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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mice infected with Plasmodium berghei K173-parasitized erythrocytes develop severe hypothermia followed by death as a consequence of murine cerebral malaria early in the second week after infection. A single intraperitoneal injection of 10(5) Units of IFN-gamma given between Day 4 and Day 6 postinfection results in a transient decrease of body temperature. No effect on parasitemia and cerebral malaria is obtained by this treatment. Daily injections of relatively low doses of IFN-gamma delays the patency of the infection for 2 days. Furthermore the proliferation rate of the parasites is reduced and the development of cerebral malaria is also delayed for 2 days. The reduction of body temperature, as found in untreated infected mice, is absent. Administration of IFN-gamma by means of a continuous delivery from intraperitoneally inserted osmotic pumps (1.2 x 10(4) Units of IFN-gamma/24 hr) also delays patency and inhibits parasitemia. Body temperature decreases during infection but mice are protected against the development of cerebral malaria. In nude mice, this treatment inhibits parasitemia to the same extent. However, reduction of body temperature was also prevented. High doses of IFN-gamma delivered by osmotic pumps (2.5 x 10(4) or 10(5) Units of IFN-gamma/24 hr) appear to be lethally toxic in conventional as well as in nude mice, independently of infection. Cerebral malaria-like symptoms are found in these mice. Treatment of infected C57BL/6J mice with antibody to IFN-gamma 4 days before and after infection as well as on the day of infection enhances parasitemia but does not affect the development of murine cerebral malaria. Single injections of anti-IFN-gamma-antibody 6 hr prior to infection or 7 days after infection have no effect. In CBA/Ca mice, treatment with anti-IFN-gamma-antibody enhances parasitemia; furthermore protection against cerebral malaria was obtained in part of the mice.
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PMID:Plasmodium berghei: recombinant interferon-gamma and the development of parasitemia and cerebral lesions in malaria-infected mice. 837 90

Despite treatment, cerebral malaria still has a high mortality. This study describes the clinical features, immediate outcome and prognostic factors for childhood cerebral malaria in Mulago Hospital, Kampala, Uganda. One hundred children who met the WHO criteria for cerebral malaria were prospectively recruited and followed up until discharge or death. Mortality was 7% and neurological sequelae occurred in 5% of survivors. Independent predictors of mortality were respiratory distress [adjusted OR 1.2 (95% CI 1.1-1.3)], circulatory failure [adjusted OR 2.1 (95% CI 1.8-2.4)], generalised hyporeflexia [adjusted OR 1.2 (95% CI 1.1-1.3)] and parasite density > or =500,000/microl [adjusted OR 1.02 (95% CI 1.01-1.2)]. Circulatory failure could be predicted by a combination of hypothermia, cold peripheries and dehydration. Death occurred within 12 hours of admission only in children with these predictors, and the risk of death increased with the number of risk factors. Multiple convulsions at admission predicted neurological sequelae [adjusted OR 12.8, 95% CI 3.0-211, p=0.014)]. Cerebral malaria mortality is predictable. Patients with respiratory distress, circulatory failure, generalised hyporeflexia and parasite density > or =500,000/microl need urgent treatment to prevent death. In primary health units, health workers may use a combination of cold peripheries, hypothermia and dehydration to predict circulatory failure.
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PMID:Immediate outcome and prognostic factors for cerebral malaria among children admitted to Mulago Hospital, Uganda. 1500 62

Malarial infections are uncommon in the United States and almost all reported cases stem from recent travelers coming from endemic countries. Cerebral malaria (CM) is a severe form of the disease usually affecting children and individuals with limited immunity. Despite proper management, mortality from CM can reach up to 25%, especially when it is associated with brain edema. Inefficient management of the edema may result in brain herniation and death. Uniform guidelines for management of CM-associated brain edema are lacking. In this report, we present a case of CM with associated severe brain edema that was successfully managed using a unique combination of therapeutic hypothermia, hypertonic saline, mannitol, and hyperventilation along with the antimalarial drugs quinidine and doxycycline. Our use of hypothermia was based on its proven benefit for improving neurological outcomes in post-cardiac arrest patients and previous in vitro research, suggesting its potential inhibitory role on malaria growth.
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PMID:Case Report: A Case of Severe Cerebral Malaria Managed with Therapeutic Hypothermia and Other Modalities for Brain Edema. 2940 3