During acute Plasmodium falciparum infection in man, plasma concentrations of platelet-specific proteins, β-thromboglobulin (βTG) and platelet factor 4 (PF4) were significantly elevated. For βTG, the mean concentration was 136.24 ± 71.58 ng/ml in patients, and 50.53 ± 25.42 ng/ml in control subjects (t = 5.3794; p = 0.0001), while for PF4 mean values were, respectively, 75.35 ± 23.09 and 18.64 ± 13.42 ng/ml (t = -6.0897; p < 0.0001). Platelet LDH loss in vitro in response to stimulation with 0.5 U of thrombin was 57.0 ± 29.5% in patient samples and 24.8 ± 16.9% (control); the values being significantly different from each other (t = 2.888; p < 0.025). With serotonin (5HT) uptake and release however, the values were essentially normal, in spite of marginal difference observed in the uptake value of patients compared to control. The data indicate that there was in vivo platelet activation during the infection, with the haemostatic balance tilted towards hypercoagulability. There was also associated easy platelet lysis with stimulation. It is also suggested that the latter finding may be one of the mechanisms of reduced circulating platelet numbers observed in patients in the acute disease.
Eight laboratories in six countries cooperated to clarify several issues concerning the phenotypes of heterozygous carriers of hemophilia “A.” Plasma levels of factor VIII (F.VIII:C, formerly VIII:C) and von Willebrand factor (VWF:Ag, formerly VIIIR:Ag) of carriers and normal women were determined by various “in-house” methods; a single lyophilized plasma standard was used for all assays. Analysis of the collated data from 336 carriers (296 obligatory carriers and 40 sporadic carriers) and 137 normal women showed that there was no difference in the F.VIII:C levels of “paternal” carriers (women who had obtained the abnormal gene from their fathers) and “maternal” carriers. Neither was there a difference in the VWF:Ag levels of normal women and either type of carrier. Age was found to have a significant effect on both F.VIII:C and VWF:Ag, values being higher at very young and very old ages, the minima occurring in the 25- to 30-year range. ABO blood type had a striking effect. Women of types A, B, and AB (designated non- O in the study), both normals and carriers, had significantly higher levels of both factors than did women of type O. Analysis by laboratories showed that differences in mean levels of both factors between laboratories were highly significant. It was concluded that age, ABO blood type, and laboratory variation should be taken into account in carrier detection.
We had earlier reported altered ADP-induced platelet aggregation in man during acute malaria infection. The present study sought to determine (i) whether the changes suggested platelet hypersensitivity to ADP and (ii) whether such changes occurred in vivo or in vitro.The aggregation response of platelets (as citrated PRP) to addition of ADP from thirty patients with acute malaria infection has been compared with that of 29 control i.e., non-infected subjects. The age range of the subjects in both groups varied from 2 to 70 years. These tests were performed before the patients took any drugs. With addition of l.0μM ADP to 1 ml of PRP, the mean aggregation amplitude (as % light transmission) obtained from 8 patients, 39.8±27.1% was significantly greater than that from 9 control subjects (5.2±6.7%; t = 3.51; P < 0.005). With higher ADP concentrations (2.4 - 5.0μM) similar response in 22 subjects (mean 89.1±14.9%) was also significantly greater than that in 20 controls (77.8±16.5%; t = 12.45; P < 0.02). These results suggest that during acute malaria infection in man, circulating platelets become hypersensitive to ADP in vitro. No instances of spontaneous aggregation were however observed in the patients.βTG was determined in 7 patients and 6 controls. The mean plasma βTG in the patients (208.3±15.6 ng/ml) was significantly higher than that in controls (59.2±15.7 ng/ml; t = 13.44; P <0.001). These latter results suggest that the platelets were probably activated in vivo to release the βTG. They further suggest that the hypersensitive changes noted earlier also probably occurred in vivo.It is suggested that acute malaria (P.falciparum) infection in man is probably another clinical condition associated with platelet hypersensitivity.
The first case of Fletcher factor deficiency from the African continent is described. This was the only case of symptomatic Fletcher factor deficiency detected in a total population survey of 40,522 persons. This patient differs from other reported cases in that the child had symptoms of severe bleeding defect such as recurrent haemarthrosis and haematoma. The clinical features appear to improve with age. Both the PTT ‘time course’ and cold-induced EACA acceleration of the thromboplastin time are useful diagnostic tests for detecting homozygous patients. Our results confirm an earlier report that the EACA test is a sensitive test for detecting heterozygotes
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