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)

Elevated plasma or serum levels of vascular cell adhesion molecule 1 (VCAM-1) have been reported in the febrile phase of falciparum malaria. However, little is known about serum VCAM-1 levels in the early post-treatment defervescent phase. Serum VCAM-1, tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and creatinine levels were determined in six Japanese patients with uncomplicated falciparum malaria during the acute febrile phase and the early post-treatment defervescent phase. The serum VCAM-1 values recorded for patients during the early post-treatment defervescent phase were significantly lower than those noted during the febrile phase (P < 0.05), but no significant difference in serum creatinine values was identified. TNF-alpha and IL-1beta levels were below the limit of detection in the serum of all patients during both the febrile phase and the early post-treatment defervescent phase. The serum levels of VCAM-1 were not related to parasitemia.
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PMID:Serum levels of vascular cell adhesion molecule 1 in the early post-treatment defervescent phase of falciparum malaria. 1119 52

Severe or complicated malaria is defined by infestation by Plasmodium falciparum into all red blood cells, especially those in the brain, causing coma and repeated convulsions; severe anemia (6 g/dl hemoglobin, 20% hematocrit); renal insufficiency (265 mcmol/l creatinine, 400 ml/day diuresis); pulmonary edema; hypoglycemia (2.2 ml/l or 0.4 g/l); shock; diffuse hemorrhaging; massive hemoglobinuria; and blood acidosis. Other possible symptoms of severe malaria are clouded thinking, changes in behavior, and inability to focus. It is most common in people with no immunity to malaria (children aged 4 and travelers in endemic zones). Pregnancy, splenectomy, corticotherapy, or poorly maintained immunity status favor severe anemia in adults. Sources of chloroquine-resistant P. falciparum have existed since 1960. Resistance has since expanded from Southeast Asia and South America to Africa, posing treatment problems. Malaria usually begins with fever (40 or more degrees Celsius), headaches, muscular pain, digestive troubles (e.g., diarrhea, nausea, or vomiting), and abdominal pain. In suspected cases of malaria, a blood sample or a thick blood smear as well as treatment (even in the absence of parasitological proof) needs to be done as soon as possible. Intravenous quinine diluted in a 5-10% glucose solution should be delivered at a rate of 24 mg/kg/day. In the case of severe jaundice, the dose should be cut in half beginning 8 hours after treatment began. If intravenous delivery is impossible, intramuscular delivery should be done. Corticosteroids, anticoagulants, and aspirin are contraindicated. In 2-4 days, oral administration (chloroquine, halofantrine, or mefloquine) is warranted. 20% of malaria-related deaths among patients who receive treatment are due to complications of the central nervous system. Protection against mosquito bites prevents malaria. Chemoprophylaxis in endemic zones should be limited to short trips to malaria zones or to pregnant women.
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PMID:[Severe malaria]. 1229 Jan 83

A case of failed peritoneal dialysis in a 5-year-old male nephrotic who developed acute renal failure following severe P. falciparum malaria infection is presented. Peritoneal dialysis (PD) failure was sequel to undetected severe dehydration which occurred during the diuretic phase of the acute renal failure. Pre-dialysis plasma potassium, bicabonate, urea and creatinine concentrations were 6.0mmol/L, 13mmol/L, 28mmol/L and 900mmol/L respectively, after about 22 hours of PD, the plasma K+, HCO-3 Ur and Cr were 5.7mmol/L, 15mmol/L, 32mmol/L and 1,090mml/L respectively. The peritoneal dialysate Ur concentration (3.5mmol and peritoneal Ur clearance (1.85ml/min/1.73m2) were grossly inadequate. There was also, intradialysis hyperglycaemia (12mmol/L owing to massive absorption of peritoneal dialysate solution which contains high concentration of glucose. Hyperglycaemia was corrected with 0.25 units/kg/dose of soluble insulin intravenously, he had two doses. Owing to similarity of clinical and biochemical features of dehydration and ARF, all efforts must be made to exclude dehydration before embarking on PD in patients with renal failure. Failure to exclude dehydration, led to PD failure in this patient.
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PMID:Failed peritoneal dialysis in a dehydrated nephrotic child, in acute renal failure: a case report. 1250 Dec 70

Malaria is widely prevalent in the tropics. Clinically significant renal and renal-related disorders commonly occur in infection with Plasmodium falciparum and P. malariae. Falciparum malaria causes fluid and electrolyte disorders, transient and mild glomerulonephritis, and acute renal failure (ARF). It appears that ARF is mediated by a complex interaction of mechanical, immunologic, cytokine, humoral, acute phase response, nonspecific factors, and hemodynamic factors. Parasitized erythrocytes play a central role in all aforementioned pathogenic factors of ARF. Antimalarial drugs are still the cornerstone of treatment of falciparum infection. Because of the hypercatabolic state of falciparum malaria-induced ARF, hemodialysis as well as peritoneal dialysis should be immediately performed when there is a rapid increase of creatinine concentration. P. malariae, in contradistinction, can cause chronic glomerulopathy that may relentlessly progress to end-stage renal disease. Antimalarial drugs, corticosteroids, and immunosuppressive agents are not effective.
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PMID:Malarial nephropathy. 1256 98

Malaria remains a major cause of morbidity and mortality in many sub Saharan countries and cerebral malaria is widely recognised as one of its most fatal forms. We studied the predictive value of routine biochemical laboratory indices in predicting the outcome of cerebral malaria in 50 Nigerian children ages 9 months to 6 years with cerebral malaria at the University College Hospital, Ibadan, Nigeria. Of the 50 children studied, 43 (68%) made a full recovery, 5 (105) developed neurological sequelae while 11(22%) died. Biochemical derangements observed among the children included azotaemia (29%), elevated plasma creatinine (20%), metabolic acidiosis (22%) and hyponatraemia (16%). Metabolic acidosis and elevated plasma creatinine on admission were significantly associated with a poor outcome (p < 0.05). Hyponatraemia and hypokalaemia were not significantly associated with outcome. On multivariated analysis, metabolic acidosis and elevated plasma creatinine on admission to hospital remained independent predictors of poor outcome after adjusting for other known risk factors. Patients with these findings require prompt referral for adequate treatment in centres equipped to manage such critically ill patients.
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PMID:Low plasma bicarbonate predicts poor outcome of cerebral malaria in Nigerian children. 1266 62

A descriptive study was carried out in 104 patients with Plasmodium vivax malaria, from the region of Turbo (Antioquia, Colombia). Clinical features and levels of hemoglobin, glycemia, serum bilirubin, alanine-aminotransferase (ALT), aspartate-aminotransferase (AST), creatinine and complete blood cell profile were established. 65% of the studied individuals were men and their mean age was 23. Of all individuals 59% had lived in the region for > 1 year and 91% were resident in the rural area. 42% were farmers and 35% had a history of malaria. The mean parasitaemia was 5865 parasites/mm3. The evolution of the disease was short (average of 4.0 days). Fever, headache and chills were observed simultaneously in 91% of the cases while the most frequent signs were palmar pallor (46%), jaundice (15%), hepatomegaly (17%), and spleen enlargement (12%). Anemia was found in 39% of the women and in 51% of the men, 8% of individuals had thrombocytopaenia and 41% had hypoglycemia.
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PMID:Clinical and laboratory findings of Plasmodium vivax malaria in Colombia, 2001. 1275 19

In a study of the influence of malaria-associated renal impairment on plasma concentrations of bilirubin, 111 Indian cases of Plasmodium falciparum malaria who had >34.2 microM total bilirubin/litre plasma were investigated. As the aim was to exclude those cases who had concomitant hepatic or (non-malarial) renal dysfunction, 19 cases who had serum concentrations of alanine aminotransferase (ALT) or alkaline phosphatase (AP) that were at least double the normal mean values were withdrawn. Of the remaining 92 patients, 47 showed evidence of renal impairment, the other 45 having plasma concentrations of creatinine that were <177 microM/litre. Plasma concentrations of the liver enzymes ALT and AP were similar for those with and without renal impairment. The plasma concentration of conjugated bilirubin (P<0.02), that of total bilirubin (P<0.05) and the ratio between the two (P<0.01) were, however, all significantly higher in the 47 patients with renal impairment than in the 45 with apparently normal renal function. The plasma concentration of creatinine was found to be not only positively correlated with the plasma concentrations of total (r=0.34; P<0.01) and conjugated (r=0.41; P<0.001) bilirubin but also negatively correlated with the urinary excretion rate for conjugated bilirubin (r=-0.34; P<0.001). The malaria-associated mortality was significantly higher among the patients with renal impairment than among those with apparently normal renal function, with 12 and three deaths, respectively (P<0.001). With increasing renal impairment there therefore appears to be a fall in the renal excretion of conjugated bilirubin. This leads to a disproportionate rise in the plasma concentration of conjugated bilirubin and this, since bilirubin can be toxic to renal tissue, may further worsen the renal impairment.
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PMID:Influence of renal impairment on plasma concentrations of conjugated bilirubin in cases of Plasmodium falciparum malaria. 1451 56

Renal failure remains a serious cause of mortality in Yemen. Our region has 1.25 million population and our hospital is the central hospital, which has a nephrology department and performs dialysis for the region. Between January 1998 and December 2002, we admitted 547 patients; including children, with acute renal failure (ARF) and chronic renal failure (CRF). CRF was observed in 400 patients, an incidence of 64 per million per year and a prevalence of 320 per million. ARF occurred in 147 persons with an incidence of 23.5 per million per year and a prevalence of 117.5 patients per million. Of all patients, 72% were adults (age range, 20-60 years) with a male preponderance. As a tropical country, malaria (27.9%), diarrhea (13.6%), and other infectious diseases were the main causes. Next most common were obstructive diseases causing CRF and ARF (26.8% and 12.9%, respectively), mainly urolithiasis, Schistosomiasis, and prostatic enlargement. However the cause of CRF in 57.5% of patients was unknown as most persons presented late with end-stage disease (64.7%), requiring immediate intervention. Other causes, such as hepatorenal syndrome, snake bite, diabetes mellitus, and hypertension, showed low occurrence rates. Patients presented to the hospital mostly in severe uremia and without a clear history of prior medications. The major findings were vomiting, acidosis, and hypertension with serum creatinine values ranging between 2.8-45 mg/dL (mean value, 13.4 mg/dL). Anemia was observed in 80.4% of CRF versus 62.6% of ARF patients. Hypertension prevalence was 65.5% among CRF patients, of whom 25% were in hypertensive crisis, whereas among ARF the prevalence was only 26.5%.
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PMID:Renal failure in Yemen. 1535 Apr 75

Data on the effects of Plasmodium gallinaceum on domesticated fowl are sparse, justifying a full investigation of its pathology. Clinical signs following blood-induced infections with the Wellcome line of strain 8A included depression, fever, anorexia, reduced weight gain, poor feed conversion, anaemia, green faeces and often death. After administration of 10(6) erythrocytic parasites, mortality 5 to 10 days after infection was 10% to 93% in chickens 7 to 84 days old. The older the birds, the lower the mortality and the longer the time to death. Onset of detectable parasitaemia occurred mostly during the second day after infection (59% of birds). Peak parasitaemia (approximately 70%) occurred on the sixth day in 85% of surviving birds. The patent period was usually 7 to 19 days. Abnormally low haematocrit values of < or =24% and high colonic temperatures of > or =42 degrees C were recorded. A febrile response is demonstrated conclusively here in P. gallinaceum malaria for the first time. Weight gain of malarious birds was reduced by approximately 18% to 51%, and feed conversion efficiency was often reduced by approximately 12% to 41%. Growth reduction was due entirely to anorexia. Liver weight relative to body weight (normally approximately 2% to 3%) increased to approximately 4.5% by 8 days, and relative spleen weight (normally approximately 0.2%) increased to 1.6% by 12 days. Specific gravities of livers and spleens in healthy and infected birds were approximately 1.09. Gall bladder volume in malarious birds 8 days after infection was approximately four times that of normal birds. Statistically significant changes occurred in the proportions of plasma proteins in malarious birds 8 days after infection; albumin and alpha2-globulin were reduced, while gamma1-globulin and gamma2-globulin were increased. Those changes coincided with significant increases in concentrations of plasma total protein and the enzymes aspartate aminotransferase, glutamate dehydrogenase and gamma-glutamyltransferase, and a decrease in creatinine. Green (biliverdin) colouration of the faeces was a consistent sign of malaria. Birds acquired non-sterile immunity after a single primary infection. The quantitative data presented facilitate selection of the most useful criteria for field diagnosis, estimation of potential economic losses, and assessment of potential avian antimalarial drugs.
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PMID:Avian malaria: clinical and chemical pathology of Plasmodium gallinaceum in the domesticated fowl Gallus gallus. 1576 37

Prostaglandins (PGs) are important mediators of macrophage activity, vascular permeability, fever, erythropoiesis, and proinflammatory responses to infection. Our recent studies have shown that plasma levels of bicyclo-PGE2 (a stable end product of PGE2 metabolism) and leukocyte cyclooxygenase (COX)-2 gene expression are suppressed in children with malarial anemia. Since the role of PGs as immunomodulators of human cerebral malaria (CM) has not been examined, we investigated urinary levels of bicyclo-PGE2/creatinine in children with varying clinical outcomes of CM. Among parasitemic children, those with asymptomatic parasitemia had the highest levels of bicyclo-PGE2/creatinine, whereas those with CM had significantly lower levels of bicyclo-PGE2. Systemic levels of bicyclo-PGE2/creatinine were not significantly associated with parasitemia, hemoglobin levels, or levels of the PG-regulatory cytokine tumor necrosis factor- alpha but were positively correlated with levels of interleukin-10. The results presented here show that impaired systemic production of PGE2 is associated with adverse outcomes of CM, whereas elevated levels of PGE2 in asymptomatic parasitemia suggest a potential role for PGs in protective immunity.
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PMID:Impaired systemic production of prostaglandin E2 in children with cerebral malaria. 1580 15


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