Medicine
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This repository contains the published and unpublished research of the Faculty of Medicine by the staff members of the faculty
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Item Mechanisms underlying early rapid increases in creatinine in paraquat poisoning(Public Library of Science, 2015) Mohamed, F.; Endre, Z.; Jayamanne, S.; Pianta, T.; Peake, P.; Palangasinghe, C.; Chathuranga, U.; Jayasekera, K.; Wunnapuk, K.; Shihana, F.; Shahmy, S.; Buckley, N.BACKGROUND: Acute kidney injury (AKI) is common after severe paraquat poisoning and usually heralds a fatal outcome. The rapid large increases in serum creatinine (Cr) exceed that which can be explained by creatinine kinetics based on loss of glomerular filtration rate (GFR). METHODS AND FINDINGS: This prospective multi-centre study compared the kinetics of two surrogate markers of GFR, serum creatinine and serum cystatin C (CysC), following paraquat poisoning to understand and assess renal functional loss after paraquat poisoning. Sixty-six acute paraquat poisoning patients admitted to medical units of five hospitals were included. Relative changes in creatinine and CysC were monitored in serial blood and urine samples, and influences of non-renal factors were also studied. RESULTS: Forty-eight of 66 patients developed AKI (AKIN criteria), with 37 (56%) developing moderate to severe AKI (AKIN stage 2 or 3). The 37 patients showed rapid increases in creatinine of >100% within 24 hours, >200% within 48 hours and >300% by 72 hours and 17 of the 37 died. CysC concentration increased by 50% at 24 hours in the same 37 patients and then remained constant. The creatinine/CysC ratio increased 8 fold over 72 hours. There was a modest fall in urinary creatinine and serum/urine creatinine ratios and a moderate increase in urinary paraquat during first three days. CONCLUSION: Loss of renal function contributes modestly to the large increases in creatinine following paraquat poisoning. The rapid rise in serum creatinine most probably represents increased production of creatine and creatinine to meet the energy demand following severe oxidative stress. Minor contributions include increased cyclisation of creatine to creatinine because of acidosis and competitive or non-competitive inhibition ofcreatinine secretion. Creatinine is not a good marker of renal functional loss after paraquat poisoning and renal injury should be evaluated using more specific biomarkers of renal injuryItem Medial temporal lobe atrophy, apolipoprotein genotype, and plasma homocysteine in Sri Lankan patients with Alzheimer's disease(Routledge, 2005) de Silva, H.A.; Gunatilake, S.B.; Johnston, C.; Warden, D.; Smith, A.D.The authors studied the association of Alzheimer's disease (AD) with total plasma homocysteine (tHcy) and apolipoprotein E (apoE)genotype, and the usefulness of measuring medial temporal lobe thickness (MTL) thickness for the diagnosis of AD in Sri Lankan patients. Using criteria of the NINCDS-ADRDA, 23 AD patients and 21 controls were recruited. All underwent MTL-oriented computed tomographic (CT) scans, measurement of plasma tHcy, and apoE genotyping. Mean plasma tHcy was significantly higher in AD patients than controls (p=.001). This association was independent of age, sex, body mass index (BMI), serum folate and vitamin B12, and serum creatinine. The frequency of apoE4 allele was significantly higher (p=.003) in AD patients, and the adjusted odds ratio of AD for the presence of one or more apoE4 alleles compared with none was 10.39 (95% CI 1.77-61.10; p=.010). The mean minimum MTL thickness was significantly higher in control subjects compared to that of AD patients (p<.001). This first report of apoE4, plasma tHcy, MTL thickness, and AD from Sri Lanka shows that high plasma tHcy, the presence of apoE4 allele, and MTL atrophy are associated with AD.Item Biochemical markers for early diagnosis of myocardial infarction(The Kandy Society of Medicine, 1996) Chandrasena, L.G.