Elevated tumor necrosis factor alpha and interleukin-6 serum levels as markers for complicated plasmodium falciparum malaria

Kern, Peter; Hemmer, Christoph Josef; Damme, Jo Van; Gruss, Hans-Jürgen; Dietrich, M.

doi:10.1016/s0002-9343(89)80688-6

Cited by 404 publications

(214 citation statements)

References 32 publications

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“…The basis of adult susceptibility to severe disease caused by primary infection with P. falciparum may lie in the production of inordinately high levels of pro-inflammatory cytokines like TNF. Clinical studies correlated TNF levels with disease severity in European adults [44,45]. Studies in a variety of animal models utilizing primary exposure to infectious agents or endotoxin demonstrated an often sharply greater susceptibility to severe disease among mature vs. immature animals [46,47].…”

Section: Discussionmentioning

confidence: 99%

Adult Javanese migrants to Indonesian Papua at high risk of severe disease caused by malaria

Baird¹,

Basri

Weina³

et al. 2003

Epidemiol. Infect.

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Migrants from Java arrive in hyperendemic Papua, Indonesia lacking exposure to endemic malaria. We evaluated records of evacuation to hospital with a diagnosis of severe malaria from a transmigration village in northeastern Papua. During the first 30 months, 198 residents with severe disease were evacuated (7·5 evacuations/100 person-years). During this period the risk of evacuation for adults (>15 years of age) was 2·8. (95% CI=2·1–3·8; P<0·0001) relative to children, despite apparently equal exposure to risk of infection. Relative risk (RR) for adults was greatest during the first 6 months (RR>16; 95% CI[ges ]2·0–129; P=0·0009), and diminished during the second 6 months (RR=9·4; 95% CI=2·7–32·8; P<0·0001) and the third 6 months (RR=3·7; 95% CI=1·7–7·9; P=0·0004). During the next two 6-month intervals, the RR for adults was 1·6 and 1·5 (95% CI range 0·8–2·6; P<0·18). Adults lacking chronic exposure were far more likely to progress to severe disease compared to children during initial exposure, but not after chronic exposure to infection.

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Section: Discussionmentioning

confidence: 99%

Adult Javanese migrants to Indonesian Papua at high risk of severe disease caused by malaria

Baird¹,

Basri

Weina³

et al. 2003

Epidemiol. Infect.

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“…There are important di¡erences between the pathology of cerebral malaria in humans and the syndrome in mice, and untangling cause from e¡ect, when confronted with a complex web of linked responses which typically have short half lives, is di¤cult. However, there is a clear relationship between serum levels of TNF-alpha and outcome in human malaria Kern et al 1989;Kwiatkowski et al 1990), and the hypothesis that this is a causal relationship rather than an epiphenomenon is strengthened by the ¢nding that human genetic polymorphisms in the promoter region of the gene for TNF-alpha (which, therefore, presumably a¡ect the level of the response) are associated with increased susceptibility to severe morbidity (McGuire et al 1996).…”

Section: (B) Cytokines and Severe Malariamentioning

confidence: 99%

Host—parasite interaction and morbidity in malaria endemic areas

Marsh

Snow

1997

Phil. Trans. R. Soc. Lond. B

121

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Severe morbidity due to Plasmodium falciparum is a major health problem in African children. The patterns of morbidity in endemic areas are modi¢ed by the immune response, and vary markedly with transmission intensity. Severe disease falls into three overlapping syndromes: coma, respiratory distress, and severe anaemia. Recently, it has become clear that metabolic acidosis plays a major role in the pathogenesis of severe disease and is particularly important in the overlap between the di¡erent clinical syndromes. We propose that the di¡erent manifestations of severe malarial morbidity arise from the interaction of a limited number of pathogenic processes: red cell destruction, toxin-mediated activation of cytokine cascades, and infected cell sequestration in tissue microvascular beds. The pattern of severe morbidity varies with age within any one endemic area, with severe anaemia predominating in the youngest children and coma having its highest incidence in older children. Between endemic areas there is a marked variation in mean age of children with severe malaria, and therefore in the importance of di¡erent clinical syndromes. The shift in mean age is due to a combination of increased challenge and more rapid development of immunity at higher levels of transmission. Recent comparative studies indicate that at higher levels of transmission the net e¡ect of these shifts may be a paradoxical reduction in total severe malarial morbidity.

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“…En los pacientes africanos con malaria se encuentra incremento en los niveles de FNTα que se relacionan con la presentación de fiebre y la gravedad de la infección (75)(76)(77). En los modelos de ratón, el exceso de FNTα contribuye al desarrollo de malaria cerebral; sin embargo, en los ensayos clínicos con agentes como anticuerpos anti-FNTα y pentoxilina (interfiere en la producción), no se ha demostrado reducción de la mortalidad y presentación de malaria cerebral en humanos (74).…”

Section: Factor De Necrosis Tumoral Alfa (Fntα)unclassified

“…Los niveles séricos de las citocinas proinflamatorias IL-1 e IL-6 se encuentran incrementados en los pacientes con malaria y se han relacionado con enfermedad grave y malaria cerebral (75,78). Estas citocinas complementan muchas de las acciones mediadas por el FNTα, como la inducción de fiebre, la activación endotelial por IL-1 y el incremento en la producción de proteínas de fase aguda por IL-6, amplificando la respuesta inflamatoria.…”

Section: Factor De Necrosis Tumoral Alfa (Fntα)unclassified

Pathogenic mechanisms in Plasmodium falciparum malaria

Vásquez

Tobón

2012

biomedica

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Se presentan los mecanismos patogénicos más conocidos en la infección por Plasmodium falciparum durante la fase eritrocitaria y extraeritrocitaria. La obstrucción vascular, explicada por los fenómenos de secuestro de glóbulos rojos parasitados y la formación de rosetas, mediados por diversos ligandos y receptores endoteliales, además de los procesos inflamatorios instaurados ante la presencia del parásito, son aspectos centrales en la patogenia de la malaria que permiten explicar los procesos de disfunción, daño y muerte celular en diferentes órganos. A partir de eventos como la lesión y la destrucción de eritrocitos, hepatocitos y células endoteliales, la pérdida de integridad del endotelio y la activación de promotores de daño celular y de apoptosis, se explican alteraciones como el aumento de la permeabilidad vascular, la hipoxia y el metabolismo anaerobio, que conducen tanto a lesiones localizadas en órganos como cerebro y pulmón, como a un estado de acidosis generalizada y falla multisistémica.Palabras clave: malaria/etiología, Plasmodium falciparum, inflamación. Pathogenic mechanisms in Plasmodium falciparum malariaThe most recognized pathogenic mechanisms of the infection with Plasmodium falciparum, during both the erythrocytic and exo-erithrocytic stages are presented. Vascular obstruction explained by the sequestration of parasitized red blood cells and erythrocyte rosetting, mediated by different endothelial ligands and receptors, in addition to the inflammatory processes induced by the presence of the parasite, are central aspects in the pathogenesis of malaria that explain the processes of damage, dysfunction and cell death in various organs. Alterations such as increased vascular permeability, hypoxia and anaerobic metabolism leading to localized lesions in organs such as brain and lung, as well as to a generalized acidotic state with multisystem failure can be explained by events such as the injury and destruction of erythrocytes, hepatocytes and endothelial cells, the loss of endothelial integrity, and the activation of cell damage and apoptosis promoters.Key words: Malaria/ethiology, Plasmodium falciparum, inflamation.Los signos y síntomas clínicos en la malaria, o paludismo, expresión del daño ocasionado en diversos órganos y sistemas, se exacerban durante el período de multiplicación del parásito en el eritrocito, mientras que el estadio hepático y la presencia de gametocitos tradicionalmente no se han asociado con la sintomatología. La malaria causa lesiones estructurales y alteraciones funcionales y metabólicas, cuya presentación clínica está en función de la edad, el estado inmunitario y las características genéticas del huésped, y por la especie, el genotipo y la virulencia del parásito. Puede conducir a un cuadro clínico grave el cual casi siempre se observa en las infecciones causadas por Plasmodium falciparum. Las complicaciones informadas con mayor frecuencia incluyen anemia grave, malaria cerebral, síndrome de dificultad respiratoria aguda y falla renal (1); en los últimos años se vien...

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Elevated tumor necrosis factor alpha and interleukin-6 serum levels as markers for complicated plasmodium falciparum malaria

Cited by 404 publications

References 32 publications

Adult Javanese migrants to Indonesian Papua at high risk of severe disease caused by malaria

Adult Javanese migrants to Indonesian Papua at high risk of severe disease caused by malaria

Host—parasite interaction and morbidity in malaria endemic areas

Pathogenic mechanisms in Plasmodium falciparum malaria

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