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 27-year old female from Nairobi was admitted to the medical wards of the Kenyatta National Hospital in May 1991. She presented with a 4-week history of productive cough, fever, weight loss, and night sweats. She acknowledged a history of contact with a patient known to have pulmonary tuberculosis. She has never received a blood transfusion. She was single and para 3 + 0. Examination revealed a sick patient, with moderate pallor, fever of 38 degrees Celsius, and who was wasted with moderate dehydration and oral thrush. There was no finger clubbing, lymphadenopathy, or pedal edema. Chest examination revealed bilateral basal pneumonia. The spleen was palpable 4 cm below the costal margin; the liver was not enlarged. The rest of the examination was normal. On admission, complete blood count showed a haemoglobin of 5.4 g/dl, total white cells were 12.5 x 10-9/L, with 82% polymorphonuclear cells and 18% lymphocytes, erythrocyte sedimentation rate (ESR) was 85 mm/hour, and platelet count was normal. The anemia was normocytic, normochromic, and no malaria parasites were seen. Urea and electrolytes and liver function tests were normal. Sputum showed no acid fast bacilli on Ziel-Neelson Stain. HIV-1 antibodies were positive by enzyme-linked immunosorbent assay (ELISA) and Western blot. Bone marrow aspirate revealed a hypercellular marrow with reversed M:E ration, dyserythropoesis, reticulum cell hyperplasia, plentiful golden yellow pigment, and clumps of Histoplasma capsulatum. Chest X-ray showed bilateral basal pneumonia. She was treated with antibiotics and intravenous fluids, but she remained febrile, her general condition progressively deteriorated, and she died a week after admission. Treatment for histoplasmosis had not been commenced, and no postmortem examination was carried out.
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PMID:Disseminated histoplasmosis in a patient with acquired immunodeficiency syndrome (AIDS): a case report. 851 33

Serum transcobalamin II (TCII) levels were determined in 56 patients with P. falciparum malaria infection. They were divided into 3 groups: severe (malarial parasite > 5% or patients with cerebral malaria or renal insufficiency), moderate (1-5% infection without complications) and mild (1% infection). Elevated serum TCII values were found only in patients with severe malaria infection. These values correlated directly with parasitemia, blood urea nitrogen and creatinine, but were not correlated with alkaline phosphatase. As 17 patients with azotemia had elevated serum TCII levels while other 3 patients with normal BUN and creatinine concentrations had serum TCII levels within the normal limits. These findings indicated that malarial patients with renal insufficiency had increased serum TCII. A possible mechanism is the reduced TCII-B12 that filtered through the glomeruli due to the reduced renal blood flow with the decreased its uptake by proximal tubular cells resulting in the decreased degradation of TCII by the tubular lysosomal enzymes. Determination of serum TCII level may be used as an indicator of renal function in malarial patients with renal insufficiency.
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PMID:Serum transcobalamin II levels in patients with malaria infection. 852 19

The present study included 426 patients with acute renal failure age range 7 months to 85 years, during 8-year period (1984-1992). Medical, surgical and obstetric causes were responsible for ARF in 68.3, 17.8, and 14% of cases respectively. The main aetiological factors encountered were volume depletion secondary to gastrointestinal fluid loss (35.2%), acute glomerulonephritis (10.3%), nephrotoxin (8.6%), falciparum malaria (4.2%), obstructive uropathy (13%), post-abortal (10.5%), and miscellaneous factors (1.4%) of patients. The overall mortality was 19.2%. Thus our observation revealed that diarrhoeal diseases (35.2%), obstructive uropathy (13.3%), and septic abortion (10.5%) were the main causes for ARF in medical, surgical, and obstetric groups respectively. In contrast to our studies, acute renal failure associated with diarrhoeal diseases, septicaemia, falciparum malaria and septic abortion are rare in European countries.
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PMID:Acute renal failure in eastern India. 864 59

The prevalence and likely cause of hyponatraemia in severe childhood malaria were investigated. One hundred and thirty two children, 47 of whom had cerebral malaria, were prospectively recruited and serial simple indices of fluid and electrolyte balance and renal function monitored during admission. In 55%, hyponatraemia (sodium < 135 mmol/l) was present on admission. Hyponatraemia was pronounced (sodium < or = 130 mmol/l) in 21%, and these children gained less weight during admission (mean weight gain 2.4% v 4.3%) than children with a normal sodium (135-145 mmol/l). Overall, 31% of survivors were at least moderately dehydrated on admission (5% weight gain by discharge). These children had higher plasma urea concentrations on admission (6.1 v 4.5 mmol/l) and were more acidotic (mean base excess -12.1 v -8.0) than children who were not dehydrated. There were changes in simple indices of renal function between admission and discharge in children who survived (creatinine 65.7 v 37.9 mumol/l and urea 5.5 v 1.9 mmol/l). The results suggest that dehydration is common in severe childhood malaria, that it may contribute to mild impairment in renal function, and that hyponatraemic children are less water depleted, showing appropriate rather than inappropriate secretion of antidiuretic hormone.
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PMID:Hyponatraemia and dehydration in severe malaria. 878 22

Thirty five patients with imported malaria were hospitalised in a period of 1980-93 in Department of Infectious Diseases of Pomeranian Medical School, Szczecin, Poland. The diagnosis of malaria was established on a base of clinical feature, the presence of Plasmodium in peripharal blood smears and, in some cases, on positive serological tests. Thirty two patients were Polish citizens, and three persons were foreigners. Malaria was caused mostly by invasion of Plasmodium falciparum (62.8), then P. vivax (31, 4), in 1 case--P. ovale and 1 case--mixed invasion occurred (P. falciparum and P. vivax). The majority of cases caused by P. falciparum were imported from Central Africa. Invasions of P. vivax were brought from North Africa, India and Middle East. Malaria in Polish patients was connected with occupational exposure and lack of proper antimalarial prophylaxis was obvious. A clinical course of disease was serious, with one mortal case. Fever, headache, abdominal pain, weakness, jaundice, insomnia were main complaints. Anemia, leucopenia, thrombocytopenia, hyperbilirubinemia, hypertransaminasemia and high serum concentration of urea were observed. A level of parasitemia in peripheral blood varied from minimal to very high (22.5%) in cases of P. falciparum invasions. In treatment chloroquine, fansidar, quinine, primaquine, halfan were used.
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PMID:[Observation of patients with malaria hospitalized during the years 1980-1993 in the Clinic of Infectious Diseases in Szczecin]. 886 94

We studied 38 patients with acute renal failure (ARF) due to malaria over a 5-year period between 1990 and 1994 at the Institute of Urology and Transplantation. There were 30 males and 8 females who ranged in age from 13 to 75 years. Most were critically ill on presentation with blood urea levels between 116 and 587 mg% and serum creatinine concentrations between 3 and 30 mg%. Anemia accompanied by hyperbilirubinemia was a result of severe hemolysis. Antimalarial therapy consisted of quinine sulfate, chloroquine, or both. Of the 38 patients, 32 required hemodialysis and eventually recovered normal (n = 29) or near normal (n = 3) function. Six patients died.
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PMID:Predictors of outcome in malarial renal failure. 887 97

Data collected from 200 children admitted to a hospital on the Kenyan coast who met a broad definition of severe acute respiratory infection (ARI) indicated that simple clinical signs alone are unable absolutely to distinguish severe ARI and severe malaria. However, laboratory data showed that marked differences exist in the pathophysiology of unequivocal malaria and unequivocal ARI. Children in the former group had a higher mean oxygen saturation (97 vs. 94, P < 0.001), mean blood urea level (5.3 vs. 1.9 mmol/L, P < 0.001) and geometric mean lactate level (4.5 vs. 2.1 mmol/L, P < 0.001), and lower mean haemoglobin level (5.3 vs. 9.0 g/dL, P < 0.001) and base excess (-9.4 vs. -2.6, P < 0.001) than those in the latter group. Using these discriminatory variables it was estimated that up to 45% of children admitted with respiratory signs indicative of severe ARI probably had malaria as the primary diagnosis. Radiological examination supported this conclusion, indicating that pneumonia characterized by consolidation was uncommon in children with respiratory signs and a high malarial parasitaemia (> or = 10,000/microliters). There is no specific radiological sign of severe malaria. In practice, all children with respiratory signs warranting hospital admission in a malaria endemic area should be treated for both malaria and ARI unless blood film examination excludes malaria. In those with malaria and clinical evidence of acidosis, but no crackles, antibodies may be withheld while appropriate treatment for dehydration and anaemia is given. However, if clinical improvement is not rapid, antibiotics should be started.
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PMID:Clinical overlap between malaria and severe pneumonia in Africa children in hospital. 901 8

Despite prompt treatment with an effective anti-malarial drug, cerebral malaria still has a mortality of 20-30%. To identify factors that may contribute to this high fatality rate, we have studied the relationship between clinical and laboratory features and a fatal outcome in 624 Gambian children with strictly defined cerebral malaria. One hundred twenty-four children (21.5%) died. Three-quarters of the deaths occurred within 24 hr of admission. Multiple logistic regression analysis showed that a cold periphery (odds ratio [OR] = 2.7), a deep coma (OR = 2.0), and hypoglycemia (OR = 4.1) were the clinical signs and laboratory parameters that predicted death most strongly. More than 90% of the children who died had at least one of these conditions. Also, children with elevated urea levels on admission or those who experienced multiple episodes of hypoglycemia or multiple convulsions subsequently were more likely to die. A combination of clinical and laboratory abnormalities can identify a group of children with cerebral malaria who are most at risk of dying, who require intensive care and who are candidates for new forms of therapy.
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PMID:Predictors of a fatal outcome following childhood cerebral malaria. 924 12

Data were prospectively collected on 306 Kenyan children, including blood gases in 258 (75%). Severe malaria caused a predominantly high-anion-gap metabolic acidosis in at least 43% of children. Children with coma and respiratory distress (CM + RD) had greater evidence of renal dysfunction, lower mean pH and higher mean plasma osmolality than those with respiratory distress (RD) or coma (CM) as isolated findings (mean urea 10.7 vs. 6.0 vs. 4.3 mmol/l; mean creatinine 97 vs. 74 vs. 58 mumol/l; mean osmolality 301 vs. 288 vs. 283 mosmol/l; and mean pH 7.16 vs. 7.29 vs. 7.39, respectively, p < 0.001 for each comparison of CM + RD vs. RD or CM). In addition, children with CM + RD had a higher mean blood lactate (6.7 vs. 3.3 mmol/l, p < 0.001), a lower mean haemoglobin (5.5 vs. 7.0 g/dl, p = 0.002) and a lower mean age (26.4 vs. 41.9 months, p < 0.001) than children with CM and accounted for 15/24 (63%) of all deaths. These and previous data implicate hypovolaemia and renal impairment in the pathogenesis of metabolic acidosis in severe childhood malaria. In children who are acidotic, anaemia is strongly associated with lactic acidaemia and may therefore contribute to its pathogenesis. These data also imply that coma in acidotic children (CM + RD) and those with an isolated encephalopathy (CM) may result from quite different pathophysiological mechanisms.
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PMID:Acidosis in severe childhood malaria. 934 54

We investigated the pathophysiology of hypoglycaemia in severe malaria in African children, especially the potential importance of glycerol as a substrate for gluconeogenesis, and whether substrate limitation contributes to hypoglycaemia in severe disease. Of 171 children with moderate or severe malaria, 16% were hypoglycaemic on admission, while at least 9% of children with severe malaria treated with quinine and a concurrent 4% dextrose infusion had a definite episode of hypoglycaemia after admission. Blood levels of gluconeogenic precursors are as high (alanine and lactate) or higher (glycerol) in those with either hypoglycaemia on or after admission as they are in children never having an episode of hypoglycaemia. Among children with severe malaria, however, those having a definite episode of hypoglycaemia at some stage are more acidotic and have greater evidence of renal impairment than those who are never hypoglycaemic (mean base excess -14.4 vs. -7.2, p < 0.001, mean creatinine 97 vs. 64, p < 0.001 and mean urea 8.1 vs. 5.8, p = 0.03, respectively). These data do not support a role for reduced gluconeogenic substrate supply in the pathogenesis of hypoglycaemia in severe childhood malaria, but do support the hypothesis that gluconeogenesis is impaired. Commonly-used bedside blood glucose monitoring devices may overestimate blood glucose measurements in the normal range, and paradoxically may also seriously overestimate the frequency of hypoglycaemia.
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PMID:Hypoglycaemia on and after admission in Kenyan children with severe malaria. 960 71


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