Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One hundred and five patients with Plasmodium falciparum were included, forty-three with cerebral malaria and sixty-two without cerebral manifestations. The main clinical presentations in cerebral malaria patients were fever (76.4%), pallor (72%), splenomegaly (60.5%), deep coma (39.5%), jaundice (18.6%), pulmonary oedema (13.9%), subconjunctival haemorrhage (13.9%), severe anemia (Hb<5mg/l) (53.5%), hypoglycemia (glucose<40mg/dl) (67.4%) and haemoglobinuria (6.9%) while in non cerebral malaria patients the clinical presentations were fever (83.8%), pallor (67.7%), splenomegaly (66%), jaundice (9.7%), severe anemia (Hb<5gm/dl) (51.6%) and hypoglycemia (glucose<40mg/dl) (3.2%). Nine patients from cerebral malaria group died after admission. Serum level of nitric oxide (nitrite plus nitrate) were assayed for all patients, serum level of nitric oxide were highly significant in patients with cerebral malaria than those without (34.6 +/- 2.3n. mol/ml VS 12.9 +/- 1.3n. mol/ml; P<0.01). In cerebral malaria, nitric oxide levels were highly elevated in patients with deeper coma than those with lighter coma (48.2 +/- 3.1n. mol/ml VS 24.4 +/- 1.3n. mol/ml; P<0.001) and also higher among patients with longer duration of coma (>72 hours) than among patients with shorter duration of coma (<72 hours) (54.5 +/- 2.8 n. mol/ml V.S. 23.6 +/- 3.1n. mol/ml; P<0.001). Also, nitric oxide levels were correlated with clinical outcome, fatal cases (9 patients) having significantly higher nitric oxide levels than survivors (56.2 +/- 3.1 n. mol/ml VS 32.5 +/- 1.3 n. mol/ml; P<0.001). Thus, higher levels of nitric oxide are associated with indices of disease severity and may predict outcome in-patients with cerebral malaria. These data are consistent with the hypothesis that nitric oxide is involved in the pathogenesis of cerebral malaria.
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PMID:Plasma levels of nitric oxide in association with severe Plasmodium falciparum in Yemen. 1256 1

(1) Check for severe malaria (coma, shock, pulmonary oedema), and take account of drug resistance in the region. (2) Mefloquine and quinine are first-line options for uncomplicated P. falciparum malaria. The atovaquone + proguanil combination can be used in patients at high risk of side effects with mefloquine
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PMID:Treatment of imported uncomplicated malaria: a medical emergency. 1260 3

Malaria in pregnancy is one of the most important preventable causes of low birthweight deliveries worldwide. It is also a major cause of severe maternal anaemia contributing to maternal mortality. It is estimated that 40% of the world's pregnant women are exposed to malaria infection during pregnancy. The clinical features of Plasmodium falciparum malaria in pregnancy depend to a large extent on the immune status of the woman, which in turn is determined by her previous exposure to malaria. In pregnant women with little or no pre-existing immunity, such as women from non-endemic areas or travellers to malarious areas, infection is associated with high risks of severe disease with maternal and perinatal mortality. Women are at particular risk of cerebral malaria, hypoglycaemia, pulmonary oedema and severe haemolytic anaemia. Fetal and perinatal loss has been documented to be as high as 60-70% in non-immune women with malaria. Adults who are long-term residents of areas of moderate or high malaria transmission, including large parts of sub-Saharan Africa, usually have a high level of immunity to malaria. Infection is frequently asymptomatic and severe disease is uncommon. During pregnancy this immunity to malaria is altered. Infection is still frequently asymptomatic, so may go unsuspected and undetected, but is associated with placental parasitization. Malaria in pregnancy is a common cause of severe maternal anaemia and low birthweight babies, these complications being more common in primigravidae than multigravidae. Preventative strategies include regular chemoprophylaxis, intermittent preventative treatment with antimalarials and insecticide-treated bednets.
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PMID:Importance and prevention of malaria in pregnancy. 1288 1

Malaria requiring intensive care is characterized by failure of one or more organ systems and/or development of several metabolic disorders secondary to the presence of Plasmodium faliciparum in the blood. Severe imported malaria in non-immunized adults causes multiple organ failure with variable degrees of altered mental status. Acute pulmonary edema is frequent, jaundice associated with mild disturbance of liver function is consistent, arterial hypertension due to hypovolemia is usual, and acute renal insufficiency is uncommon. Coagulation disorders are generally low-grade, acidosis is an unfavorable prognostic factor, severe hypoglycemia can occur after the beginning of quinine treatment, and anemia is an consistent but discrete symptom. In endemic areas emphasis should be placed on the complications of severe malaria in pregnant women due to the high incidence of hypoglycemia and pulmonary edema. Severe malaria can develop early in children in endemic zones. Presenting signs include cerebral malaria in older children and severe anemia in young children. Quinine is the reference treatment with a bolus of 17 mg/kg followed by a daily maintenance dose of 24 mg/kg. Use of artemether should be restricted to quinine-resistant forms. Total blood exchange transfusion is not recommended. Supportive symptomatic treatment, e.g. mechanically assisted ventilation and kidney dialysis, is required. In endemic zones over 90% of deaths involve children without access to intensive care facilities. Mortality rates associated with management of severe imported malaria in intensive care range from 10 to 30%.
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PMID:[Severe malaria in intensive care units in 2003]. 1457 63

Five black-footed penguins (Spheniscus demersus) admitted to the Southern African Foundation for the Conservation of Coastal Birds, in Cape Town, South Africa, died from malaria infection. Evidence for malaria as the cause of death included antemortem clinical signs, parasitemia, splenomegaly, pulmonary edema, and the presence of histologically visible schizonts in the reticuloendothelial system. A portion of the malarial small subunit ribosomal ribonucleic acid gene was detected by polymerase chain reaction from postmortem blood samples from all the birds. A species-specific variable region of this gene was compared with the same region on genes from other known avian malarial organisms, establishing that Plasmodium juxtanucleare was involved.
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PMID:Plasmodium Juxtanucleare associated with mortality in black-footed penguins (Spheniscus demersus) admitted to a rehabilitation center. 1458 86

Plasmodium falciparum is the most common cause of severe and life-threatening malaria. Falciparum malaria causes over one million deaths every year. In Africa, a vast majority of these deaths occur in children under five years of age. The presentation of severe malaria varies with age and geographical distribution. The mortality rate is higher in adults than in children but African children develop neuro-cognitive sequelae following severe malaria more frequently. The management of severe malaria includes prompt administration of appropriate parenteral anti-malarial agents and early recognition and treatment of the complications. In children, the complications include metabolic acidosis (often caused by hypovolaemia), hypoglycaemia, hyperlacticacidaemia, severe anaemia, seizures and raised intracranial pressure. In adults, renal failure and pulmonary oedema are more common causes of death. In contrast, concomitant bacterial infections occur more frequently in children and are associated with mortality in children. Admission to critical or intensive care units may help reduce the mortality, and the frequency and severity of sequelae related to severe malaria.
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PMID:Management of severe falciparum malaria. 1504 99

Falciparum malaria affect all ages with multiple-systemic complications which varies in different age group. We studied 242 children with complicated Falciparum malaria with a median age of 6.5 years to look for occurrence of different complications in younger and older age groups and overall mortality picture. Unarousable coma (40.5%), severe anemia (26.03%), repeated seizures (46.2%) and hepatopathy (32.2%) were commonest complications. Under five children had higher risk of development of cerebral malaria (P<0.01), severe anemia (P<0.05) and seizures (P<0.001); whereas above five children had higher risk of acute renal failure (P<0.05) and malarial hepatopathy (P<0.02). Over all mortality was 9.9%, cerebral malaria being the commonest cause (6.6%). Multi-system involvement was seen in 58.4% cases of death. Children having pulmonary edema, shock and cerebral malaria had high case fatality rate.
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PMID:Severe falciparum malaria. 1505 76

Until recently, the sequestration of erythrocytes infected with Plasmodium falciparum has been thought to be due to one of a number of protein-protein interactions. In this article, Stephen Rogerson and Graham Brown summarize the emerging evidence that, in vitro, infected erythrocytes can also adhere to the glycosaminoglycan chondroitin sulphate A (CSA) expressed on the surface of cells and immobilized on plastic. In vivo, binding of infected erythrocytes to CSA could be crucial to the development of malarial infection of the placenta, and possibly to sequestration in the lung and brain. The consequences of this may include maternal morbidity and mortality, low birth weight in the infant, pulmonary oedema and cerebral malaria. They discuss the need to characterize the molecular basis of this interaction, and to investigate the possible therapeutic role of CSA in malaria. Chondroitin sulphates are nontoxic compounds already in use for other diseases in humans. Vaccines based on inhibiting this receptor-ligand interaction could also be appropriate.
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PMID:Chondroitin sulphate A as an adherence receptor for Plasmodium falciparum-infected erythrocytes. 1527 26

A 57-year-old man who had been intermittently taking one 300-mg tablet of quinine sulfate orally for leg cramps experienced transient acute pulmonary edema and hypotension 30-40 minutes after ingestion on two consecutive occasions. He was not taking any concomitant drugs, and there was no alternative explanation for either event. Serial troponin T tests and electrocardiograms, obtained on admission to the hospital, followed by an outpatient echocardiogram and a coronary angiogram, were essentially normal. We compared this case with one previously published and nine previously unpublished reports of quinine-associated pulmonary edema and conclude that some cases of pulmonary edema or adult respiratory distress syndrome in patients with malaria may be caused by an adverse reaction to quinine. Although infrequent, clinicians should be aware of this potentially serious and costly adverse reaction.
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PMID:Acute pulmonary edema caused by quinine. 1546 Jan 83

The natural killer complex (NKC) is a genetic region of highly linked genes encoding several receptors involved in the control of NK cell function. The NKC is highly polymorphic, and allelic variability of various NKC loci has been demonstrated in inbred mice. Making use of BALB.B6-Cmv1r congenic mice, in which the NKC from disease-susceptible C57BL/6 mice has been introduced into the disease-resistant BALB/c background, we show here that during murine malaria infection, the NKC regulates a range of pathophysiological syndromes such as cerebral malaria, pulmonary edema, and severe anemia, which contribute to morbidity and mortality in human malaria. Parasitemia levels were not affected by the NKC genotype, indicating that control of malarial fatalities by the NKC cells does not operate through effects on parasite growth rate. Parasite-specific antibody responses and the proinflammatory gene transcription profile, as well as the TH1/TH2 balance, also appeared to be influenced by NKC genotype, providing evidence that this region, known to control innate immune responses via NK and/or NK T-cell activation, can also significantly regulate acquired immunity to infection. To date, NKC-encoded innate system receptors have been shown mainly to regulate viral infections. Our data provide evidence for critical NKC involvement in the broad immunological responses to a protozoan parasite.
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PMID:The natural killer complex regulates severe malarial pathogenesis and influences acquired immune responses to Plasmodium berghei ANKA. 1578 73


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