Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A total of 740 consecutive children aged between 6 months and 12 years who presented with acute encephalopathic illnesses during a three year period were assessed both clinically and by laboratory investigations. Cerebrospinal fluid was examined for the presence of cells or other abnormal substances, and any organisms were cultured. Blood examination included white cell count and estimations of haemoglobin, urea, glucose, and electrolyte concentrations and serum alanine aminotransferase and aspartate aminotransferase. A firm diagnosis was established in 278 patients (38%). Pyogenic meningitis (n = 134), measles encephalopathy (n = 38), and electrolyte imbalance (n = 23) were important causes in this group, cerebral malaria (n = 4) was uncommon and there were no cases of Reye's syndrome. The diagnoses of the remaining 462 were combined under the heading 'acute unexplained encephalopathy'. Altogether 394 of the 462 patients underwent virological investigations for arboviruses and 92 (23%) had one or more indicators of Japanese encephalitis. No other arboviruses could be isolated. Throat swabs from 187 patients with acute unexplained encephalopathy were studied on monkey kidney tissue cell lines of which 14 were positive (8%). These were identified as adenovirus, parainfluenza, influenza, poliomyelitis, Coxsackie, and echovirus; in two cases the virus was untypable. Japanese encephalitis is an important cause of acute childhood encephalopathy in this region. Clinical features of the illness may be mimicked by several disorders which require specific treatment. Thirty four of the 92 died (37%).
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PMID:Virological investigations of acute encephalopathy in India. 203 25

Reye's syndrome virtually disappeared from much of the world after the use of salicylate in febrile children was successfully discouraged. This severe sepsis-like disease was thought to be caused by a hypersensitivity to salicylates in children with mild viral infections, although no mechanism consistent with this proposal was ever established. Salicylate toxicity in African children has been noted to have many clinical features in common with severe falciparum malaria, including acidosis, altered consciousness, convulsions, and hypoglycaemia. Salicylates are widely available in various formulations in many African countries, and are commonly used for initial treatment of the symptoms that malaria shares with other diseases. There is now experimental evidence that salicylate increases and prolongs the activity of key elements along the signalling pathway through which interferon gamma generates inducible nitric oxide synthase (iNOS), and we have shown that iNOS is strongly expressed in fatal malaria and other acute fevers in African children. We further propose that, in areas where salicyaltes are still used to treat the symptoms of febrile illnesses in children, this mechanism could exacerbate potentially serious infectious diseases, including falciparum malaria. In contrast, the absence of salicylate use in children in some Pacific islands could contribute to the milder outcome of falciparum malaria than is observed in Africa. Widespread expression of iNOS has also been seen in the tissues of a patient with fatal clinically defined Reye's syndrome. This finding suggests that Reye's syndrome can be mediated through salicylate enhancement of iNOS expression, the initial trigger in this instance usually being a viral infection.
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PMID:Salicylates, nitric oxide, malaria, and Reye's syndrome. 1150 38

A common clinical presentation of Plasmodium falciparum is parasitemia, complicated by an encephalopathy for which other explanations cannot be found, termed cerebral malaria-an important cause of death in young children in endemic areas. Our objective was to study hepatic histopathology in Malawian children with fatal encephalopathy, with and without P falciparum parasitemia, to assess the contributions of severe malaria. We report autopsy results from a series of 87 Malawian children who died between 1996 and 2008. Among 75 cases with P falciparum parasitemia, 51 had intracerebral sequestered parasites, whereas 24 without sequestered parasites had other causes of death revealed by autopsy including 4 patients with clinicopathologic findings which may represent Reye syndrome. Hepatic histology in parasitemic cases revealed very limited sequestration of parasites in hepatic sinusoids, even in cases with extensive sequestration elsewhere, but increased numbers of hemozoin-laden Kupffer cells were invariably present with a strong association with histologic evidence of cerebral malaria by quantitative analysis. Of 12 patients who were consistently aparasitemic during their fatal illness, 5 had clinicopathologic findings which may represent Reye syndrome. Hepatic sequestration of parasitized erythrocytes is not a feature of fatal malaria in Malawian children, and there is no structural damage in the liver. Reye syndrome may be an important cause of fatal encephalopathy in children in Malawi with and without peripheral parasitemia and warrants close scrutiny of aspirin use in malaria-endemic areas.
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PMID:Liver pathology in Malawian children with fatal encephalopathy. 2139 81

Dengue Fever (DF) is only rarely considered as a cause of acute liver failure even globally and only a few case reports of acute hepatic failure and encephalopathy occurring in DF in adults are available. We report a case of Acute Liver Failure due to Dengue during a major outbreak in 2010 in Chitwan. A 20 year old previously healthy female presented to the emergency department of Chitwan Medical College with fever, jaundice and altered sensorium. She was tested positive for Dengue IgM. Her biochemical and clinical parameters were suggestive of acute liver failure with total billirubin of 10.1 mg/dL, direct billirubin of 5.2 mg/dL, ALT 5760 IU, AST 14100 IU, alkaline phosphatase of 1250 IU, PT INR of 1.76 and platelet count of 30,000/mm3. Other causes for acute hepatic failure like acute viral hepatitis, leptospirosis, malaria, Reyes syndrome were ruled out. The patient was admitted and managed in the ICU with supportive care and platelet transfusion. With treatment she made a significant clinical and biochemical improvement with AST of 105 IU, ALT of 120 IU and platelet count of 150,000/mm3. She was discharged after 11 days of hospital stay.
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PMID:Fulminant hepatic failure due to dengue. 2261 Aug 74

Cerebral malaria caused by P. falciparum is the severest form of the disease resulting into morbidity of a huge number of people worldwide. Development of effective curatives is essential in order to overcome the fatality of cerebral malaria. Earlier studies have shown the presence of salicylic acid in malaria parasite P.falciparum which plays a critical role in the manifestation of cerebral malaria. Further, the application of salicylic acid for the treatment of acute symptoms in cerebral malaria increases the activity of iNOS leading to severe inflammation mediated death, also called as Reye's syndrome. Therefore, modulation of the level of salicylic acid might be a novel approach to neutralize the symptoms of cerebral malaria. The probable source of parasite salicylic acid is the shikimate pathway which produces chorismate, a precursor to aromatic amino acids and other secondary metabolites like salicylic acid in parasite. In this work, we performed the immunological, pathological and biochemical studies in mice infected with chorismate synthase knocked out P. berghei ANKA which does not produce salicylic acid. Less cerebral outcomes were observed as compared to the mice infected with wild type parasite. The possible mechanism behind this protective effect might be the hindrance of salicylic acid mediated induction of autophagy in parasite, which helps in its survival in the stressed condition of brain microvasculature during cerebral malaria. The absence of SA leading to reduced parasite load along with the reduced pathological symptoms contributes to less fatality outcome by cerebral malaria.
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PMID:Chorismate synthase mediates cerebral malaria pathogenesis by eliciting salicylic acid dependent autophagy response in parasite. 3326 32