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)

Liver function tests were performed in 165 hospitalized patients suffering from P. falciparum malaria with complications. Serum bilirubin was found increased in 33 patients, and 22 of them had unconjugated hyperbilirubinaemia. Serum alanine aminotransferase was increased in 5 patients, but only to mild to moderate levels. Serum alkaline phosphatase was increased in 11 patients, gamma-glutamyl transpeptidase in 3 patients. Serum total protein and albumin were significantly decreased but these were considered more as indicator of acute phase response. Liver cell necrosis was observed in one patient, and oedema and mononuclear cell infiltration in two patients. Though hepatomegaly and mild elevation of enzymes can be observed in a significant proportion of patients, involvement of liver leading to acute hepatitis or liver cell necrosis is a relatively uncommon complication in P. falciparum malaria.
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PMID:Hepatic changes in P. falciparum malaria. 128 32

A variety of tubular marker proteins, as compared to healthy controls, are excreted at an increased rate in the urine of patients with renal damage. Beside cytoplasmic glutathione-S-transferase and lysosomal beta-N-acetyl-glucosaminidase (beta-NAG) the majority of kidney-related urine proteins derives from membrane surface components of the most vulnerable proximal tubule epithelia, among them ala-(leu-gly)-aminopeptidase, gamma-glutamyl transpeptidase (GGT), the tubular portion of angiotensinase A, the major brush border glycoprotein 'SGP-240' and adenosine-deaminase-binding protein. Urinary tissue proteins, e.g. brush border (BB) microvilli, are immunologically identical with those antigens prepared from cell membranes of the human kidney itself. BB antigens are shed into the urine of patients with glomerulonephritis, interstitial nephritis, systemic diseases, e.g. systemic lupus erythematosus (SLE), diabetes mellitus and multiple myeloma, arterial hypertension, infectious diseases (malaria, AIDS) and after operations, renal grafting and administration of X-ray contrast media, aminoglycosides or certain cytostatics (cis-platinum). Tissue proteinuria of tubular proteins is determined by enzyme-kinetic or quantitative immunological assays applying either poly- or monoclonal antikidney antibodies. Clinical, ultrastructural and histochemical studies support the idea that both 'soluble' and high-molecular-weight membrane particles (vacuolar blebs, greater than 10(6) dalton) as well as microfilamental components of the epithelial cytoskeleton contribute to tubular 'histuria' which appears as a sensitive parameter in monitoring tubular damage under clinical conditions at a very early phase.
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PMID:Urinary proteins of tubular origin: basic immunochemical and clinical aspects. 225 76

A randomized double blind study in long term malaria chemoprophylaxis was performed to compare the tolerability of Fansimef (1 tablet containing 250 mg mefloquine + 500 mg sulfadoxine + 25 mg pyrimethamine per week) with chloroquine (300 mg per week). 211 Austrian industrial workers and their families in Warri, Nigeria, participated in this study; 101 received Fansimef and 110 chloroquine for 3-18 months (mean 41 weeks). Prophylaxis was discontinued because of adverse effects in 7 volunteers in the Fansimef group (mainly insomnia, palpitations, dizziness, nausea and headache) and in 2 volunteers of the chloroquine group (headache and loss of hair in one volunteer, nausea, dizziness and vomiting in the other). Most of the adverse effects could be due to the mefloquine component. A few minor complaints of burning eyes, nausea and gastric pain were reported in both groups. Laboratory checks performed at 3-monthly intervals showed a slight, transient and clinically irrelevant (but statistically significant) increase of serum glutamic-oxalacetic transaminase and gamma-glutamyl transpeptidase at month 3 in the Fansimef group. An attack of acute Plasmodium falciparum malaria occurred in one volunteer 6 weeks after discontinuation of prophylaxis with Fansimef. Antibodies against blood stage parasites could be demonstrated by the indirect immunofluorescence test at different stages of the study, indicating that these two antimalarials are not causal prophylactic agents.
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PMID:Tolerability of long-term malaria prophylaxis with the combination mefloquine + sulfadoxine + pyrimethamine (Fansimef): results of a double blind field trial versus chloroquine in Nigeria. 290 58

A 67-year-old man was referred to us for tonic-clonic convulsions. A review of his history revealed that he had been hospitalized for loss of consciousness, hypotension, and suspected apoplexy at age 67. He had experienced prior tonic-clonic convulsions at age 72 and age 74. He had malaria and tuberculosis in his history but had been otherwise generally well. Physical examination was normal, and his blood pressure was 100/80 mmHg. Laboratory findings were normal except alcalinephosphatase (292 U/l) and gamma-glutamyl transpeptidase(60 U/l). Neurological examination showed alert consciousness, mild upper gaze palsy, slight right-side hemiparesis and left Babinski signs was present. Cranial magnetic resonance imaging showed no abnormality, but cerebral angiography revealed bilateral carotid artery occlusion. There were abundant leptomeningeal anastomoses, and the posterior communicating artery was supplied by the left vertebral artery. Electroencephalography showed a spike wave in the temporal lobe and rebuild-up phenomenon in the right hemisphere. Brain atrophy in the anterior and temporal lobes progressed, and the patient experienced gradual disorientation, delirium and hypobulia. He was eventually bedridden. He also demonstrated repetitive tonic-clonic convulsions. After one convulsion, he remained unconscious and died of pneumonia. Autopsy revealed thickening of the intima and internal elastic lamina in the occluded internal carotid artery. The anterior and middle cerebral arteries showed the same pathological changes. Multiple small infarctions restricted to grey matter were present in the cerebral cortex and may have caused the progressive brain atrophy. There was no myelin pallor in the white matter of the cerebrum. Atherosclerotic changes, senile plaque, and neurofibrillary tangles were seen but were within normal limits. These pathological findings were strongly suggestive of moyamoya disease.
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PMID:[An autopsy case of bilateral carotid artery occlusion with repetitive epilepsy and brain atrophy in a senile patient]. 1068 97