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)

In order to determine the prevalence of deficient activity of the enzyme glucose-6-phosphate dehydrogenase (G-6-PD) among the inhabitants of the east African Republic of Djibouti, we analyzed by the methaemoglobin reduction test the blood of 170 Djiboutian males, 81 Afars and 89 Somalis. Eight subjects were found to be G-6-PD deficient, 1 Afar and 7 Somalis (1.2% versus 8%; P = 0.02). We conclude that in Djibouti, health care providers should consider the presence of potential G-6-PD deficiency in their patients, especially in males of the Somali ethnic group. Indeed, many medications are contraindicated in the G-6-PD deficient subjects, and primaquine and pyrimethamine-sulfadoxine (FANSIDAR) have to be considered dangerous anti-malarial drugs for Somali males as long as their level of G-6-PD activity has not been determined. Since in Djibouti many acute falciparum cases are presenting with severe icteric anaemia, we hypothesize that some of these haemolytic anaemias might not be caused by the parasitic infection alone, but that some malaria patients might become aggravated through the administration of haemolytic drugs in case they are G-6-PD deficient. Finally, we propose that our study should be expanded to include the systematic determination of the variants of the enzyme in all subjects found G-6-PD deficient, since the clinical manifestations of G-6-PD deficiency are directly related to the type of variant present.
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PMID:[Dissimilar glucose-6-phosphate dehydrogenase (G-6-PD) deficiency in the Afars and the Somalis of Djibouti]. 189 21

Renal failure in malaria appears to be a complication less well known than anaemia and cerebral malaria. Thirty-one non-immune patients treated for Plasmodium falciparum malaria at Hannover Medical School were reviewed. Nine patients (29%) had acute renal failure, seven of whom required dialysis, and five patients needed mechanical ventilation. Cerebral symptoms were seen in nine patients, and three of the patients died. In a second series, information about patients who died of malaria in Germany and Austria was gathered. Thirty-six reports were obtained and analysed retrospectively. Thirty-four patients (94%) had acute renal failure. Eighteen patients received dialysis while five other patients with high central venous pressure or hyperkalaemia would have benefitted from dialysis. Cerebral involvement was seen in 34 patients, and 20 patients showed respiratory failure. It was concluded that renal failure in P. falciparum malaria is as common in non-immune adults as cerebral malaria. As untreated renal failure may have a deleterious influence on cerebral and respiratory functions, early dialysis-treatment in patients with severe P. falciparum malaria and signs of deteriorating renal function is recommended.
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PMID:Renal failure is a common complication in non-immune Europeans with Plasmodium falciparum malaria. 189 68

Fulminant malaria infections are characterised by hypoglycaemia and potentially lethal lactic acidosis. In young adult Wistar rats (n = 26) infected with Plasmodium berghei (ANKA strain), hyperparasitaemia (greater than 50%), anaemia (PCV 19.6 +/- 5.3%; mean +/- SD) hypoglycaemia (1.04 +/- 0.74 mmol/litre), hyperlactataemia (13.2 +/- 2.20 mmol/litre), hyperpyruvicaemia (0.51 +/- 0.12 mmol/litre) and metabolic acidosis (arterial pH 6.96 +/- 0.11) developed after approximately 14 days of infection. Hypoglycaemia was associated with appropriate suppression of plasma insulin concentrations. In a second series of experiments the metabolic effects of treatment with glucose (500 mg/kg/hr), quinine (5 mg/kg bolus followed by 10 mg/kg over 1 hr) and a potent activator of pyruvate dehydrogenase, dichloroacetate (300 mg/kg) were studied over a 1-hr period. In control animals quinine had no measurable effects, but dichloroacetate significantly reduced arterial blood lactate (74%) and pyruvate (80%). In infected animals, glucose infusion attenuated the rise in lactate (38% compared with 82%; P less than 0.01) but quinine had no additional metabolic effects. Dichloroacetate further attenuated the rise in lactate (14%; P less than 0.01).
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PMID:Plasmodium berghei: lactic acidosis and hypoglycaemia in a rodent model of severe malaria; effects of glucose, quinine, and dichloroacetate. 190 Dec 69

Seventy children from 7 months to 15 years old have been treated for malaria at Hospital Trousseau (Paris) during years 1987 and 1988. Thirty nine of them were living in France usually. The infection was one chiefly in Africa (68 cases), and by P. falciparum in 78% of children. The digestive symptoms were frequent (40/70); splenomegaly was observed in 40 children and hepatomegaly in 31. Anemia was present in 59 cases and mild thrombopenia for 31 cases. The C. reactive protein raised in 92% of cases. The diagnosis was late in 31 patients. Only one cerebral malaria case was observed. The chemoprophylaxis was unfitted or absent in 74% of children living in Paris. The chloroquino-resistance was clinically present in 17 cases and the mefloquine was more often used during 1988 year.
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PMID:[Malaria of importation in the child: epidemiological, clinical and therapeutic analysis. Apropos of 70 cases observed in a pediatric hospital in Paris]. 191 46

The case records of 64 patients with malaria over a five year period admitted to the University Hospital, Kuala Lumpur were examined. There were 32 cases of P. falciparum, 26 cases of P. vivax and two cases of mixed infections. Four cases of P. malariae were recorded. The clinical findings, biochemical and haematological parameters were examined for any indication of a pernicious syndrome. A high index of suspicion of a malarial infection may be based on the findings of anaemia, thrombocytopaenia, hyponatraemia, renal failure and abnormal liver function tests in the face of a negative blood film. These pernicious syndromes occur more often in malignant tertian malaria (anaemia 50%, hyponatraemia 39.1%) but a high percentage of the other malarial species show these abnormalities (P. vivax anaemia 57.7%, hyponatraemia 19.2%). When these abnormalities are present but blood films for malaria parasites are negative, repeat blood films are warranted until a parasitological diagnosis is achieved and correct treatment may be started.
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PMID:Recognition of pernicious syndromes in malaria infections. 192 72

Out of 604 Gambian children admitted with falciparum malaria to one hospital between September and December, 1988, 308 had cerebral malaria and 203 were severely anaemic (haemoglobin less than 60 g/l). 14% of those with cerebral malaria died, as did 7.8% of those with severe anaemia. 32 (12%) of children surviving cerebral malaria had residual neurological deficit. 69 other children were admitted with clinical features strongly suggestive of cerebral malaria but with negative blood films; 16 of these died and 3 had residual neurological deficits. The commonest sequelae of cerebral malaria were hemiplegia (23 cases), cortical blindness (11), aphasia (9), and ataxia (6). Factors predisposing to sequelae included prolonged coma, protracted convulsions, severe anaemia, and a biphasic clinical course characterised by recovery of consciousness followed by recurrent convulsions and coma. At follow up 1-6 months later over half these children had made a full recovery, but a quarter were left with a major residual neurological deficit. Cerebral malaria in childhood may be an important cause of neurological handicap in the tropics.
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PMID:Neurological sequelae of cerebral malaria in children. 197 27

To investigate the relation of tumor necrosis factor-alpha (TNF alpha) to Plasmodium falciparum infection, plasma TNF alpha concentrations were measured in Zairian children with severe malaria, mild malaria, or other illnesses. The initial geometric mean plasma concentration of TNF alpha among 61 children with P. falciparum infection, (71 pg/ml) was higher than the level in 26 severely ill, aparasitemic children (10 pg/ml; P less than .001). Among 29 parasitemic children, initial geometric mean TNF alpha levels decreased from 77 to 5 pg/ml (P less than .001) at day 7. TNF alpha levels increased with parasite density and were associated with hyperparasitemia, severe anemia, hypoglycemia, and young age but not with cerebral malaria or fatal outcome. However, TNF alpha levels were elevated equally in children with cerebral malaria and with other signs of severe malaria. With multiple linear regression, TNF alpha levels were elevated independently in children with hyperparasitemia (P = .001) and severe anemia (P = .04). In this study, high TNF alpha levels were associated with several manifestations of severe malaria and were not specific to cerebral malaria.
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PMID:Tumor necrosis factor and severe malaria. 198 82

Malaria must be included in the differential diagnosis of all febrile patients. Malaria is classified 'complicated' or 'uncomplicated', according to clinical findings (cerebral malaria, generalized convulsions, pulmonary edema, severe anemia, hyperthermia, renal failure, haemoglobinuria, shock, spontaneous bleeding) and laboratory results (parasitemia greater than 5%, haemoglobin less than 5 g%, creatinine greater than 265 mumol/l, glucose less than 2.2 mmol/l, DIC, pH less than 7.2, bilirubin greater than 50 mumol/l). Plasmodium (P.) vivax, P. ovale and P. malariae cause uncomplicated disease as a rule, whereas P. falciparum may result in either of both. Complicated falciparum malaria is always at risk for a lethal outcome. Only microscopic evidence of malaria parasites proofs the diagnosis. The thick smear is good for screening, thin films are necessary to determine the species. Serology and cultures are not helpful in diagnosing acute malaria. Tests for drug resistance await to be applicable for emergency situations.
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PMID:[Clinical aspects and diagnosis of malaria]. 199 79

Over a period of 6 months in 1988, 104 patients with severe and complicated falciparum malaria were admitted to the Gonder College Hospital (GCH), Gonder, Ethiopia; 85 male (81.7%) and 19 female (18.3%). The age ranged between 14 and 70 years with a mean age of 31 years. Eighty-one patients (78.3%) had moved from a nonendemic to a malariaendemic area shortly before their illness. Altered state of consciousness, hyperparasitaemia and severe anaemia were the most frequent complications found. Fifty-three patients (51.0%) died. Non-immune status and unknown duration of symptoms were significantly associated with mortality. Among those who died, comatose state on admission, hyperparasitaemia and acute renal failure were more frequently seen. Forty-six (86.8%) had developed two or more complications and 15 (28.3%) had superimposed bacterial infections. Inadequate preventive measures and treatment facilities may be two important factors accounting for the high mortality.
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PMID:Clinical and laboratory features of severe and complicated falciparum malaria the experience from Gonder Hospital. 200 87

A hypothesis presented in the paper discusses the role of valine substitution in p21 protein of H-ras, a product of ras family oncogene. The event was followed by a marked decrease in GTPase activity of the protein and alteration of its function in the cell. Recent results of X-ray structural analysis were compared with the model suggested by the authors earlier. The role of valine substitution in sickle-cell anemia held to be a genetic mechanism of protection against malaria is discussed. Based on similarity of valine substitution in p21 protein and hemoglobin, a relationship between certain forms of malignant transformation and malaria at molecular level is suggested.
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PMID:[The role of "valine substitution" in oncogene functioning (a hypothesis)]. 201 2


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