View clinical trials related to Acidosis, Lactic.
Filter by:This project looks at the time course of lactic acid rise (if any) after seizures. Salivary and capillary lactic acid are tested. This type of measurement may be useful in signalling the occurrence or recent history of a seizure.
Expanded access to DCA as continued treatment for congenital lactic acidosis.
In resolving lactic acidosis among children with severe malarial anemia, there is no difference between those transfused with blood of longer storage compared to shorter storage age
The objective of this study is to determine whether preoperative parenteral thiamin supplementation does prevent the intra and early postoperative increase of lactate and whether this effect is related to the extent of thiamine deficiency in patients undergoing heart surgery. In addition the prevalence of major thiamin deficiency in patient undergoing heart surgery will be determined.
From a central registry at the National Board of Health and Welfare in Sweden collect all patients in the city of Malmö prescribed metformin during two years. Glomerular filtration rate (eGFR) was estimated from the CKD-EPI formula (n=5408) and compared to a control material (n=2815) from the same town. All cases of severe lactic acidosis rendering ICU admission were also sought. The study hypothesis is that metformin is prescribed to patients with lower GFR than anticipated with very few cases of lactic acidosis registered.
The purpose of this study is to investigate whether entecavir treatment increases the incidence of lactic acidosis compared to another nucleoside/nucleotide reverse transcriptase inhibitors (NRTI), lamivudine, and/or no NRTI treatment, in patients with cirrhosis or hepatic failure whose Model for End stage Liver Disease (MELD) scores are over 18.
MP4OX is a novel oxygen therapeutic agent being developed as an ischemic rescue therapy to enhance perfusion and oxygenation of tissues at risk during hemorrhagic shock. MP4OX is a pegylated hemoglobin-based colloid. Due to its molecular size and unique oxygen dissociation characteristics, MP4OX targets delivery of oxygen to ischemic tissues. This study will evaluate the safety and efficacy of MP4OX treatment in trauma patients suffering from lactic acidosis due to severe hemorrhagic shock. The study hypothesis is that MP4OX will reverse the lactic acidosis by enhancing perfusion and oxygenation of ischemic tissues and thereby prevent and reduce the duration of organ failure and improve outcome in these patients.
Blood lactate levels in patients receiving typical or atypical antipsychotics have not been described in the literature. The goal of this study is to assess the dynamics of lactate levels in the blood from typical or atypical antipsychotics not confounded by prior antipsychotic treatments, the investigators conducted a prospective study of lactate levels in patients receiving antipsychotic medication. The investigators hypothesized that 6 months of treatment with haloperidol or olanzapine would result in a change in blood lactate levels and extrapyramidal side effects.
MP4OX is a novel oxygen therapeutic agent specifically developed to perfuse and oxygenate tissue at risk for ischemia and hypoxia. MP4OX is a pegylated hemoglobin-based colloid and and as a result of its molecular size and unique oxygen dissociation characteristics, targets oxygen delivery to ischemic tissues by selectively off-loading oxygen in tissues predisposed to low oxygen tension. Sangart is currently evaluating MP4OX to reduce organ dysfunction and failure in trauma patients with lactic acidosis due to severe hemorrhagic shock.
Metformin is the first line drug of choice for the treatment of type II diabetes. Lactic acidosis can develop as a side effect, especially when renal failure leads to drug accumulation. Lactic acidosis is usually attributed to an abnormal inhibition of hepatic lactate clearance. Growing evidence suggest that metformin can dose-dependently inhibit hepatocyte mitochondrial function. Whether a similar effect occurs in extra-hepatic human tissues remains unknown. The investigators hypothesize that mitochondrial dysfunction occurs during metformin intoxication even in tissues other than the liver, thus contributing to the development of lactic acidosis. The aim of this study is to investigate mitochondrial integrity in circulating platelets of patients with lactic acidosis due to metformin intoxication.