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

Thirty-two patients of smear positive Plasmodium falciparum malaria having jaundice were analysed retrospectively. Majority of the cases were in the age group of 31-40 years. Serum bilirubin levels ranged from 2 mg to 40 mg%. Fourteen (42.6%) had serum bilirubin above 10 mg%. Conjugated bilirubinaemia was found in twenty one patients (65.5%), unconjugated in 4 (12.5%) while 7 patients (21.8%) had a mixed pattern. Serum transaminases were high in 21.8% patients. Twenty five patients (78%) had associated azotaemia, 11(34.3%) had intravascular haemolysis and 3(9.3%) had possible cerebral malaria. Hepatosplenomegaly was seen in all the 32 patients. Mortality was 21% but none died of hepatic encephalopathy. Histologically the most consistent finding in liver biopsies was reticulo-endothelial cell hyperplasia. Pigmentation in kupffer cells, fatty change, sinusoidal and portal infiltration and cholestasis were the other features seen.
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PMID:Jaundice in Plasmodium falciparum. 268 27

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

A retrospective analysis of fifty cases where falciparum malaria was detected at autopsy, was done. Histopathological sections from all organs were taken. Cerebral malaria was seen in 44 cases on histology. Plugging of cerebral vasculature by parasitised erythrocytes (pRBC) was seen in all cases while Durck granulomas were seen in 5 cases. Multiple organ involvement was seen in form of sequestration of pRBC in all the cases. Positive peripheral smear was obtained in only 20 cases (antemortem). Twenty-nine patients had jaundice of which 18 had altered sensorium. They were clinically diagnosed as hepatic failure with or without hepatic encephalopathy. Fever as a symptom was seen in 19 patients. Age varied from 14 years to 80 years. Twenty-three patients died within 12 hours of admission, 12 other patients expired within a day. Only two cases survived more than a week. Specific antimalarial therapy was administered to 29 patients of which only 11 cases received quinine.
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PMID:Plasmodium falciparum malaria--a diagnostic dilemma. 900 76

A 53-year-old patient, after return from a short visit to the Ivory Coast, was admitted for suspicion of hepatic encephalopathy. An acute pernicious malaria was diagnosed with associating altered consciousness, hyperthermia, icterus, hepatomegaly, and oliguria. Blood tests showed acute renal failure, pancytopenia, disseminated intravascular coagulation, metabolic acidosis and parasitaemia at 12%. An intravenous therapy with quinine and doxycycline was started without delay. One day later, an exchange blood transfusion including a erythrapheresis and plasmapheresis was undertaken. The patient's general condition improved, and he was discharged from the ICU 22 days later. The indications for exchange blood transfusion in acute pernicious malaria are discussed.
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PMID:[Acute pernicious malaria treated with exchange transfusion]. 1042 88

West Nile encephalitis (WNE) has become endemic in the United States since 1999. The clinical spectrum of WNE includes aseptic meningitis, meningoencephalitis, or encephalitis with or without flaccid paralysis. The severity of WNE ranges from asymptomatic serum conversion to severe neurologic deficits or a fatal outcome. Several systemic disorders may present with encephalitis as part of the clinical presentation, for example, Legionnaires' disease, neoplasms with metastases to the central nervous system, Mycoplasma meningoencephalitis, brucellosis, Listeria, Rocky Mountain spotted fever, ehrlichiosis, and malaria. The most common infectious causes of encephalitis that need to be differentiated from WNE include herpes simplex virus 1, meningoencephalitis, and enteroviral meningoencephalitis. We present a case of apparent hepatic encephalopathy secondary to pancreatic carcinoma with liver involvement that presented as hepatic encephalopathy mimicking WNE. We conclude that patients presenting with encephalitis in the summer months should have serum/cerebrospinal fluid serologic studies sent for WNE even if an alternate explanation seems to explain the clinical syndrome.
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PMID:West Nile viral encephalitis mimicking hepatic encephalopathy. 1564 37

Jaundice is a common clinical presentation in severe malaria, seen in approximately 2.5% patients with falciparum infection but hepatitis is unusual. Although hepatic dysfunction is unusual and hepatic encephalopathy is almost never seen in malaria, yet, cases of hepatic dysfunction are being increasingly reported in patients with P.falciparum infection, from different parts of world. The extent of hepatocellular dysfunction varies from mild abnormalities in liver function tests to hepatic failure. Patients with hepatocellular dysfunction in malaria are more prone to develop complications, but have a favorable outcome if hepatic involvement is recognized early and managed properly. It is important to meticulously look for hepatic dysfunction in patients with severe malaria, distinguish it from fulminant hepatic failure and manage it aggressively.
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PMID:Malarial hepatopathy. 1710 60

Malaria is a major cause of morbidity and mortality with an annual death toll exceeding one million. Severe malaria is a complex multisystem disorder, including one or more of the following complications: cerebral malaria, anemia, acidosis, jaundice, respiratory distress, renal insufficiency, coagulation anomalies, and hyperparasitemia. Using a combined in vivo/in vitro metabolic-based approach, we investigated the putative pathogenic effects of Plasmodium berghei ANKA on brain, in a mouse strain developing malaria but resistant to cerebral malaria. The purpose was to determine whether the infection could cause a brain dysfunction distinct from the classic cerebral syndrome. Mice resistant to cerebral malaria were infected with P. berghei ANKA and explored during both the symptomless and the severe stage of the disease by using in vivo brain magnetic resonance imaging and spectroscopy. The infected mice did not present the lesional and metabolic hallmarks of cerebral malaria. However, brain dysfunction caused by anemia, parasite burden, and hepatic damage was evidenced. We report an increase in cerebral blood flow, a process allowing temporary maintenance of oxygen supply to brain despite anemia. Besides, we document metabolic anomalies affecting choline-derived compounds, myo-inositol, glutamine, glycine, and alanine. The choline decrease appears related to parasite proliferation. Glutamine, myo-inositol, glycine, and alanine variations together indicate a hepatic encephalopathy, a finding in agreement with the liver damage detected in mice, which is also a feature of the human disease. These results reveal the vulnerability of brain to malaria infection at the severe stage of the disease even in the absence of cerebral malaria.
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PMID:Magnetic resonance spectroscopy reveals an impaired brain metabolic profile in mice resistant to cerebral malaria infected with Plasmodium berghei ANKA. 1736 63

A study on the clinicoepidemiology of cerebral malaria (CM) and mild malaria (MM) among adults and children attending NSCB medical college hospital Jabalpur and civil hospital Maihar, Satna, in central India was undertaken. Of 1,633 patients, 401 were Plasmodium falciparum and 18 P. vivax. Of 401, 199 CM patients and 112 MM patients were enrolled. Severe complications among CM patients were jaundice (26%), acute renal failure (22%), respiratory distress (22%), severe malaria anemia (18%), hypotension (17%), hepatic encephalopathy (7.0%), and hematuria (5%). Among CM cases, seizures and severe malaria anemia were significantly higher in children (P < 0.0001) compared with adults, whereas jaundice (P < 0.0025), acute renal failure (P < 0.0001), and hematuria (P <or= 0.05) were significantly higher among adults. Mortality was high among adults with multiple organ failures. Overall case fatality rate was 21%. Neurologic sequelae at discharge from the hospital were 3%, whereas at follow-up, only 1% had persistent neurologic sequelae.
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PMID:Burden of cerebral malaria in central India (2004-2007). 1884 Jul 56

Leptospirosis in humans is a common zoonotic disease. It is often under-diagnosed, especially when associated with neurological features, resulting in significant morbidity and mortality. This subgroup of patients with neurological manifestations is often empirically treated for cerebral malaria, dengue fever, tuberculous meningitis, hepatic encephalopathy, viral encephalitis, etc. Hence it is important to be aware of uncommon manifestations of this disease. We report one such patient, which highlights the importance of considering leptospirosis as the diagnostic possibility with hepato-renal, pulmonary and nervous system involvement, particularly where diagnostic supports and resources are limited.
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PMID:Leptospirosis presenting as acute meningoencephalitis. 2035 61

Malaria remains an overwhelming problem in the tropical developing countries, with 300 to 500 million new cases and about a million deaths per year (Mishra et al., 2003). Malaria is a potentially life-threatening disease in the tropics. Jaundice is one of the severe manifestations of falciparum malaria. Its incidence (Mishra et al., 2003). varies between 10 and 45% in different reports and is seen more in adults than in children. Jaundice may vary from mild to very severe. However, clinical signs of hepatic encephalopathy (such as liver flaps) are never seen unless there is presence of concomitant viral hepatitis (WHO, 2000). Our case is a 6-year-old female child presented with fever, jaundice, and anasarca. Peripheral smear showed trophozoites and schizonts of Plasmodium (P.) vivax and trophozoites and gametocytes of P. falciparum. Viral markers for hepatitis were negative. She developed fulminant hepatic failure and expired after 26 hours of admission.
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PMID:A Rare Case Report of Fatal Fulminant Hepatic Failure in a Child due to Mixed vivax and falciparum Infection. 2260 19


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