 000/μl or if no significant increase was noted after 14 days. After treatment, platelets increased in the recombinant human erythropoietin group (from a baseline value of 70 000±11 184 to 101 250±37 625/μl), while no difference was noted in the placebo group (70 714±9928 vs 70 000±10 231/μl). The increase in the platelet count in the recombinant human erythropoietin group was significant, both compared to baseline values (paired Student's t-test, t=-3.80, p<0.005) and to the results of treatment in the placebo group (unpaired Student's t-test, t=2.71, p<0.02). Eight out of 12 recombinant human erythropoietin-treated patients (66%) reached ≥100 000/μl platelets while four (33%) did not. In comparison to responders, non-responders had a significantly lower baseline platelet count (58 500±7937 vs 75 750±7498/μl, t=-3.69, p=0.004) and failed more frequently than responders to improve their haematocrit in response to recombinant human erythropoietin (Pearson χ²=4.687, p=0.03). When treatment was discontinued, the platelet count reverted to baseline in a few weeks. In conclusion, recombinant human erythropoietin treatment transiently corrected mild thrombocytopenia in patients with chronic liver disease. The failure to increase circulating thrombocytes with recombinant human erythropoietin treatment occurred in patients with a lower steady-state value in the balance between excessive platelet destruction and compensatory production.