Haemostatic defect in non-immune patients with falciparum malaria: no evidence of diffuse intravascular coagulation.

Abstract

This inhibition would be expected to inhibit viral DNA synthesis and thus to end viral replication. But we found that 42-nm ("infective virus") particles did not disappear from the blood during treatment, presumably because, although virus replication was inhibited, the clearance rate of the circulating particles was relatively slow in relation to the duration of treatment. Similarly, HBe antigen, a marker for the presence of infective virus, did not disappear from the blood during treatment. The slow clearance of viral particles was similar to that observed after inhibition of virus-specific DNA polymerase by human leucocyte interferon treatment in chronic hepatitis.12 In these studies the serum titre of HBe fell several weeks after the fall in DNA polymerase activity, and not until then did HBsAg titres fall. The results of vidarabine treatment were also similar to those of interferon in that DNA polymerase activity increased after treatment was stopped. Nevertheless, in the case of interferon continued treatment produced a sustained effect, and vidarabine will probably do the same.The advantage of vidarabine is ease of synthesis, so that sufficient quantities could be made at low cost for treating the many HBsAg carriers throughout the world. This is in contrast to interferon, which is difficult to prepare, costly, and so in short supply. Whether inhibition of viral replication by vidarabine will permanently clear HBsAg and so arrest chronic liver disease remains to be determined. At the least this form of treatment may, by reducing the concentration of circulating virus particles, reduce the infectivity of the patient, thereby restricting the spread of the infection. Furthermore, its effectiveness may be enhanced, and hence duration of treatment reduced, by the concurrent use of immunostimulants which accelerate the clearance of existing infected cells,13 while vidarabine prevents further viral replication. Medical3Journal, 1978, 2, 533-535 Summary and conclusions Nine non-immune patients with imported falciparum malaria were examined for signs of diffuse intravascular coagulation (DIC). Although all had thrombocytopenia initially and some later had a decline in plasma fibrinogen concentrations, DIC was never detected, even in severely affected patients with coma and kidney damage. None of the patients were given heparin and all recovered without residual symptoms. Heparin administration should probably be considered only when clear-cut DIC, which possibly never occurs in falciparum malaria, has been demonstrated.

Haematological Alterations in Acute Malaria

“…Thrombocytopenia is regularly encountered in malaria (Maegraith & Desowitz 1967, Beale et a1 1972, Skudowitz et a1 1973, Vreeken & Cremer-Goote 1978. 4/5 of our patients had subnormal platelet counts, more than half of whom had severe thrombocytopenia (platelet count < 50 x 109/l).…”

Thrombocytopenia and Release of Activated von Willebrand Factor during EarlyPlasmodium falciparumMalaria

“…Activation of the coagulation system may also cause platelet consumption. However, the coagulation is usually only mildly activated during malaria, and disseminated intravascular coagulation is rare, even during severe malaria [31].…”

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“…Our findings agree with previous reports that cerebral malaria infection causes accelerated turnover of haemostatic mechanism arising from possible disorders of platelet. And also, Vreeken 8 reported that due to reduced humoral immune response to the sporozoite in which diagnosis is made in patients that show evidence of neurologic dysfunction e.g. seizure, convulsion, disturbance of consciousness not readily explained by metabolic abnormalities or severe febrile reactions.…”

“…Anaemia is an almost inevitable consequence of malaria infection but its pathophysiology is complex and has relatively little in common with anaemia of other infections 4 . Cerebral malaria occurs in approximately 2% of patients with acute falciparum malaria 8 . Cerebral malaria is suspected in any child with malaria whose level of consciousness is deteriorating and where no other cause is found.…”