Patient-specific formulations improve efficacyPotentially fewer side effects compared to current delivery methodsApproach can potentially be extended to treat alkylosis or other ailments affecting body chemistry
技术应用
Better treatment of acute metabolic acidosisImprove distribution of pH-influencing materials in general
详细技术说明
Professors Thomas Mason and Jeffrey Kraut in UCLA’s Department of Chemistry and School of Medicine, respectively, have developed improved materials and methods of treating acute metabolic acidosis. By examining the effects of experimental treatments based on formulations of sodium carbonate and sodium bicarbonate, the inventors have developed methods to optimize more effective ratios of sodium carbonate and sodium bicarbonate that take into account the extent of a patient’s acidosis. Additionally, the investigators have conceived new methods of delivering these formulations. By delivering the treatment solution in a time- and spatially-varying manner, caustic exposure is distributed, thereby reducing tissue damage resulting from current methods.
申请号码
20150196708
其他
State Of Development
The investigators have composed an enabling description based on calculations, to the extent that one skilled in the art can practice the invention. Additionally, ex vivo experiments using acidotic mammalian blood have established proof-of-concept. Currently, development is focused on optimizing delivery by formulating mixed solutions, and by implementing a computer-controlled system to administer time-varying solution mixtures. Further downstream, plans are also in place to test these optimized solutions and delivery methods using in vivo models of acidosis.
Background
Metabolic acidosis is a condition in which blood pH becomes abnormally acidic. It can lead to severe neurological and cardiac complications if left unchecked. Currently, treatment consists of eliminating the underlying cause, and administering an intravenous sodium bicarbonate solution. However, this approach has shown no more benefit than similar quantities of sodium chloride, and failed to reduce morbidity or mortality in patients with ketoacidosis or lactic acidosis. This failure has been attributed in part to the cell generating carbon dioxide in response to the administration of bicarbonate, thereby resulting in a reduction in intracellular pH. There is therefore a need to develop a new base that raises both extracellular and intracellular pH and eliminate. Ideally, this new base will also reduce carbon dioxide levels in tissues.
