Case 1: A 27-year-old woman, referred to our hospital because of relapsing fever after travel to Thailand, was given a diagnosis of vivax malaria. Clinical investigation revealed thrombocytopenia, elevated platelet-associated IgG (PAIgG), and negative antibody against Plasmodium vivax antigen. After antimalarial treatment, the levels of both the platelets and PAIgG returned to normal. Case 2: A 28-year-old Sri Lankan man was admitted to our hospital with a complaint of fever. The patient had thrombocytopenia, elevated PAIgG, and positive antibody against Plasmodium vivax antigen. He contracted malaria in Sri Lanka about 6 months prior to this admission. After treatment, the platelet count and PAIgG level returned to normal. In these two cases, high levels of PAIgG may have been involved in the development of the thrombocytopenia. In the first patient, in particular, the thrombocytopenia was thought to be induced by some immunological mechanism prior to the detection of antimaralial antibodies in serum.
Tissue factor activity (TFA) of 10(8) leukemia cells was measured in 82 patients with acute nonlymphoid leukemia by the clotting method. The TFA bore a significant correlation to the development of disseminated intravascular coagulation (DIC) in these cases. Mean TFA value with standard deviation (SD) was 8.3 +/- 6.3 U in 48 cases with DIC, which was significantly higher than 0.3 +/- 4.2 U in 34 cases without DIC. Whereas Mean TFA in non-M3 was 0.9 +/- 6.3 U which was significantly lower than 37.2 +/- 2.3 U in M3, some non-M3 showed TFA as high as M3 and were complicated by DIC. In heparin treatment, dosage of heparin could not be controlled by either APTT or AcCT but was controlled by the extent of TFA of leukemia cells. Retrospective analysis of clinical features revealed that 97000X + 9000 units/day (X = logarithm value of TFA) of heparin is an adequate dosage for the successful treatment of DIC when TFA of leukemia cells is 0.8 U or more.
SummaryUsing clotting assay and radioimmunoassay (RIA), tissue factor activity (TFA) and TF related antigen (TFR:AG) were determined in an extracellular culture medium of HL-60 cells. After 12 h incubation, TFA and TFR:AG in the medium with endotoxin (EDX: 1 μg/ml) reached maximums which were 1.8 and 2.1 times greater than those in the medium without EDX, respectively. In the leukemic cells of 10 patients with acute nonlymphoid leukemia (ANLL), TFR:AG showed a significant correlation with TFA (p <0.01). On day 1 of the induction chemotherapy, TFR:AG in the 7 patients with DIC significantly increased to 288.9 ± 153.1 ng/ml (p <0.01), whereas no increase in TFR: AG was recognized in the 3 patients without DIC. These results suggest that TF may be released from leukemic cells into the culture medium or blood stream, and that this may correlate with the development of DIC.
Case 1: A 27-year-old woman, referred to our hospital because of relapsing fever after travel to Thailand, was given a diagnosis of vivax malaria. Clinical investigation revealed thrombocytopenia, elevated platelet-associated IgG (PAIgG), and negative antibody against Plasmodium vivax antigen. After antimalarial treatment, the levels of both the platelets and PAIgG returned to normal. Case 2: A 28-year-old Sri Lankan man was admitted to our hospital with a complaint of fever. The patient had thrombocytopenia, elevated PAIgG, and positive antibody against Plasmodium vivax antigen. He contracted malaria in Sri Lanka about 6 months prior to this admission. After treatment, the platelet count and PAIgG level returned to normal. In these two cases, high levels of PAIgG may have been involved in the development of the thrombocytopenia. In the first patient, in particular, the thrombocytopenia was thought to be induced by some immunological mechanism prior to the detection of antimaralial antibodies in serum. Am.
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