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hydrogen carbonate and Encephalomyelitis, Subacute Necrotizing

hydrogen carbonate has been researched along with Encephalomyelitis, Subacute Necrotizing 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.

Research Excerpts

ExcerptRelevanceReference
" The partial correction of lactic acidosis with oral sodium bicarbonate chronic therapy may result in a slow evolution of the clinical symptoms."3.68Congenital 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)
"We suggest that respiratory alkalosis (hypocapnia) of Leigh syndrome patients with SURF1 mutations results from compulsory hyperventilation and speculate that hypocapnia may contribute to Leigh-like brain damage in the SURF1-deficient patients as well as in other patients presenting with Leigh-like syndrome."1.31Compulsory hyperventilation and hypocapnia of patients with Leigh syndrome associated with SURF1 gene mutations as a cause of low serum bicarbonates. ( Karczmarewicz, E; Piekutowska-Abramczuk, DH; Popowska, E; Pronicka, E; Pronicki, M; Sykut-Cegielskâ, Y; Taybert, J, 2001)

Research

Studies (2)

TimeframeStudies, this research(%)All Research%
pre-19900 (0.00)18.7374
1990's1 (50.00)18.2507
2000's1 (50.00)29.6817
2010's0 (0.00)24.3611
2020's0 (0.00)2.80

Authors

AuthorsStudies
Pronicka, E1
Piekutowska-Abramczuk, DH1
Popowska, E1
Pronicki, M1
Karczmarewicz, E1
Sykut-Cegielskâ, Y1
Taybert, J1
Federico, A1
Dotti, MT1
Fabrizi, GM1
Palmeri, S1
Massimo, L1
Robinson, BH1
Malandrini, A1
Guazzi, GC1

Clinical Trials (1)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
Phase 3 Trial of Coenzyme Q10 in Mitochondrial Disease[NCT00432744]Phase 324 participants (Actual)Interventional2007-01-31Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

McMaster Gross Motor Function (GMFM 88)

The McMaster Gross Motor Function is a validated scale ranging from 0 to 100 (the higher the better). Since there was the possibility of a subject becoming totally disabled our FDA peer reviewed design called for its use as follows: If the subject completed both periods, the score was calculated as the difference in scores between the end of Period 2 (at 12 months) minus that at the end of Period 1 (6 months). If a subject became totally disabled, this difference was considered as plus infinity if it occurred in period 1 (Penalizes period 1), and minus infinity if it occurred in Period 2 (Penalizes period 2). The two treatments were compared via the Wilcoxon test, and the effect size was estimated using Kendall's Tau-B. This is interpreted in a similar manner to correlation with positive values favoring COQenzyme10 and negative values favoring placebo. One of the links in this report is to the the GMFM scale and how it is scored. A link to the instrument is included. (NCT00432744)
Timeframe: Taken at 6 and 12 Months

Interventionunits on a scale (Median)
Placebo First-0.002
CoenzymeQ10 Frist-0.12

Non-parametric Hotelling T-square Bivariate Analysis of GMGF 88 and OPeds QOL.

This is a multivariate analysis of the first two outcomes: Period 2 minus Period 1 GMFM88 and Peds Quality of Life, analyzed as follows: First, to be in the analysis, subjects must contribute at least one of these endpoints. Second, if the subject became totally disabled during period 1, the difference was defined as + infinity, (highest possible evidence favoring period 2), and if the subject became totally disabled in period 2, the subject was scored as - infinity (highest possible evidence favoring period 1). Period 2 minus period 1 differences were ranked form low to high with missing values scores at the mid-rank. The Hotelling T-square was computed on these ranks and the P-value was obtained from 100,000 rerandomizations as the fraction of rerandomizations with T-sq at least as large as that observed. (NCT00432744)
Timeframe: end of 12 month minus end of 6 month difference.

Interventionparticipants (Number)
Placebo First7
CoenzymeQ10 Frist8

Pediatric Quality of Life Scale

"The Pediatric Quality of Life Scale is a validated scale ranging from 0 to 100 (the higher the better). Since there was the possibility of a subject becoming totally disabled our FDA peer reviewed design called for its use as follows: If the subject completed both periods, the score was calculated as the difference in scores between the end of Period 2 (at 12 months) minus that at the end of Period 1 (6 months). If a subject became totally disabled, this difference was considered as plus infinity if it occurred in period 1 (Penalizes period 1), and minus infinity if it occurred in Period 2 (Penalizes period 2). The two treatments were compared via the Wilcoxon test, and the effect size was estimated using Kendall's Tau-B. This is interpreted in a similar manner to correlation with positive values favoring COQenzyme10 and negative values favoring placebo. Goggle pedsQL and Mapi to browse the copyrighted manual. A link to the instrument is included." (NCT00432744)
Timeframe: At 6 and 12 Months

Interventionunits on a scale (Median)
Placebo First-1.1
CoenzymeQ10 Frist-11.9

Other Studies

2 other studies available for hydrogen carbonate and Encephalomyelitis, Subacute Necrotizing

ArticleYear
Compulsory hyperventilation and hypocapnia of patients with Leigh syndrome associated with SURF1 gene mutations as a cause of low serum bicarbonates.
    Journal of inherited metabolic disease, 2001, Volume: 24, Issue:7

    Topics: Alkalosis, Respiratory; Bicarbonates; Carbon Dioxide; Child; Child, Preschool; Female; Humans; Hydro

2001
Congenital lactic acidosis due to a defect of pyruvate dehydrogenase complex (E1). Clinical, biochemical, nerve biopsy study and effect of therapy.
    European neurology, 1990, Volume: 30, Issue:3

    Topics: Acidosis, Lactic; Bicarbonates; Biopsy; Brain Diseases, Metabolic; Child; Fibroblasts; Humans; Leigh

1990