In vitro effect of sodium phenobarbital and diethylnicotinamide (coramine) on the protein binding of bilirubin

Khanna, Narinder N.; Harpur, Eleanor R.; Stern, Leo

doi:10.1016/s0009-9120(68)80091-8

Cited by 11 publications

(3 citation statements)

References 9 publications

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“…The pharmacological properties of phenobarbital and nicethamide, the two substances chosen for induction, have been known for a long time. Antagonistic action of phenobarbital against nicethamide and vice versa was offset on a recipropal basis in the intended way by the dosage used for Group V. There is no evidence that either nicethamide (4, 5 , 17) or phenobarbital (4, 17) will free bilirubin linked to albumin. Prophylactic routine use of the enzyme inductor combination phenobarbital/nicethamide in the manner used in Group V, is therefore recommended as a preferred method to prevent the development of hyperbilirubinemia in premature infants.…”

Section: Discussionmentioning

confidence: 97%

An Enzyme Inductor Combination for the Prevention of Hyperbilirubinemia in Premature Infants

et al. 1974

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GDR). Enzyme inductor combination to prevent hyperbilirubinaemia in premature in-. fants. Acta Paediatr Scand, 63: 393, 1974.-In the management of physiologic hyperbilirubinemia in newborn infants, phenobarbital and nicethamide (diethylnicotinamide), as an enzyme inductor combination, are found to have a cumulative effect and, consequently, are clearly superior to the use of phenobarbital alone. Four different dosages were compared and the most favourable variant proved to be phenobarbital, 10 mg/kg body weight pro die from day 1 to day 3 (after birth), combined with nicethamide, 100 mg/kg per diem from day 1 to day 4. Exchange transfusion was no longer necessary in 400 premature infants who had received this type of prophylactic combination and thus the routine use of this inductor regimen can now be recommended.

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Section: Discussionmentioning

confidence: 97%

An Enzyme Inductor Combination for the Prevention of Hyperbilirubinemia in Premature Infants

et al. 1974

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“…Caffeine complexation was shown to reduce the rate of transport in vitro of salicylic acid, ethyl p-hydroxybenzoate, dehydroacetic acid, and aspirin (Bates et al 1970). Caffeine sodium benzoate also decreased in vitro the percent of bilirubin that was protein-bound (Khanna et al 1969). Caffeine was ineffective against the depressant actions of alcohol on motor coordination, but decreased simple auditory and visual reaction times which could in itself lead to a false sense of fitness (Franks et al 1975).…”

Section: Pharmacological Actionsmentioning

confidence: 94%

The Pharmacology and Toxicology of Caffeine

Lachance

1982

Journal of Food Safety

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The widespread use of caffeine is most commonly linked to the stimulatory action it has on the central nervous system. Generally, adverse effects include gastrorrhea, insomnia, and diuresis. Tolerance and withdrawal symptoms have been observed and excessive consumption can lead to an anxiety neurosis condition (caffeinism). The actions of caffeine may involve its effects on neurotransmitter turnover and metabolism; its promotion of the cellular messenger, cAMP; its sensitization of the calcium releasing mechanisms of cellular reticulum; or its antagonism of the autacoid, adenosine. Caffeine lethality is rare in man but caffeine poisoning with its gastrointestinal, CNS, and cardiovascular stimulation could especially be hazardous to children. Most of the mutagenicity work has been performed in organisms whose cellular DNA synthesis and repair mechanism vary significantly from those found in man. The work in human cell lines suggests that caffeine‐induced chromosomal breakage, with its lack of chromatid exchange would promote cell lethality, not muta‐genticity. Nothing but circumstantial evidence implicates caffeine as a human carcinogen or teratogen. Involvement of caffeine as a cocarcinogen or a coteratogen (which includes effects on gamete production or fetal development) appears far more likely, but neither has even begun to be truly evaluated. Basic metabolism of caffeine involves the processes of N‐demethylation, hydration, and oxidation; and most likely requires the cytochrome P1‐450 system. Though various metabolites of caffeine are pharmacologically active, the extent of involvement of individual metabolites in the pharmacological or toxicological responses of caffeine in man is still unknown.

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“…It may be that measurement of the 'free' bilirubin level will eventually prove a better index of the likelihood of brain damage in infants with hyperbilirubinaemia (Odell, Storey, and Rosenberg, 1970). It is already known that phenobarbitone does not act to lower serum bilirubin levels by displacing indirect bilirubin from its binding sites in the blood (Khanna, Harpur, and Stern, 1969).…”

mentioning

confidence: 99%

Sequential Trial of Effect of Phenobarbitone on Serum Bilirubin of Preterm Infants

Carswell¹,

Kerr²,

Dunsmore³

1972

Archives of Disease in Childhood

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In vitro effect of sodium phenobarbital and diethylnicotinamide (coramine) on the protein binding of bilirubin

Cited by 11 publications

References 9 publications

An Enzyme Inductor Combination for the Prevention of Hyperbilirubinemia in Premature Infants

An Enzyme Inductor Combination for the Prevention of Hyperbilirubinemia in Premature Infants

The Pharmacology and Toxicology of Caffeine

Sequential Trial of Effect of Phenobarbitone on Serum Bilirubin of Preterm Infants

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