Among 111 patients referred to our outpatient clinic for isolated thrombocytopenia
during a 24-month period, 17 (15.3%) cases of EDTA-dependent pseudothrombocytopenia
(EDTA-PTCP) were identified. EDTA-PTCP represented the
second most frequent cause of thrombocytopenia in this population. The diagnosis
was confirmed by the following findings: (a) normal platelet numbers immediately
after blood withdrawal; (b) progressive fall of platelet counts and evident
platelet clumping over time, only in EDTA-anticoagulated blood. A simple,
inexpensive and quick diagnostic method was devised, that consists in evaluating
the platelet number in a blood sample anticoagulated with EDTA immediately
after blood withdrawl and 4 h later.
Among 111 patients referred to our outpatient clinic for isolated thrombocytopenia during a 24-month period, 17 (15.3%) cases of EDTA-dependent pseudothrombocytopenia (EDTA-PTCP) were identified. EDTA-PTCP represented the second most frequent cause of thrombocytopenia in this population. The diagnosis was confirmed by the following findings: (a) normal platelet numbers immediately after blood withdrawal; (b) progressive fall of platelet counts and evident platelet clumping over time, only in EDTA-anticoagulated blood. A simple, inexpensive and quick diagnostic method was devised, that consists in evaluating the platelet number in a blood sample anticoagulated with EDTA immediately after blood withdrawal and 4 h later.
A patient with a combined hereditary deficiency of factors VII and VIII is presented together with a family study. The main bleeding manifestations were easy bruising and bleeding after tooth extractions. No hemarthrosis was ever observed. The main laboratory features consisted in a mild prolongation of prothrombin time and of partial thromboplastin time. TG test was abnormal and was corrected by the addition of adsorbed normal plasma. Specific assays revealed a moderate defect of factors VII and VIII. All other clotting factors were within normal limits. The factor VII antigen in the propositus was normal or nearly normal. The factor- VIII-associated antigen was also normal. Five additional family members presented the same coagulation pattern and were variably symptomatic. The hereditary transmission pattern seems to be autosomal dominant. The defect appears to be due to a structural abnormality of a gene controlling factors VII and VIII activation.
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