hydrogen carbonate has been researched along with Pyruvate Dehydrogenase Complex Deficiency Disease in 2 studies
Bicarbonates: Inorganic salts that contain the -HCO3 radical. They are an important factor in determining the pH of the blood and the concentration of bicarbonate ions is regulated by the kidney. Levels in the blood are an index of the alkali reserve or buffering capacity.
hydrogencarbonate : The carbon oxoanion resulting from the removal of a proton from carbonic acid.
Pyruvate Dehydrogenase Complex Deficiency Disease: An inherited metabolic disorder caused by deficient enzyme activity in the PYRUVATE DEHYDROGENASE COMPLEX, resulting in deficiency of acetyl CoA and reduced synthesis of acetylcholine. Two clinical forms are recognized: neonatal and juvenile. The neonatal form is a relatively common cause of lactic acidosis in the first weeks of life and may also feature an erythematous rash. The juvenile form presents with lactic acidosis, alopecia, intermittent ATAXIA; SEIZURES; and an erythematous rash. (From J Inherit Metab Dis 1996;19(4):452-62) Autosomal recessive and X-linked forms are caused by mutations in the genes for the three different enzyme components of this multisubunit pyruvate dehydrogenase complex. One of the mutations at Xp22.2-p22.1 in the gene for the E1 alpha component of the complex leads to LEIGH DISEASE.
| Excerpt | Relevance | Reference |
|---|---|---|
| " The partial correction of lactic acidosis with oral sodium bicarbonate chronic therapy may result in a slow evolution of the clinical symptoms." | 3.68 | Congenital lactic acidosis due to a defect of pyruvate dehydrogenase complex (E1). Clinical, biochemical, nerve biopsy study and effect of therapy. ( Dotti, MT; Fabrizi, GM; Federico, A; Guazzi, GC; Malandrini, A; Massimo, L; Palmeri, S; Robinson, BH, 1990) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 1 (50.00) | 18.2507 |
| 2000's | 1 (50.00) | 29.6817 |
| 2010's | 0 (0.00) | 24.3611 |
| 2020's | 0 (0.00) | 2.80 |
| Authors | Studies |
|---|---|
| Neiberger, RE | 1 |
| George, JC | 1 |
| Perkins, LA | 1 |
| Theriaque, DW | 1 |
| Hutson, AD | 1 |
| Stacpoole, PW | 1 |
| Federico, A | 1 |
| Dotti, MT | 1 |
| Fabrizi, GM | 1 |
| Palmeri, S | 1 |
| Massimo, L | 1 |
| Robinson, BH | 1 |
| Malandrini, A | 1 |
| Guazzi, GC | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Pharmacotoxicology of Trichloroethylene Metabolites: Short-term Effect of DCA on in Vivo Tyrosine Catabolism and MAAI Expression[NCT00865514] | 2 participants (Actual) | Interventional | 2011-08-31 | Terminated (stopped due to Difficulty in obtaining the solution from the compounding pharmacies caused a two year delay in start-up; the funding ended prior to study completion.) | |||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
2 other studies available for hydrogen carbonate and Pyruvate Dehydrogenase Complex Deficiency Disease
| Article | Year |
|---|---|
Renal manifestations of congenital lactic acidosis.
Topics: Acidosis, Lactic; Adolescent; Adult; Bicarbonates; Blood Urea Nitrogen; Calcium; Child; Child, Presc | 2002 |
Congenital lactic acidosis due to a defect of pyruvate dehydrogenase complex (E1). Clinical, biochemical, nerve biopsy study and effect of therapy.
Topics: Acidosis, Lactic; Bicarbonates; Biopsy; Brain Diseases, Metabolic; Child; Fibroblasts; Humans; Leigh | 1990 |