View clinical trials related to Acidosis, Lactic.
Filter by:To establish the relationship between human MAAI haplotype and DCA and tyrosine metabolism. This aim test the postulates that MAAI haplotype determines, and thus can predict,1) dose-dependent DCA kinetics and biotransformation.
The purpose of this study is to analyze the gene expression patterns associated with various microenvironmental stresses in tumors to understand their roles in tumor progression and treatment responses. To achieve this goal, we will perform gene expression analysis of the tumor samples collected from an IRB-approved study (IRB #: 4516-05-2R2) International Phase III Study of Chemoradiotherapy versus Chemoradiotherapy Plus Hyperthermia for Locally Advanced Cervical Cancer directed by Dr. Mark Dewhirst. We will correlate the gene expression signatures of different microenvironmental stresses with the measured physiological parameters to understand their role in tumor progression, treatment response and clinical outcomes.
Lactic acidosis is a potentially life-threatening disease associated with the treatment of chronic HIV infection. Although acidosis is rare, hyperlactatemia is common and may have long term consequences yet to be recognized. Lactic acidosis is a manifestation of mitochondrial toxicity; consequences which have yet to be fully recognized and understood. In this study, we propose to look at lactate clearance and production by two methods, in four treatment groups, including HIV positive subjects on highly active antiretroviral therapy (HAART) treatment regimes and without HAART regimes, with liver steatosis and without, and compared with HIV negative controls. Supplementation with cofactors thiamine, niacin and L-carnitine, which may have a positive effect on lactate metabolism by facilitating mitochondrial function, will be studied as well.
The purpose of this study is to determine the best way to treat people on d4T (stavudine) with high levels of lactic acid. Switching from d4T to abacavir will be assessed. Adding riboflavin and thiamine will also be assessed. Participants will be randomly assigned to one of four groups: - Group 1 participants will continue to take d4T as part of their antiretroviral (ARV) regimen, and will be given the vitamin supplements - Group 2 will continue to take d4T without vitamin supplements - Group 3 will switch from d4T to abacavir and receive the vitamins - Group 4 will switch from d4T to abacavir without vitamin supplements. The study plans to involve eighty participants from Canada and Argentina for a treatment period of 16 weeks and a follow-up visit at week 24.
This is a study to determine the safety of dichloroacetate (DCA) with a low-tyrosine diet given with or without nitisinone (NTBC) in children with chronic lactic acidosis (CLA).
Dichloroacetate (DCA) is a product of water chlorination and a metabolite of certain industrial solvents, thus making it a chemical of environmental concern. However, DCA is also used as an investigational drug for treating various diseases of adults and children, at doses far greater than those to which humans are normally exposed in the environment. Our research involves how DCA is metabolized by healthy adults and by children with a fatal genetic disease, congenital lactic acidosis (CLA) who are treated with DCA.
OBJECTIVES: I. Determine the pharmacokinetics of sodium dichloroacetate (DCA) in patients with congenital lactic acidemia. II. Determine the efficacy of DCA in decreasing the frequency and/or severity of acute episodes of acidotic illness, improving linear growth, improving neurological or developmental function, or slowing neurological or developmental deterioration in these patients.
OBJECTIVES: I. Compare the safety of sodium dichloroacetate (DCA) vs placebo in children with congenital lactic acidosis. II. Determine the quality of life of these patients. III. Determine the pharmacokinetics and metabolic fate of DCA over the course of drug administration in these patients.
OBJECTIVES: I. Study the metabolism of pyruvate and related problems in patients with lactic acidemia. II. Define the nature of the metabolic defect.