Malaria, one of the major global public health events, is a leading cause of mortality and morbidity among children and adults in tropical and subtropical regions(mainly in sub-Saharan Africa), threatening human health. It is well known that malaria can cause various complications including anemia, blackwater fever, cerebral malaria, and kidney damage. Conventionally, cardiac involvement has not been listed as a common reason affecting morbidity and mortality of malaria, which may be related to ignored cases or insufficient diagnosis. However, the serious clinical consequences such as acute coronary syndrome, heart failure, and malignant arrhythmia caused by malaria have aroused great concern. At present, antimalarials are commonly used for treating malaria in clinical practice. However, inappropriate medication can increase the risk of cardiovascular diseases and cause severe consequences. This review summarized the research advances in the cardiovascular complications including acute myocardial infarction, arrhythmia, hypertension, heart failure, and myocarditis in malaria. The possible mechanisms of cardiovascular diseases caused by malaria were systematically expounded from the hypotheses of cell adhesion, inflammation and cytokines, myocardial apoptosis induced by plasmodium toxin, cardiac injury secondary to acute renal failure, and thrombosis. Furthermore, the effects of quinolines, nucleoprotein synthesis inhibitors, and artemisinin and its derivatives on cardiac structure and function were summarized. Compared with the cardiac toxicity of quinolines in antimalarial therapy, the adverse effects of artemisinin-derived drugs on heart have not been reported in clinical studies. More importantly, the artemisinin-derived drugs demonstrate favorable application prospects in the prevention and treatment of cardiovascular diseases, and are expected to play a role in the treatment of malaria patients with cardiovascular diseases. This review provides reference for the prevention and treatment of malaria-related cardiovascular complications as well as the safe application of antimalarials.
Child ; Adult ; Humans ; Antimalarials/pharmacology* ; Cardiovascular Diseases/drug therapy* ; Artemisinins/pharmacology* ; Quinolines ; Malaria, Cerebral/drug therapy* ; Heart Failure/drug therapy* ; Arrhythmias, Cardiac/drug therapy*

The pathogenesis of cerebral malaria is biologically complex and involves multi-factorial mechanisms such as microvascular congestion, immunopathology by the pro-inflammatory cytokine and endothelial dysfunction. Recent data have suggested that a pleiotropic T-cell immunomodulatory protein (TIP) could effectively mediate inflammatory cytokines of mammalian immune response against acute graft-versus-host disease in animal models. In this study, we identified a conserved homologue of TIP in Plasmodium berghei (PbTIP) as a membrane protein in Plasmodium asexual stage. Compared with PBS control group, the pathology of experimental cerebral malaria (ECM) in rPbTIP intravenous injection (i.v.) group was alleviated by the downregulation of pro-inflammatory responses, and rPbTIP i.v. group elicited an expansion of regulatory T-cell response. Therefore, rPbTIP i.v. group displayed less severe brain pathology and feverish mice in rPbTIP i.v. group died from ECM. This study suggested that PbTIP may be a novel promising target to alleviate the severity of ECM.
Animals ; Brain ; Cytokines ; Down-Regulation ; Estrogens, Conjugated (USP) ; Graft vs Host Disease ; Injections, Intravenous ; Malaria, Cerebral ; Membrane Proteins ; Mice ; Models, Animal ; Pathology ; Plasmodium berghei ; Plasmodium ; Staphylococcal Protein A ; T-Lymphocytes

No abstract available.
Malaria, Cerebral* ; Plasmodium falciparum*

A 51-year-old man diagnosed with Plasmodium vivax malaria was transferred to our clinic with newly developed drowsy mentality and myoclonus after the initiation of hydroxychloroquine therapy. Following therapy to treat the vivax malaria and supportive care, the patient recovered completely with no sequelae. Cerebral complications caused by vivax malaria are very rare worldwide, and only two cases have been reported in Korea. Here, we report the third published case of P. vivax infection with cerebral complications in Korea.
Humans ; Hydroxychloroquine ; Korea ; Malaria, Cerebral ; Malaria, Vivax ; Middle Aged ; Myoclonus ; Plasmodium ; Plasmodium vivax

Cerebral malaria is a severe neurological complication of Plasmodium falciparum infection. Cerebral malaria can lead to cerebral infarction by several mechanisms including systemic inflammatory response. The systemic inflammatory response is known to rarely occur in Plasmodium vivax infection. We report a patient who developed multiple cerebral infarctions following Plasmodium vivax infection.
Cerebral Infarction ; Humans ; Malaria, Cerebral ; Plasmodium ; Plasmodium falciparum ; Plasmodium vivax

A 51-year-old man diagnosed with Plasmodium vivax malaria was transferred to our clinic with newly developed drowsy mentality and myoclonus after the initiation of hydroxychloroquine therapy. Following therapy to treat the vivax malaria and supportive care, the patient recovered completely with no sequelae. Cerebral complications caused by vivax malaria are very rare worldwide, and only two cases have been reported in Korea. Here, we report the third published case of P. vivax infection with cerebral complications in Korea.
Humans ; Hydroxychloroquine ; Korea ; Malaria, Cerebral ; Malaria, Vivax ; Middle Aged ; Myoclonus ; Plasmodium ; Plasmodium vivax

Animals ; Apraxias ; congenital ; Cogan Syndrome ; diagnosis ; etiology ; Coma ; Diagnosis, Differential ; Humans ; Malaria, Cerebral ; complications ; diagnosis ; parasitology ; Male ; Middle Aged ; Plasmodium falciparum ; isolation & purification ; Tomography, X-Ray Computed

Astrocytes are the most abundant cells in the central nervous system that play roles in maintaining the blood-brain-barrier and in neural injury, including cerebral malaria, a severe complication of Plasmodium falciparum infection. Prostaglandin (PG) D2 is abundantly produced in the brain and regulates the sleep response. Moreover, PGD2 is a potential factor derived from P. falciparum within erythrocytes. Heme oxygenase-1 (HO-1) is catalyzing enzyme in heme breakdown process to release iron, carbon monoxide, and biliverdin/bilirubin, and may influence iron supply to the P. falciparum parasites. Here, we showed that treatment of a human astrocyte cell line, CCF-STTG1, with PGD2 significantly increased the expression levels of HO-1 mRNA by RT-PCR. Western blot analysis showed that PGD2 treatment increased the level of HO-1 protein, in a dose- and time-dependent manner. Thus, PGD2 may be involved in the pathogenesis of cerebral malaria by inducing HO-1 expression in malaria patients.
Animals ; Astrocytes/*enzymology ; Blotting, Western ; Cell Line ; Gene Expression Profiling ; Heme Oxygenase-1/*biosynthesis ; Humans ; Malaria, Cerebral/*pathology ; Malaria, Falciparum/*complications/*pathology ; Plasmodium falciparum/*pathogenicity ; Prostaglandins/*metabolism ; Reverse Transcriptase Polymerase Chain Reaction

Plasmodium vivax malaria is an endemic disease in Korea, which rarely causes severe complications including those occurring in the cerebrum. There are limited numbers of complicated cases that have been reported around the world. We experienced a case of vivax malaria with cerebral complication: cognitive impairment and ataxia. A 55-year-old female with diabetes mellitus presented to the emergency department with acute fever of two days' duration. She did not have any history of travelling abroad or receiving blood transfusions. Peripheral blood smear revealed vivax malaria with parasitemia density of 0.53 percent. She demonstrated loss of orientation, especially regarding time and place, and ataxia. Although the initial hydroxychloroquine treatment for malaria was successful, cognitive impairment and ataxia persisted and were not recovered. Brain MRI showed no structural abnormality. Brain PET showed diffuse hypometabolism in right parieto-temporal lobe of the brain.
Ataxia ; Blood Transfusion ; Brain ; Cerebrum ; Diabetes Mellitus ; Emergencies ; Endemic Diseases ; Female ; Fever ; Humans ; Hydroxychloroquine ; Hypogonadism ; Korea ; Malaria ; Malaria, Cerebral ; Malaria, Vivax ; Middle Aged ; Mitochondrial Diseases ; Ophthalmoplegia ; Orientation ; Parasitemia ; Plasmodium ; Plasmodium vivax

Plasmodium vivax malaria is an endemic disease in Korea, which rarely causes severe complications including those occurring in the cerebrum. There are limited numbers of complicated cases that have been reported around the world. We experienced a case of vivax malaria with cerebral complication: cognitive impairment and ataxia. A 55-year-old female with diabetes mellitus presented to the emergency department with acute fever of two days' duration. She did not have any history of travelling abroad or receiving blood transfusions. Peripheral blood smear revealed vivax malaria with parasitemia density of 0.53 percent. She demonstrated loss of orientation, especially regarding time and place, and ataxia. Although the initial hydroxychloroquine treatment for malaria was successful, cognitive impairment and ataxia persisted and were not recovered. Brain MRI showed no structural abnormality. Brain PET showed diffuse hypometabolism in right parieto-temporal lobe of the brain.
Ataxia ; Blood Transfusion ; Brain ; Cerebrum ; Diabetes Mellitus ; Emergencies ; Endemic Diseases ; Female ; Fever ; Humans ; Hydroxychloroquine ; Hypogonadism ; Korea ; Malaria ; Malaria, Cerebral ; Malaria, Vivax ; Middle Aged ; Mitochondrial Diseases ; Ophthalmoplegia ; Orientation ; Parasitemia ; Plasmodium ; Plasmodium vivax