Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: KEGG:D01453 (caffeine)
21,611 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Caffeine, which has a wide range between therapeutic and toxic levels, is a widely used medication for prevention and treatment of apnoea of prematurity. Despite its safety, caffeine overdose and intoxication has been previously reported in the literature. We present a 30-day-old 28-week preterm newborn who was exposed to 300 mg.kg-1 caffeine base by mouth accidentally. The patient exhibited agitations, irritability, tachycardia, tachypnoea, diuresis, electrolyte abnormalities, hyperglycaemia and metabolic acidosis, for which he received supportive treatment. No seizure activity was observed. The effects of intoxication lasted for 96 h and then completely resolved.
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PMID:Caffeine intoxication in a premature neonate. 1169 54

Apnea of prematurity is a common problem of the premature infant under 30 weeks gestation. Theophylline and caffeine, two methylxanthines, are widely used to treat this condition. The drugs are equally effective in preventing apnea in the premature infant. Caffeine citrate has many advantages over theophylline, however, including once-a-day dosing, more predictable plasma concentrations, earlier onset of action, and minimal side effects. Caffeine is therefore the initial drug of choice for apnea of prematurity.
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PMID:Theophylline or caffeine: which is best for apnea of prematurity? 1194 72

In the last decade, knowledge regarding the neurodevelopment and functional aspects of the respiratory centers during postnatal maturation has increased substantially. However, an increase in such knowledge has not provided a basis for change in practice. The diagnosis of apnea of prematurity (AOP) is one of exclusion. All causes of secondary apnea must be ruled out before initiating treatment for AOP. Treatment will depend on the etiology as well as effectiveness and tolerability of the treatment by the patient. The primary goal of any treatment of AOP is to prevent the frequency of apnea lasting >20 seconds, and/or those that are shorter, but associated with cyanosis and bradycardia. The clinical management of AOP is not much different today than it was two decades ago, with pharmacologic and nonpharmacologic treatment options remaining the mainstay of therapy. Methylxanthines are still the most widely used pharmacologic agents. Due to the wider therapeutic index of caffeine and ease of once daily administration, it should be the preferred agent. Doxapram, or nonpharmacologic treatment measures such as nasal continuous positive airway pressure, may be considered in infants who are unresponsive to methylxanthine treatment alone. Treatment should be continued until there is complete resolution of apnea, and for some time thereafter. The choice of method for weaning treatment remains one of individual physician preference. Discharge from hospital after apnea requires close monitoring and some infants will require home apnea monitors. The decision to provide a home apnea monitor should be individualized for each patient, depending on the effectiveness of treatment and clinical response.
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PMID:Treatment of apnea of prematurity. 1260 84

OBJECTIVE: To review medical literature related to apnea of prematurity. SOURCES: Extensive literature search and clinical practice-oriented concepts. SUMMARY OF THE FINDINGS: Apnea is one of the most common respiratory disorders in the neonatal period. Immaturity of the central nervous system is associated with instability of respiration. Therefore, apnea manifests itself in other systems, causing problems such as hypoglycemia, hypothermia, infection, or patent ductus arteriosus. Apnea may be central, obstructive or mixed depending on the presence of air flow through the upper airways. Diagnosis should involve careful observation by unit personnel and the monitoring of heart rate, respiratory frequency or arterial oxygen saturation. Initially, the treatment consists of xanthines (caffeine and aminophylline). If respiratory failure occurs, then continuous positive airway pressure (CPAP), and mechanical ventilation should be used. CONCLUSIONS: Preterm newborns are susceptible to respiratory problems, having apnea as a clinical manifestation of disorders in many organs and systems.
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PMID:[Neonatal apnea] 1467 97

The methylxanthines aminophylline, theophylline and caffeine have been used for more than 30 years to treat apnoea of prematurity. Today, they are among the most commonly prescribed drugs in neonatal medicine. Methylxanthines reduce the frequency of idiopathic apnoea and the need for mechanical ventilation by acting as non-specific inhibitors of adenosine A(1) and A(2a) receptors. However, recent and rapidly growing research into the actions of adenosine and its receptors raises concerns about the safety of methylxanthine therapy in very preterm infants. Possible adverse effects include impaired growth, lack of neuroprotection during acute hypoxic-ischaemic episodes and abnormal behaviour. An international controlled clinical trial is underway to examine the long-term efficacy and safety of methylxanthine therapy in very low birth weight babies.
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PMID:Controversies surrounding xanthine therapy. 1505 Feb 17

Methylxanthine therapy reduces the frequency of apnea and the need for mechanical ventilation. Recent research has raised concerns about the safety of methylxanthines in very preterm infants. Possible adverse effects include poor growth, worsening of hypoxic-ischemic brain damage and abnormal childhood behavior. Over 2,000 infants with birth weights 500-1,250 g have been randomized in the international placebo-controlled Caffeine for Apnea of Prematurity (CAP) trial to examine the long-term efficacy and safety of methylxanthine therapy for the management of apnea of prematurity. Additional therapies such as continuous positive airway pressure were used as necessary to control apneic attacks. At 18 months we measure the combined rate of death or survival with one or more of the following impairments: cerebral palsy, cognitive deficit, blindness and deafness. This outcome was chosen because of the need to evaluate the impact of common neonatal therapies beyond discharge from the intensive care unit. However, several potential long-term consequences of methylxanthine therapy may not become apparent until the study cohort reaches pre-school age. We will therefore extend the follow-up to age 5 years. The main outcome at 5 years will be a composite of death or survival with severe disability in at least one of six domains: cognition, neuromotor function, vision, hearing, behavior, and general health. Once this project is completed, caffeine will be one of the most rigorously evaluated neonatal therapies.
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PMID:Methylxanthine therapy for apnea of prematurity: evaluation of treatment benefits and risks at age 5 years in the international Caffeine for Apnea of Prematurity (CAP) trial. 1621 Aug 43

Caffeine (1,3,7-trimethylxanthine) is an alkali that easily crosses the placental barrier and can interfere in the growth and development of fetal cells and compromise fetal oxygenation. Considering the widespread consumption of foods containing caffeine in Brazil, the aim of this study was to evaluate the association between total caffeine consumption (including its food sources) and prematurity. A case-control study of 140 cases (newborns with gestational age less than 37 weeks) and 162 controls (newborns with 37 weeks gestational age or greater) evaluated caffeine consumption during pregnancy. Intake measurement used a semi-quantitative food frequency questionnaire based on the following foods: coffee, tea, and powdered chocolate. Total caffeine consumption (including food sources) during pregnancy was not associated with prematurity, and most intakes were less than 300 mg/ day. Caffeine consumption in the present study does not support guidelines against caffeine consumption by Brazilian pregnant women.
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PMID:[Caffeine intake and food sources of caffeine and prematurity: a case-control study]. 1641 Aug 79

Apnea of prematurity (AOP) is found in >50% of premature infants and is almost universal in infants who are <1000 g at birth. The literature clearly defines clinically significant apnea in infants (breathing pauses that last for >20 seconds or for >10 seconds if associated with bradycardia or oxygen desaturation), but there is no consensus about the duration of apnea, the degree of change in oxygen saturation, or severity of bradycardia that should be considered pathologic. Although caregivers are able to respond successfully to apnea events with drugs (as well as physical and mechanical interventions) in the NICU, it remains unproven whether such interventions have any long-term effects. One of the most effective drugs, caffeine citrate, is currently labeled for short-term use only and within a limited gestational-age population. Clinicians often use off-label drugs that have been approved for gastroesophageal reflux disease, which is common in premature infants, with the belief that such treatments also have an impact on AOP, although this link has never been demonstrated. Key treatment issues include (1) lack of standardization for definition, diagnosis, and treatment of AOP, (2) unproven benefit of intervention, (3) lack of real-time data documenting AOP events, (4) unevaluated sustained treatment improvement at 7 days or later, (5) failure to address confounding conditions, (6) unsubstantiated AOP-gastroesophageal reflux disease relationship, and (7) undetermined role of AOP affecting long-term neurodevelopmental outcomes. In addressing study-design issues, the pulmonary group identified (1) key questions about neonatal apnea, (2) methodologic requirements for study, (3) appropriate outcome measures, and (4) ethical considerations for future studies. This article describes a sample framework for the study of apnea in neonates and identifies future research needs. Plenary-session discussion points are also listed.
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PMID:Summary proceedings from the apnea-of-prematurity group. 1677 22

Caffeine, an unspecific antagonist of adenosine receptors, is commonly used to treat the apnea of prematurity. We have defined the effects of caffeine on the carotid body (CB) chemoreceptors, the main peripheral controllers of breathing, and identified the adenosine receptors involved. Caffeine inhibited basal (IC50, 210 microm) and low intensity (PO2 approximately 66 mm Hg/30 mm K+) stimulation-induced release of catecholamines from chemoreceptor cells in intact preparations of rat CB in vitro. Opposite to caffeine, 5'-(N-ethylcarboxamido)adenosine (NECA; an A2 agonist) augmented basal and low-intensity hypoxia-induced release. 2-p-(2-Carboxyethyl)phenethyl-amino-5'-N-ethylcaboxamido-adenosine hydrochloride (CGS21680), 2-hexynyl-NECA (HE-NECA) and SCH58621 (A2A receptors agents) neither affected catecholamine release nor altered the caffeine effects. The 8-cycle-1,3-dipropylxanthine (DPCPX; an A1/A2B antagonist) and 8-(4-{[(4-cyanophenyl)carbamoylmethyl]-oxy}phenyl)-1,3-di(n-propyl)xanthine (MRS1754; an A2B antagonist) mimicking of caffeine indicated that caffeine effects are mediated by A2B receptors. Immunocytochemical A2B receptors were located in tyrosine hydroxylase positive chemoreceptor cells. Caffeine reduced by 52% the chemosensory discharges elicited by hypoxia in the carotid sinus nerve. Inhibition had two components with pharmacological analysis indicating that A2A and A2B receptors mediate, respectively, the low (17 x 10(-9) m) and high (160 x 10(-6) m) IC50 effects. It is concluded that endogenous adenosine, via presynaptic A2B and postsynaptic A2A receptors, can exert excitatory effects on the overall output of the rat CB chemoreceptors.
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PMID:Caffeine inhibition of rat carotid body chemoreceptors is mediated by A2A and A2B adenosine receptors. 1680 51

Caffeine is commonly used to treat respiratory instabilities related to prematurity. However, the role of adenosinergic modulation and the potential long-term effects of neonatal caffeine treatment (NCT) on respiratory control are poorly understood. To address these shortcomings, we tested the following hypotheses: 1) adenosine A(1)- and A(2A)-receptor antagonists modulate respiratory activity at rest and during hypercapnia; 2) NCT has long-term consequences on adenosinergic modulation of respiratory control. Rat pups received by gavage either caffeine (15 mg/kg) or water (control) once a day from postnatal days 3 to 12. At day 20, rats received intraperitoneal injection with vehicle, DPCPX (A(1) antagonist, 4 mg/kg), or ZM-241385 (A(2A) antagonist, 1 mg/kg) before plethysmographic measurements of resting ventilation, hypercapnic ventilatory response (5% CO(2)), and occurrence of apneas in freely behaving rats. In controls, data show that A(2A), but not A(1), antagonist decreased resting ventilation by 31% (P = 0.003). A(1) antagonist increased the hypercapnic response by 60% (P < 0.001), whereas A(2A) antagonist increased the hypercapnic response by 42% (P = 0.033). In NCT rats, A(1) antagonist increased resting ventilation by 27% (P = 0.02), but the increase of the hypercapnic response was blunted compared with controls. A(1) antagonist enhanced the occurrence of spontaneous apneas in NCT rats only (P = 0.005). Finally, A(2A) antagonist injected in NCT rats had no effect on ventilation. These data show that hypercapnia activates adenosinergic pathways, which attenuate responsiveness (and/or sensitivity) to CO(2) via A(1) receptors. NCT elicits developmental plasticity of adenosinergic modulation, since neonatal caffeine persistently decreases ventilatory sensitivity to adenosine blockers.
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PMID:Disruption of adenosinergic modulation of ventilation at rest and during hypercapnia by neonatal caffeine in young rats: role of adenosine A(1) and A(2A) receptors. 1713 26


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