- General Drug Summary
- Description
- NADH is the reduced form of NAD+, and NAD+ is the oxidized form of NADH, A coenzyme composed of ribosylnicotinamide 5'-diphosphate coupled to adenosine 5'-phosphate by pyrophosphate linkage. It is found widely in nature and is involved in numerous enzymatic reactions in which it serves as an electron carrier by being alternately oxidized (NAD+) and reduced (NADH). It forms NADP with the addition of a phosphate group to the 2' position of the adenosyl nucleotide through an ester linkage.(Dorland, 27th ed)
- Also Known As
- beta-DPNH; beta-NADH; Coenzyme I, reduced; Cozymase I, reduced; dihydrodiphosphopyridine nucleotide; dihydronicotinamide adenine dinucleotide; Diphosphopyridine nucleotide; diphosphopyridine nucleotide reduced; DPN; DPN+; DPNH; NAD-reduced; NAD+; NADH+H+; NADH2; Nicotinamide adenine dinucleotide; nicotinamide adenine dinucleotide reduced; Nicotinaminde-Adenine-Dinucleotide
- Groups
- approved; nutraceutical
- Structure
- Summary In Neonatal Jaundice
-
2 record(s) for NADH NA in Neonatal Jaundice.
- PMID
- Drug Name
- Efficacy
- Evidence
- Summary
- Glucose-6-phosphate dehydrogenase (G-6-PD) is an enzyme in the first step of the hexose-monophosphate shunt required for the generation of nicotinamide adenine dinucleotide phosphate (NADPH). G-6-PD activity is low in a number of jaundiced patients.
- Glucose-6-phosphate dehydrogenase (G-6-PD) levels in jaundiced neonates in Calabar. Nigerian journal of medicine : journal of the Nati, [Go to PubMed]
- Glucose-6-phosphate dehydrogenase (G-6-PD) is an enzyme in the first step of the hexose-monophosphate shunt required for the generation of nicotinamide adenine dinucleotide phosphate (NADPH). Red blood cells of neonates with deficient G-6-PD are potentially susceptible to acute severe haemolysis and may result in haemolytic jaundice. This study was to determine the association between neonatal jaundice and G-6-PD activity and the degree of deficiency of this enzyme among the affected neonates.
G-6-PD levels in jaundiced neonates admitted into the Special Care Baby Unit (SCBU) of the University of Calabar Teaching Hospital were assayed between May 2000 and April 2001 using Biotic (London) diagnostic assay kit method. Data was analyzed using SPSS (base 705) data Editor (Microsoft Windows 95).
A total of 102 jaundiced neonates between ages 1 and 10 days were studied. Out of the 102 jaundiced neonates, 39 (38.2%) were G-6-PD deficient with G-6-PD concentration of 48.89 +/- 72 mU/10(12) erythrocyte compared to 129.51 +/- 0.92 mU/10(12) erythrocyte in the remaining 63 subjects. The prevalence rate of G-6-PD deficiency among jaundiced neonates was 38% which is significantly high (p < 0.05) considering the study sample size. There was no significant difference (p > 0.05) in G-6-PD level in the males and females.
G-6-PD activity is low in a number of jaundiced patients. Routine assay of G-6-PD in jaundiced patients is recommended.
- 16225031
- NADH
- NA
- Clinical Trial
- Summary
- Glucose-6-phosphate dehydrogenase deficiency causes Neonatal hyperbilirubinemia.The conversion of nicotinamide adenine dinucleotide phosphate to its reduced form in erythrocytes is the basis of diagnostic testing for the deficiency.
- Diagnosis and management of G6PD deficiency. American family physician, 2005 Oct 1 [Go to PubMed]
- Glucose-6-phosphate dehydrogenase deficiency, the most common enzyme deficiency worldwide, causes a spectrum of disease including neonatal hyperbilirubinemia, acute hemolysis, and chronic hemolysis. Persons with this condition also may be asymptomatic. This X-linked inherited disorder most commonly affects persons of African, Asian, Mediterranean, or Middle-Eastern descent. Approximately 400 million people are affected worldwide. Homozygotes and heterozygotes can be symptomatic, although the disease typically is more severe in persons who are homozygous for the deficiency. The conversion of nicotinamide adenine dinucleotide phosphate to its reduced form in erythrocytes is the basis of diagnostic testing for the deficiency. This usually is done by fluorescent spot test. Different gene mutations cause different levels of enzyme deficiency, with classes assigned to various degrees of deficiency and disease manifestation. Because acute hemolysis is caused by exposure to an oxidative stressor in the form of an inection, oxidative drug, or fava beans, treatment is geared toward avoidance of these and other stressors. Acute hemolysis is self-limited, but in rare instances it can be severe enough to warrant a blood transfusion. Neonatal hyperbilirubinemia may require treatment with phototherapy or exchange transfusion to prevent kernicterus. The variant that causes chronic hemolysis is uncommon because it is related to sporadic gene mutation rather than the more common inherited gene mutation.