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

Clinical and pathological data on 25 fatal cases of tropical malaria were obtained from several hospitals in a retrospective survey. The patients originated, without exception, from non-malaria endemic regions (non-immunes). Death occurred in nine patients despite elimination of the parasitaemia with schizontocides. Life threatening complications were complex and apparently interacting. Manifestations of the disease included (1) initial acute renal failure, (2) disturbance of water and electrolyte balance, (3) cerebral oedema resulting in microhaemorrhages, (4) lung oedema, and increasing respiratory insufficiency even after elimination of the parasitaemia (in 4 cases there was histological evidence of shock lung), (5) myocarditis (histological evidence of cellular myocardial infiltration obtained in 4 cases), (6) hepatocellular damage, (7) complications associated with intensive-care treatment in 2 cases. The data allow no conclusions on the intensity and nature of blood clotting disturbances. According to this analysis the clinical manifestations of advanced malaria resemble protracted shock conditions having other aetiologies. However, specific cerebral and cardiac complications and homeostatic disturbances do apparently occur, the treatment of which requires experience with the clinical syndrome.
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PMID:[Fatal complications of tropical malaria in non-immune patients. A retrospective clinico-pathologic analysis of 25 cases]. 389 70

A double-blind, randomized, dose-finding, phase II mefloquine trial was carried out in 147 adult male patients suffering from acute, uncomplicated, falciparum malaria and admitted to the Hospital for Tropical Diseases, Bangkok, between January 1980 and April 1981. Mefloquine was administered as a single oral dose of 500, 750, or 1000 mg (base) in the form of the hydrochloride. The clinical and parasitological responses were satisfactory with all three dosage regimens. The cure rates for the 1000-, 750-, and 500-mg doses were 100%, 92.5%, and 95% respectively, over an observation period of 63 days.The side-effects, which were transient and generally mild, included nausea, vomiting, and diarrhoea. No significant changes were noted in haematological or biochemical parameters in any of the three groups. Sinus bradycardia, which started 4-7 days after drug administration and lasted for a few weeks, was seen in 10 patients. It was symptomless and needed no treatment.Acute brain syndrome was observed in one patient on day 21 after receiving a 1000-mg dose of mefloquine.Mefloquine was well tolerated in one case of acute renal failure, in 10 cases of moderately severe malaria with jaundice, in 13 cases with glucose-6-phosphate dehydrogenase deficiency, and in one case of thalassaemia.Mefloquine showed no effect on either gametocytes of Plasmodium falciparum or tissue forms of P. vivax.Mefloquine hydrochloride was found to be an effective drug for the treatment of falciparum malaria and tended to produce a more rapid clinical and parasitological response at the highest tested dose of 1000 mg (base).
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PMID:A phase II clinical trial of mefloquine in patients with chloroquine-resistant falciparum malaria in Thailand. 634 13

The case of an Angolan woman who underwent, in her country, an hysterectomy requiring the transfusion of two whole blood units is reported. In the immediate postoperative period, acute renal failure with anuria set in, justifying the patient's transfer to an intensive care unit in France. Upon admission, she had a thick blood film and serology work-up for Plasmodium falciparum, both of which were negative. On the 20th day, the patient presented a pernicious malarial crisis with a concurrent rise in IgG and IgM titres, indicating recent contamination. The mode of infection is discussed: contaminating anopheline bites associated with the interruption of chemoprophylaxis rigorously followed up till then; post transfusion malaria, almost unavoidable in an endemic country; accidental inoculation by Plasmodium falciparum of the dialysis equipment. Finally, the possibility of pernicious malaria aggravating the initial acute renal failure and hypocalcaemia is also discussed.
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PMID:[Postoperative pernicious malarial attack in a subject, a native of an endemic zone]. 638 31

Generalized circulatory changes, manifesting as pulmonary oedema, acute renal failure, liver damage and severe hypotension, are well recognized aspects of acute falciparum malaria. The organ pathology is thought to be associated with a restricted local blood flow. These aspects of falciparum malaria are strikingly analogous to the shock syndrome which follows trauma, the injection of indotoxin, or some bacterial infections. Two of the cyclooxygenase products of arachidonic acid, thromboxane A2 and prostacyclin, acting through their opposing effects on vasoactivity and platelet aggregation, are emerging as the major controlling influences of vascular homeostasis. The effects of thromboxane, which constricts blood vessels and aggregates platelets, appear to dominate during traumatic or endotoxic shock. Thus thromboxane is potentially one of the main mediators of endotoxicity, and as such, from our previously published model, is likely to be important in the pathogenesis of the circulatory disturbances seen in acute malaria. This suggestion is consistent with earlier evidence that the autonomic nerve supply and bradykinin may have an important role in the pathogenesis of the haemodynamic changes in this disease. It also implies that pharmacological antagonists of thromboxane may provide useful specific therapy for the main life-threatening aspects of acute falciparum malaria.
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PMID:Thromboxane may be important in the organ damage and hypotension of malaria. 727 28

109 (9.8%) of 1103 malaria patients examined in Sabah were deficient in glucose-6-phosphate dehydrogenase (G6PD). 69 of these G6PD-deficient patients were randomly allocated to 1 of 3 treatment regimes with chloroquine, chloroquine and primaquine, or sulfadoxine-pyrimethamine (Fansidar). No hemolysis was observed in the 1st group; except for a single mild case, no case of hemolysis was seen in the 3rd group. However, in the 2nd group of 23 patients, hemolysis occurred in 7 of 16 patients who had complete G6PD deficiency. Of these 7, 5 required blood transfusion and the other 2 developed acute renal failure, 1 even requiring peritoneal dialysis. In the Fansidar group, 4 of 22 patients took more than 15 days to clear the parasitemia. Chloroquine resistance to falciparum infection was common in the patients given this antimalarial drug.
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PMID:The treatment of malaria in glucose-6-phosphate dehydrogenase deficient patients in Sabah. 732 35

Thirty patients with severe falciparum malaria were each given a total of 1600-mg artesunate suppository over three consecutive days followed by 1250 mg mefloquine per os, divided into two doses which were given 12 h apart. All patients were admitted for 28 days to the Bangkok Hospital for Tropical Diseases, so that the efficacy and tolerability of the treatment could be assessed. All the patients showed clinical improvement, with mean (S.D.) parasite and fever clearance times of 50.4 (13.0) and 70.7 (44.9) h, respectively. Two patients with unrousable coma (Glasgow coma score < or = 8) on admittance regained consciousness 46 and 48 h post-treatment. One other patient had acute renal failure and required dialysis. Most patients (80%) were initially hyperparasitaemic, with a mean density of 184,344 parasites/microliters blood. No deaths occurred. Efficacy was evaluated in 25 of the patients. The cure rate 28 days post-treatment was 92%. None of the patients had major adverse effects although two had tenesmus and passed stools immediately after each suppository was administered. A fresh suppository had to be inserted when this occurred. The results indicate that artesunate suppositories followed by oral mefloquine constitute a well-tolerated regimen with a high cure rate. The combination is suitable as an alternative treatment for severe malaria, particularly in children. Further, large-scale studies are required.
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PMID:Efficacy and tolerability of a sequential, artesunate suppository plus mefloquine, treatment of severe falciparum malaria. 749 60

Thirty-five children with G6PD deficiency, who presented with acute intravascular haemolysis, were evaluated to define its aetiology, clinical features and ultimate outcome. All were boys with ages ranging from 6 months to 12 years. Pallor of abrupt onset and passage of cola-coloured urine were universal presenting symptoms. Incriminating factors responsible for haemolysis include hepatitis (7), malaria (4), bacterial sepsis (3) and drug intake (24), with more than one predisposing condition existing in some children. Marked elevations in serum bilirubin, coinciding with intravascular haemolysis, was a feature in all the seven children with hepatitis. Azotaemia was noted in 20 patients, of whom 14 did not have oliguria. All four children with malaria presented with protracted renal failure. Therapy focused on maintaining a high urine output in those without oliguria. A total of 15 peritoneal dialyses and five haemodialyses were required in six patients with acute renal failure, all of whom were oliguric. Supportive therapy consisted of blood transfusions and treatment of the predisposing diseases. Thirty-two children recovered completely while three died, the cause of death being severe anaemia and congestive cardiac failure, malaria with oliguric renal failure and hepatic encephalopathy, respectively.
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PMID:Acute intravascular haemolysis in glucose-6-phosphate dehydrogenase deficiency. 750 89

The APACHE II (Acute Physiology and Chronic Health Evaluation) severity-of-disease classification system was used to stratify the prognosis of 72 adult patients with cerebral malaria. Overall mortality was 13.89%. With the cut-off point at a score of 24, the APACHE II score stratified the patients' mortality outcome with 95.8% accuracy. High APACHE II score, deep unconsciousness, acute renal failure and acidaemia were identified as poor prognostic factors. We suggest that the APACHE II system is useful for stratifying the prognosis of group outcome in cerebral malaria patients.
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PMID:APACHE II scoring for predicting outcome in cerebral malaria. 763 22

Disturbances in calcium metabolism in acute renal failure (ARF) remain incompletely understood. Most data are from patients with rhabdomyolysis. As renal impairment commonly accompanies severe malaria in the absence of rhabdomyolysis, falciparum malaria provides an alternative model of mineral homoeostasis in ARF. We studied 25 Vietnamese subjects, aged 18-63 yr, with severe malaria and 10 controls. Fourteen patients had a serum creatinine level of 250 mumol/L or less during treatment (group 1), five developed ARF but were not dialyzed (group 2a), and six required dialysis (group 2b). Group 1 patients presented with mild hypocalcemia (mean +/- SD serum ionized calcium, 1.18 +/- 0.05 vs. 1.23 +/- 0.02 mmol/L in controls; P = 0.01) that persisted until discharge in the presence of normal serum phosphate, PTH, and vitamin D metabolite levels. Group 2 patients were more hypocalcemic on admission (1.10 +/- 0.08 mmol/L; P < 0.0001 vs. controls), especially those in group 2b whose serum ionized calcium fell to 0.88 +/- 0.13 mmol/L when renal dysfunction was maximal. In group 2 patients, the admission serum PTH level was raised (5.4 +/- 3.8 vs. 2.7 +/- 0.9 pmol/L in controls; P < 0.02) and changed reciprocally with calcemia. Significant rises in serum phosphate occurred only in group 2b patients who had depressed serum free 1,25-dihydroxyvitamin D levels throughout. Hypercalcemia did not accompany the diuretic phase of ARF. These data suggest that parathyroid gland dysfunction is a cause of hypocalcemia in severe malaria without ARF, as seen in group 1 patients; in patients with ARF, the effect of the combination of phosphate retention and altered vitamin D metabolism on skeletal PTH sensitivity is of prime significance.
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PMID:Mineral homoeostasis in acute renal failure complicating severe falciparum malaria. 767 21

We report two patients who had cerebral malaria, heavy parasitemia, hyperbilirubinemia, hypercatabolism with rapid rises of blood urea and serum creatinine and acute renal failure. There was no evidence of intravascular hemolysis. Renal biopsy was consistent with acute tubular necrosis. Both patients responded to treatment with intravenous quinine and dialysis.
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PMID:Acute renal failure in falciparum malaria. 767 79


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