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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

South African canine babesiosis is caused by the virulent Babesia canis rossi. In recent years, this common disease has been detected in 12% of dogs presented at the outpatients' division of the University of Pretoria's (Onderstepoort) Veterinary Academic Hospital, and 31% of the affected dogs have been hospitalized as seriously ill. Of these hospitalized cases, 50% had severe anaemia at presentation, 32% had moderate anaemia and 18% were non-anaemic (often polycythaemic), frequently with central-nervous-system signs or multiple organ failure. A retrospective survey of 662 hospitalized cases revealed that the haematology, clinical biochemistry and patient profile (signalment) of the severely anaemic dogs were distinct from those of the non-anaemic, indicating that the babesiosis in these two groups of dogs should be viewed as two different disease in terms of the postulated, underlying, 'pathomechanisms'. The severely anaemic dogs exhibited hypoxic hepatic disease and an increase in serum urea (without a concomitant increase in creatinine), seldom had profound electrolyte imbalances and tended to have a much more profound leucocytosis, consisting of a left-shifted inflammatory leucogram, with higher numbers of circulating metamyelocytes, lymphocytosis and monocytosis. In contrast, the non-anaemic dogs exhibited severe azotaemia (which could be of renal or pre-renal origin) and often showed a marked electrolyte disturbance (reflecting acid-base abnormalities) and a very mild leucocyte response; such dogs often presented as leucopenic, many being lymphocytopenic. These results indicate that the severely anaemic dogs had developed haemolytic disease (possibly immune-mediated), whereas the non-anaemic dogs had developed an acute and overwhelming inflammatory response. The mean age of the non-anaemic dogs (2.66 years) was less than the dogs in the 'severe anaemia group' (0.83 years). Dogs belonging to the traditional fighting breeds (bull terriers, pit bull terriers and Staffordshire bull terriers) were noticeably over-represented in the non-survivors of the acute inflammatory response, possibly indicating an underlying genetic basis for the different presentations. It is evident that the inflammatory-response disease presentation, which is similar to complicated falciparum malaria in humans, amy serve as an animal model for the disease.
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PMID:Canine babesiosis in South Africa: more than one disease. Does this serve as a model for falciparum malaria? 968 1

The role of inducible nitric oxide synthase (iNOS) and nitric oxide (NO) in the pathophysiology of severe falciparum malaria remains unclear. We conducted a retrospective case-control study of Vietnamese adults with severe malaria to determine the relationship between outcome and admission plasma reactive nitrogen intermediates (RNI), the stable metabolites of NO. The study was designed to take into account the potential confounders of recent dietary nitrogen intake and renal function. Seventy-six patients who died from severe malaria were matched for age and sex with 76 survivors from a prospectively studied series of 560 patients. Median untransformed unadjusted plasma RNI levels were slightly higher in fatal cases (45 mumol/L, range 0-482) than in survivors (24.1 mumol/L, range 1.4-466) (P = 0.031, Wilcoxon signed-rank). There was a significant positive correlation between RNI levels and plasma creatinine (Spearman's rho = 0.35, P < 0.0001), and the addition of plasma creatinine as a covariate in a multivariate analysis abolished the trend towards higher RNI levels in fatal cases (P for the coefficient for RNI = 0.96). There was no association between RNI levels and either depth of coma on admission or time to regain consciousness. These findings do not support a pivotal role for systemic generation of NO in the pathogenesis of severe malaria in general, or cerebral malaria in particular.
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PMID:Reactive nitrogen intermediates and outcome in severe adult malaria. 976 23

Malaria remains an overwhelming problem in tropical developing countries, with 300 to 500 million new cases and 1.5 to 3.5 million deaths per year. Malaria is a potentially life-threatening disease for travelers to the tropics. Imported malaria is an important clinical problem in nonendemic areas of the world because of increasing numbers of travelers, overseas workers, and immigrants from endemic areas. According to the World Health Organization's criteria, the recognition of one or more of the following clinical features should raise the suspicion of severe malaria: cerebral malaria (unrousable coma), severe anemia (hemoglobin <5 g/dL), renal failure (serum creatinine >3 mg/dL), pulmonary edema or adult respiratory distress syndrome, hypoglycemia (glucose <40 mg/dL), circulatory collapse or shock, disseminated intravascular coagulation, repeated generalized convulsions, acidosis (pH <7.25), macroscopic hemoglobinuria, hyperparasitemia (>5 percent of the erythrocytes infested by parasites), or jaundice (bilirubin >3 mg/dL). Although only a small proportion of patients with malaria develops severe manifestations, these patients require the most urgent and intensive care. Mortality among patients with cerebral malaria, even when treated in modern intensive care units, exceeds 30%, and when complicated by the adult respiratory distress syndrome, it may approach 80%. Among travelers, mortality remains a serious issue because of failure to obtain and use preventive measures, delay in seeking medical attention, and misdiagnosis.
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PMID:Imported severe falciparum malaria in Israel. 977 25

Elevated plasma or serum levels of thrombomodulin (TM), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin have been reported in several diseases. However, plasma or serum levels of TM, ICAM-1, VCAM-1, and E-selectin have not been investigated in the acute phase of Plasmodium vivax malaria. Serum TM, ICAM-1, VCAM-1, E-selectin, and creatinine levels were determined in six Japanese patients in the acute phase of vivax malaria and in seven healthy Japanese controls. Parasitemias of the peripheral blood were < 0.1% in five patients and 0.8% in one patient. The patients' mean +/- SD serum levels of TM, ICAM-1, VCAM-1, and E-selectin were 5.7 +/- 1.3 Fujirebio units/ml, 709 +/- 397 ng/ml, 2,112 +/- 782 ng/ml, and 99 +/- 28 ng/ml, respectively, and all were significantly greater than those in the controls (TM; P < 0.005, ICAM-1; P < 0.025, VCAM-1; P < 0.005, E-selectin; P < 0.025). However, no significant difference was identified between patients and controls for serum creatinine values. The serum levels of TM and VCAM-1 were not related to parasitemia. The elevation of serum TM levels suggests that endothelial cell damage occurs in the acute phase of vivax malaria.
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PMID:Serum levels of thrombomodulin, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and E-selectin in the acute phase of Plasmodium vivax malaria. 1007 44

To establish the effects of chloroquine on kidney function we monitored renal parameters in age and sex matched control subjects and patients who presented with acute transient fever. The patients were immediately treated with chloroquine diphosphate in the recommended dosage. Blood samples for creatinine, urea, Na+ and K+ determinations were collected before treatment (Day 0), on the 3rd day of treatment (Day 3) and two days after the last dose of chloroquine (Day 5). 24 h urine collections were collected for five consecutive days from the second day of treatment. Spot urine samples showed the absence of blood cells, bilirubin, glucose, protein and ketones. Examination of thick blood smears over three days did not reveal any forms of malaria parasites. Urinary tract infection in the patients was also excluded. Therefore, these patients were a suitable group to assess the effects of chloroquine on renal function. The blood pressure in females and males decreased significantly after two days of chloroquine treatment compared with Day 0. The plasma concentration of creatinine in females and females was increased by chloroquine 2 days after the last dose by comparison with the Day 0 (females, 66 +/- 2 mumol/L versus 83 +/- 2 mumol/L n = 20, p < 0.01 and males, 78 +/- 6 mumol/L versus 81 +/- 9 mumol/L, n = 20, p < 0.01). This was paralleled by a reduction in urinary creatinine excretion during the same period (females 15 +/- 1 mg/kg body weight/24 h versus 12 +/- 1 mg/kg body weight/24 h and males 23 +/- 3 mg/kg/24 h versus 18 +/- 2 mg/kg/24 h, p < 0.01 in both instances). Urinary urea excretion in females was reduced from 290 +/- 6 mumol/kg/24 h to 215 +/- 5 mumol/kg/24 h 2 days after treatment. The results of the study suggest that the effects of chloroquine in patients with acute transient fever include lowered urinary urea and creatinine excretion.
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PMID:Chloroquine influences renal function in rural Zimbabweans with acute transient fever. 1008 79

Kidney function was studied in 80 Gambian children with cerebral malaria, 73 children with mild malaria, and in 19 children with other febrile illnesses. Serum creatinine was measured, and the excretion in urine of immunoglobulin G, transferrin, albumin and alpha 1 microglobulin was determined. Twenty-five percent of children with cerebral malaria, and 4% of children with mild malaria had an elevated serum creatinine above 62 mumol/l. Increased urinary protein excretion was frequent: 53% of children with cerebral malaria had a glomerulo-tubular pattern of protein excretion, and 46% a tubular pattern. Median albuminuria was 68 mg/l in children with cerebral malaria, 18 mg/l in children with mild malaria, and 9 mg/l in febrile children with other diseases (P < 0.0001). There was no significant association between the proteinuria and height of fever or the degree of parasitaemia, and there was no significant association between death and signs of renal impairment. Renal involvement is common in children with malaria in The Gambia, with prerenal, glomerular, and tubulo-interstitial factors contributing. It is more pronounced in children with cerebral malaria than in those with mild malaria. However, renal dysfunction is relatively mild and does not indicate a worse prognosis.
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PMID:Renal involvement in Gambian children with cerebral or mild malaria. 1040 76

Falciparum malaria is a disease of tropical climates which affects 270 million people annually and has an overall mortality of 1%. While the incidence of acute renal failure in malaria is less than 1%, mortality is reported to be as high as 45% in those with renal failure. We report the clinical course and outcome in 5 patients with falciparum malaria-induced acute renal failure treated at the Singapore General Hospital between June and July 1997. All 5 males, with mean age of 35.2 +/- 13.1 years, were admitted with history of fever and reported travel to a known malarious zone. Mean laboratory parameters upon admission included serum creatinine 725 +/- 515 mumol/L and serum urea 47 +/- 31 mmol/L. Three patients with hypotension on admission were started on haemodiafiltration, of whom 2 were subsequently converted to haemodialysis as their haemodynamics improved. Two remaining patients were started on intermittent bicarbonate haemodialysis. The overall mortality in our series was 20%, with 1 patient having died of complications of adult respiratory distress syndrome, disseminated intravascular coagulation and multiorgan failure. The remaining 4 survived and recovered their renal function. The single patient mortality occurred in the patient with admission serum creatinine of 1632 mumol/L, a value significantly higher than that of the 4 patients who survived (mean serum creatinine, 499 +/- 106 mumol/L, P < 0.002). These results suggest that falciparum malaria associated with acute renal failure is associated with a high morbidity, but early presentation and intervention with appropriate antimalarial and renal replacement therapy is associated with improved survival and recovery of renal function.
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PMID:A case series of falciparum malaria-induced acute renal failure. 1056 76

Biochemical evidence of skeletal muscle damage is common in malaria, but rhabdomyolysis appears to be rare. To investigate the relationship between serum creatine kinase and myoglobin levels, muscle histology, and renal function in Plasmodium falciparum infections, we studied 13 patients with uncomplicated malaria, 13 with severe noncerebral malaria, and 10 with cerebral malaria. A muscle biopsy specimen was obtained from each patient for light microscopy and electron microscopy. Mean serum creatine kinase concentrations +/- SD were raised but similar for the three groups (258 +/- 277, 149 +/- 158, and 203 +/- 197 U/L, respectively; P = .5). The mean serum myoglobin level +/- SD was highest in cerebral malaria (457 +/- 246 vs. 170 +/- 150 and 209 +/- 125 ng/mL in uncomplicated and severe malaria, respectively; P < .01) and correlated with the mean serum creatinine level (r = .39 for 36 patients; P = .02). The number of intravascular parasites, proportion of mature forms, and glycogen depletion were highest in biopsy specimens from patients with cerebral malaria. Myonecrosis was not observed. Muscle appears to be an important site for P. falciparum sequestration, which could contribute to metabolic and renal complications.
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PMID:Skeletal muscle involvement in falciparum malaria: biochemical and ultrastructural study. 1058 98

Of 51 consecutive children with cerebral malaria, fever, convulsions, and drowsiness were the commonest presenting symptoms. Decerebrate and decorticate postures and absent cornea reflex were the commonest brain stem signs. Opening lumbar cerebrospinal (CSF) pressure was raised in all but one of 24 children in whom it was reliably measured [mean 15.2 +/- 5.7 mmHg, range 6-24]. Hyponatraemia occurred in 17 (33%). Acute renal failure was not uncommon; the combination of hypercreatininaemia (plasma creatinine > 100 mumol/L) and hyperkalaemia (plasma potassium > 6.0 mumol/L) was fatal in 5 out of 7 patients in whom it occurred. Disturbances of acid-base status were present in all 40 children in whom it was assessed on admission. Mortality rate was 16% (8 patients). Neurological deficits occurred in 7 (14%) of the survivors and included cortical blindness [3], aphasia [3], hypertonia [3], hearing loss [2], and dystonia [1]. In addition to the present measures aimed at reducing morbidity and morality in children with cerebral malaria, efforts should be directed at rapid assessment of renal function and prompt correction of such dysfunction if found.
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PMID:Clinical study of cerebral malaria in African children. 1089 20

Acute renal failure (ARF) associated with liver disease is a commonly encountered clinical problem of varied etiology and high mortality. We have prospectively analyzed patients with liver disease and ARF to determine the etiology, clinical spectrum, prognosis and factors affecting the outcome. Other than hepatorenal syndrome patients, out of 221 cases, 66 developed ARF secondary to various liver disease like cirrhosis (n = 29, mortality 8, risk factors-older age p < 0.01, grade III/IV encephalopathy p < 0.05), fulminant hepatic failure (n = 25, mortality 15, risk factor-prolonged prothrombin time p < 0.01), and obstructive jaundice (n = 12, mortality 7, risk factor-sepsis p < 0.01). In these three groups the factors leading to ARF were volume depletion (24), gastrointestinal bleed (28), sepsis (34), drugs (27) [aminoglycosides (9) and NSAID (18)] along with hyperbilirubinemia. Various types of ARF with contemporaneous liver injury were malaria (n = 37, mortality 15, risk factors-higher bilirubin p < 0.001, higher creatinine p < 0.05, anuria p < 0.05 and dialysis dependency p < 0.05), sepsis (n = 36, mortality 22, risk factors-age p < 0.001, higher bilirubin p < 0.01, oliguria p < 0.05), hypovolemia with ischemic hepatic injury (n = 14, mortality 5, risk factors-higher creatinine p < 0.05 and SGPT p < 0.01), acute pancreatitis (n = 12, mortality 4, risk factors-higher bilirubin p < 0.001, higher SGPT p < 0.01, dialysis dependency p < 0.05), rifampicin toxicity (n = 10, no mortality), paroxysmal nocturnal hemoglobinuria (n = 3, no mortality), CuSO4 poisoning (n = 3 mortality 2), post abortal (n = 11, mortality 6, risk factors higher creatinine p < 0.05 and SGPT p < 0.01), ARF following delivery including HELLP syndrome (n = 12, mortality 4, risk factors-higher bilirubin p < 0.01 and SGPT p < 0.01), and of uncertain etiology (n= 14 mortality 4). 133 patients (60.2%), required hemodialysis hemodialfiltration or peritoneal dialysis. ARF associated with liver disease is having high mortality (42.5%). Avoidance of dehydration, hypotension, nephrotoxic drugs and sepsis, with promote dialytic support are necessary to reduce mortality and morbidity.
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PMID:Acute renal failure associated with liver disease in India: etiology and outcome. 1104 Dec 94


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