Article Abstract:
Malaria is an infectious disease caused by the parasite Plasmodium. Infection with Plasmodium falciparum is associated with an increase in the number of platelets (cells involved in blood clotting) and changes in blood flow that promote coagulation. These effects may be due to tumor necrosis factor/cachectin (TNF alpha), which is a cytokine, or growth-regulating factor. TNF-alpha was shown to reduce levels of protein C (PC), which prevents blood coagulation, and increase levels of a protein that enhances blood coagulation. The relation between the severity of P. falciparum malaria, parasitemia (the presence of parasites in the blood) and hemostatic (blood flow-related) changes was assessed in 47 patients with P. falciparum malaria. The levels of certain factors that control blood coagulation were measured, including the anticoagulant PC and several factors that enhance coagulation: coagulation factor IX, TNF-alpha, and thrombin-antithrombin III(TAT). Before treatment with antimalarial agents, the blood levels of TNF-alpha and TAT were increased, whereas the levels of PC and its inhibitor, referred to as PCI-1, were decreased. These trends were correlated with the severity of malaria and number of parasites in the blood. However, coagulation factor IX was not changed. When endothelial cells, which line the surface of some tissues, were exposed to the blood of a patient with severe malaria under laboratory conditions, the coagulation activity and genetic material that codes for coagulant factors in the endothelial cells increased. These findings show that P. falciparum infection results in the development of conditions that enhance blood coagulation. The changes in blood flow may be a reaction to P. falciparum infection, because hemostatic changes are correlated with the number of parasites in the blood and can be restored to normal conditions by antimalarial therapy. (Consumer Summary produced by Reliance Medical Information, Inc.)
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Article Abstract:
Following decades of decreasing worldwide incidence of malaria, the disease is once again on the rise. Travelers from developed countries who visit areas where malaria is endemic are susceptible to the disease. One type of malaria is caused by the organism Plasmodium falciparum, which has become increasingly resistant to standard treatments and can be deadly if not detected early. Physicians need to be aware of the symptoms and treatments for this disease so that it can be effectively treated before the patient's life is endangered. This study examined the case of a 28-year-old woman who contracted Plasmodium falciparum malaria after traveling to Africa. She became ill with fever and headaches 10 days after her return. Upon examination at a hospital, P. falciparum was found in her blood. Examination of the smears by doctors estimated the parasitemia (extent of parasites in blood) to be 0.05 percent. This level is not considered severe, so treatment for mild malaria was given, including oral quinine therapy. A blood smear 12 hours later found the parasitemia had increased to 22 percent, an extremely high level. Intravenous quinidine therapy was immediately begun and the patient eventually recovered. This case highlights the fact that initial blood smear readings can be misleading in such cases. Multiplication of the parasite alone could not have accounted for the massive increases seen. Normally, once malaria has been diagnosed, further blood smears are considered unnecessary. Nevertheless, frequent blood smears are needed in the initial diagnosis of malaria to detect cases that are much more severe than they initially appear to be. This can lead to earlier use of aggressive therapy when necessary. (Consumer Summary produced by Reliance Medical Information, Inc.)
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Article Abstract:
Hemophilia type A is an inherited bleeding disorder that is caused by a deficiency of factor VIII (a blood protein required for blood clot formation). An acquired form of hemophilia can develop in nonhemophiliacs when the immune system begins making autoantibodies that inhibit the activity of a small portion of the factor VIII molecule called factor VIII:C. This antibody is known as factor VIII:C inhibitor. Acquired hemophilia has been treated by giving intravenous injections of purified factor VIII:C. The clinical effectiveness of this form of treatment is related to the amount of factor VIII:C inhibitor present in the blood. Factor VIII:C purified from pig (porcine) blood has been used because it is less likely to react with the factor VIII:C inhibitors present in the patient's blood than factor VIII:C purified from human blood. This means that less of the porcine factor VIII:C will interact with the inhibitors (autoantibodies) and more will be available to prevent bleeding. Transfusion reactions are rare following treatment with porcine factor VIII:C. Adverse reactions of any type to porcine factor VIII:C occur in 7 to 13 percent of patients, and most of these reactions are mild or transient. Severe reactions are uncommon. Using porcine factor VIII:C instead of human factor VIII:C reduces the transmission of AIDS and hepatitis. (Consumer Summary produced by Reliance Medical Information, Inc.)
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