PharmGKB summary

Thorn, Caroline F.; Aklillu, Eleni; McDonagh, Ellen M.; Klein, Teri E.; Altman, Russ B.

doi:10.1097/fpc.0b013e3283505d5e

Cited by 92 publications

(35 citation statements)

References 40 publications

(62 reference statements)

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“…As coffee intake in teenager individuals was reported to be lower than in adults ( 42 ), elevated theobromine concentrations in young patients may be attributed to consumption of other products than coffee, including chocolate foods and beverages, which provide low caffeine but constitute the major source of dietary theobromine ( 51 ). Moreover, theobromine accounts for only 7–8% of caffeine metabolism ( 52 , 53 ) and in the present study, the calculated theobromine/caffeine ratio was close to 1, further supporting that the present plasma levels of theobromine result from other sources than from caffeine metabolism exclusively.…”

Section: Discussionsupporting

confidence: 85%

Association Between Plasma Caffeine and Other Methylxanthines and Metabolic Parameters in a Psychiatric Population Treated With Psychotropic Drugs Inducing Metabolic Disturbances

et al. 2018

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Importance: Multiple studies conducted in the general population identified an association between self-reported coffee consumption and plasma lipid levels. To date, no study assessed whether and which plasma methylxanthines (caffeine and/or its metabolites, i.e., paraxanthine, theophylline, and theobromine) are associated with plasma lipids. In psychiatric patients, an important coffee consumption is often reported and many psychotropic drugs can induce a rapid and substantial increase of plasma lipid levels.Objective: To determine whether plasma methylxanthines are associated with metabolic parameters in psychiatric patients receiving treatments known to induce metabolic disturbances.Design, Setting, and Participants: Data were obtained from a prospective study including 630 patients with metabolic parameters [i.e., body mass index (BMI), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), non-high-density lipoprotein cholesterol (non-HDL-C), and fasting triglycerides (TG)] monitored routinely during psychotropic treatment.Exposures: Plasma methylxanthines levels.Main Outcomes and Measures: Metabolic variables including BMI and plasma lipid levels.Results: Multivariate analyses indicated that BMI, TC, HDL-C, and non-HDL-C increased significantly with increasing total methylxanthines (pcorrected ≤ 0.05). In addition, compared to patients with plasma caffeine concentration in the lowest quartile, those with caffeine concentration in the highest quartile were twice more prone to suffer from non-HDL hypercholesterolemia (pcorrected = 0.05), five times more likely to suffer from hypertriglyceridemia (pcorrected = 0.01) and four times more susceptible to be overweight (pcorrected = 0.01).Conclusions and Relevance: This study showed that plasma caffeine and other methylxanthines are associated with worsening of metabolic parameters in patients receiving psychotropic treatments known to induce metabolic disturbances. It emphasizes that important caffeine consumption could be considered as an additional environmental risk factor for metabolic worsening in patients receiving such treatments.

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Section: Discussionsupporting

confidence: 85%

Association Between Plasma Caffeine and Other Methylxanthines and Metabolic Parameters in a Psychiatric Population Treated With Psychotropic Drugs Inducing Metabolic Disturbances

et al. 2018

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“…Biotransformation of caffeine by the microsomal cytochrome P450 mono-oxygenases and partially by xanthine oxidases is essentially a conversion to N-3 (paraxanthine), N-7 (theophylline) and N-1 (theobromine) demethylation. 11 The main route of metabolism in adults is through N-3 demethylation to paraxanthine (70-80%); 11 the predominant process in preterm infant is N-7 demethylation which matures at about four months of age. 12 The demethylation process in infants is postnatal age-dependent regardless of gestational age or birth weight.…”

Section: Pharmacology Of Caffeine In Premature Neonatesmentioning

confidence: 99%

Caffeine, Bronchopulmonary Dysplasia and Neurodevelopmental Outcomes in Premature Infants

Kumar¹

2018

Pediatr Neonatal Nurs Open J

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Caffeine, a stimulant is the most widely used drug in the world in adults with increasing usage in children. It is commonly used in the treatment of apnea of prematurity in premature infants. Caffeine in a randomized trial has been shown to reduce the incidence of bronchopulmonary dysplasia in infants <1250 grams birth weight when used to treat apnea of prematurity in these infants. In the same cohort of infants, caffeine improved neurodevelopmental outcomes and survival at 18 months of age and was found to be safe without any adverse events up to 11 years of age. Caffeine is an adenosine receptor antagonist and inhibits adenosine receptors at physiologic concentrations with important effects on behavior and cognitive functions. However, higher doses of caffeine may inhibit the enzyme phosphodiesterase and affect vascular smooth muscle function. Anti-oxidant, anti-inflammatory and antiapoptotic properties of caffeine and its ability to scavenge reactive oxygen species may contribute to its lung and neuroprotective effects in premature infants. Animal studies on whether caffeine is protective to the lung are not conclusive at this time. Similarly, caffeine is demonstrated to have adverse effects on brain development in animal studies. Despite the beneficial effects of caffeine in premature infants when administered in the neonatal period, the long-term effects on adult-oriented disease such as cardio-metabolic disease and neurobehavioral states in children and adults needs further study.

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“…Paraxanthine, a metabolite of caffeine, can undergo acetylation by NAT2 to form 5-acetylamino-6-formylamino-3-methyluracil (AFMU) (see PharmGKB Caffeine Pathway, Pharmacokinetics http://www.pharmgkb.org/pathway/PA165884757) [150]. Caffeine can be used as a non-toxic probe drug in vivo for predicting acetylator phenotype; by measuring metabolite ratio AFMU/1-methyl xanthine (1X) in urine after caffeine consumption, a bi- or tri-modal pattern in a given population is observed [39, 115, 151].…”

Section: Pharmacogeneticsmentioning

confidence: 99%