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)

Seventy-two patients with severe falciparum malaria are described. Twenty-four (33.3%) were complicated by acute renal failure. Comparing patients with renal failure and those without, statistically significant differences occurred regarding presence of cerebral malaria (83% vs 46%), jaundice (92% vs 33%), and death (54% vs 17%). A significantly higher number of patients with renal failure were nonimmune visitors to malaria endemic regions. Renal failure was oliguric in 45% of cases. Dialysis was indicated in 38%, 29% died in early renal failure, and 33% recovered spontaneously. It is concluded that falciparum malaria is frequently complicated by cerebral malaria and renal failure. As nonimmune individuals are prone to develop serious complications, malaria prophylaxis and vigorous treatment of cases is mandatory.
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PMID:Acute renal failure due to falciparum malaria. 223 18

22 cases of adult cerebral malaria were observed between July 1987 and June 1989, either associated or not: parasitemia 5%, consciousness disorders, acute renal failure, thrombocytopenia. Two patients died (9%). Increased frequency of attacks is underlined. They are due to chloroquino-resistant parasite strains, even polychemoresistant, occurred in French speaking Tropical Africa since 1985. Therapeutic strategy is described. The necessity to use increased doses of quinine has been admitted, correlatively underlining importance of strict monitoring of the patients because, in first instance, the risk of hypoglycemia (eased by injecting too quickly high doses of quinine) and of acute pulmonary oedema (eased by too quick perfusions and/or transfusions).
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PMID:[Adult cerebral malaria. Actual experience of the Infectious Diseases Intensive Care Department at the Claude Bernard Hospital]. 236 52

Cellular Ca2+ influx during the reperfusion period after an ischemic insult has been proposed to be a crucial pathogenetic factor in the development of experimental acute renal failure (ARF). The present study, therefore, examined the potential beneficial effect of intrarenal verapamil, a calcium entry blocking agent, on ARF in patients. Twelve patients were enrolled in the study. Six ARF patients (experimental group)--ARF caused by malaria (4 patients) and leptospirosis (2 patients)--had a catheter placed in their renal artery; verapamil was infused at 100 micrograms/min for 3 h and intravenous furosemide, 0.8 mg/kg/h x 24 h was also administered. Another six ARF patients (control group)--ARF caused by malaria (5 patients) and leptospirosis (1 patient)--were treated with intravenous furosemide alone. Baseline renal function was comparable in both groups; GFR (3.16 +/- 3.24 vs 0.7 +/- 1.5 mL/min, NS), serum creatinine (Scr), (9.1 +/- 2.1 vs 11.3 +/- 2.2 mg/dL, NS), and urine volume (V) (41.79 +/- 4.77 vs 34.54 +/- 13.52 mL/h, NS), were comparable in the experimental and control groups. Twenty-four hours posttreatment, the increment of GFR (9.66 +/- 4.25 vs 1.32 +/- 0.50 mL/min, P less than .02) and V (181.8 +/- 61.7 vs 79 +/- 18 mL/h, P less than .04), were significantly greater in the experimental group as compared to the control group. The course of ARF was also shorter in the experimental group (6.5 +/- 2.1 vs 13 +/- 1.1 days, P less than .05), who also required less dialysis. Thus, combination of a renal arterial infusion of verapamil and intravenous furosemide significantly improves the renal function in tropical ARF as compared to intravenous furosemide alone.
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PMID:Beneficial effect of intrarenal verapamil in human acute renal failure. 248 83

The effects of furosemide and furosemide with dopamine on renal function were studied in 23 patients with acute renal failure due to falciparum malaria whose serum creatinine ranged from 230 to 947 mumol/l. Furosemide given intravenously at the dosage of 200 mg 6 hourly for a period of 4 days did not alter the clinical course of renal failure. Intravenous administration of furosemide (200 mg 6 hourly) with dopamine (1 microgram/kg/min) for 4 days increased creatinine clearance and arrested the progress of renal failure when the serum creatinine was less than 400 mumol/l, but failed to alter the course of renal failure when the serum creatinine exceeded 600 mumol/l.
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PMID:Furosemide and dopamine in malarial acute renal failure. 265 49

Life threatening hypoglycaemia has been closely associated with the use of quinine, but the effect of quinidine and the synthetic antimalarials on the homoeostasis of glucose has not been investigated. In volunteers given a fixed dose of 500 mg base and patients with malaria given a quinidine loading dose (15 mg base/kg) mean (SEM) plasma insulin concentrations rose from 6.1 (1.5) mU/l to 10.9 (4.4) mU/l (p less than 0.02) and 10.4 (2.0) mU/l to 18.5 (5.3) mU/l (p less than 0.04), respectively. Plasma glucose concentrations fell from 4.5 (1.1) mmol/l (81 (20) mg/100 ml) to 4.0 (0.3) mmol/l (72 (5) mg/100 ml) in volunteers (p less than 0.04) and from 5.7 (1.3) mmol/l (102 (23) mg/100 ml) to 4.8 (1.6) mmol/l (86 (29) mg/100 ml) in patients (p less than 0.05). One of two patients with cerebral malaria and acute renal failure became profoundly hypoglycaemic (plasma glucose concentration 1.4 mmol/l (25 mg/100 ml), plasma insulin concentration 3.1 mU/l). Hypoglycaemia may occur in any severely ill fasting patient given parenteral quinidine. The other antimalarials tested, chloroquine, amodiaquine, mefloquine, and halofantrine, did not stimulate the release of insulin, an important advantage that should be taken into account when treatment is chosen for Plasmodium falciparum malaria.
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PMID:Hypoglycaemia and antimalarial drugs: quinidine and release of insulin. 308 30

Severe falciparum malaria complicated by acute renal failure resulted in very high mortality. Ten patients with acute renal failure from falciparum malaria (infected rbc up to 80%) were continuously dialysed using Tenckhoff peritoneal catheter. Five were oliguric and BUN was maintained between 60 to 80 mg/dl (21.4 to 28.6 mmol/l) by hourly 1 to 1.5 liter dialysate exchange during the acute phase. The peritoneal urea clearance (mean +/- SD) was 12.1 +/- 1.2 ml/min with urea nitrogen removal of 13.4 +/- 2.3 g/day. In nonoliguric cases dialysis was also needed for additional removal of waste products since the remaining renal function could not cope with the hypercatabolic state. Peritoneal glucose absorption (135 to 565 g/day) gave considerable caloric supply without volume load and also contributed to the prevention of hypoglycemia. Varying degree of acute respiratory failure developed in all patients with 5 cases (2 oliguric and 3 nonoliguric) progressing to pulmonary edema. Swan-Ganz catheterization and hemodynamic study suggested the role of increased capillary permeability and volume overload from endogenous water formation in the development of pulmonary complication. Continuous removal of fluid and waste products minimized these problems and may prevent the progression of respiratory failure. One patient died of severe sepsis and the other nine survived. This study showed the beneficial contribution of continuous peritoneal dialysis in the management of acute renal failure from severe falciparum malaria.
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PMID:Continuous peritoneal dialysis in acute renal failure from severe falciparum malaria. 312 24

A non-immune, 31-year-old woman developed an acute infection with Plasmodium falciparum after travelling to Kenia. The parasites proved resistant to chloroquine and sulfadoxine/pyrimethamine. The course of the disease was complicated by acute renal failure, hepatocellular damage, disorders of blood coagulation, thrombocytopenia, hemolysis and cerebral involvement. Despite a very high level of parasitemia (50% parasitized erythrocytes) a rapid clinical improvement was achieved by plasmapheresis and hemodialysis. Our experience shows that plasmapheresis and hemodialysis are excellent additive methods which rapidly improve clinical symptoms and may reduce morbidity and mortality in severe malaria tropica.
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PMID:Successful treatment of malaria tropica with acute renal failure and cerebral involvement by plasmapheresis and hemodialysis. 322 May 82

A 42-year-old man was admitted to hospital with, previously wrongly diagnosed, fulminant falciparum malaria, 14 days after a two-week trip to Kenya. He had a high fever and was jaundiced, with severe anaemia and thrombocytopenia. He was given quinine intravenously and pyrimethamine/sulfadoxine (Fansidar) by mouth. He developed acute renal failure and increasingly severe cerebral symptoms, at times coma. An exchange transfusion and several plasmaphereses were, therefore, performed. The cerebral symptoms quickly abated during the exchange transfusion, but renal function failed to improve. Because of continuing fever, mefloquin (Lariam) and doxy-cycline (Vibramycin) were also administered. After several dialysis periods the patient improved gradually and was discharged after three weeks in generally good condition with normal renal function.
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PMID:[Exchange transfusion and (or) plasmapheresis: effective measures in severe tropical malaria?]. 328 61

The monitoring of quinine by HPLC in 3 patients suffering from cerebral malaria with acute renal failure and treated by haemofiltration is reported. The recommended dose of quinine in this situation is reduced to 10 to 15 mg.kg-1.day-1. However, in the first patient, when given quinine 10 mg kg-1.day-1 the plasma concentration was mainly below the recommended therapeutic range of 5 to 15 mg/l. In consequence, the dose of quinine in the second patient was elevated to quinine dihydrochloride 15.1 mg.kg-1.day-1 which produced plasma concentrations in the low therapeutic range. In the third patient, an unreduced dose of quinine dihydrochloride 25.7 mg.kg-1.day-1 was employed, resulting in plasma concentrations above 15 mg/l, which is generally assumed to be toxic, although, no sign of acute quinine toxicity was seen. The antimalarial effect in all three patients was satisfactory. Quinine was estimated in the haemofiltrate in two patients and was found to be below the limit of sensitivity (0.25 mg/l). Plasma quinine did not change during or shortly after haemofiltration. It is concluded that in case of acute renal failure in cerebral malaria the dose of quinine should be reduced, but that the common recommendation of 10 to 15 mg.kg-1.day-1 may be too low, and that haemofiltration has no marked influence on the total body clearance of quinine.
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PMID:Drug monitoring of quinine by HPLC in cerebral malaria with acute renal failure treated by haemofiltration. 331 49

Eleven of 43 nonimmune patients with falciparum malaria had one or several organ complications: cerebral malaria, acute respiratory failure, acute renal failure, secondary infection, autoimmune haemolysis, spontaneous spleen rupture, and acute pancreatitis. Parasitaemia was 0.1 to 60%. Initial antiparasitic therapy with quinine given parenterally resulted in rapid regression of parasitaemia. An additional schizonticide agent was given depending on parasitic resistance. Supportive therapy comprised intensive-care monitoring including fluid and electrolyte balance and, if necessary, early haemodialysis and (or) endotracheal intubation with PEEP breathing. In one patient with excessive parasitaemia exchange transfusion was performed. Heparin was given only in proven disseminated intravascular coagulation, corticosteroids only in persistent autoimmune haemolysis. All patients survived without suffering permanent defects. Retrospective analysis shows that, apart from rapid specific therapy, supportive treatment of the individual organ complications determines course and prognosis of complicated falciparum malaria.
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PMID:[Complicated malaria tropica: specific and supportive therapy in the imported diseases]. 351 46


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