Cardiovascular Guarana is produced from the guarana plant (Paullina cupana), the seeds of which contain 3.6-5.8% caffeine.
• A 25-year-old woman, who had pre-existing mitral valve prolapse and a history of having had bouts of palpitation with caffeine, developed intractable ventricular fibrillation after consuming a "natural energy" guarana health drink containing a high concentration of caffeine (1A ). At autopsy, she was found to have sclerosis and myxoid changes in the mitral valve leaflets. The caffeine concentration in her aortic blood was 19 mg/l.
This case highlights the need for more careful regulation of "natural" products, including warning for patients with underlying health problems, and clear labeling to document the presence of any constituents with potentially toxic effects. It also shows the need for medical practitioners to be familiar with the more widely used "natural remedies" and their tox-icological profiles. Following the death of this patient, the Western Australian Coroner recommended that Race 2005 Energy Blast should be removed from the local market, and the product was recalled nationally in August 1999.
Nervous system Red Bull, a widely consumed "power drink", a mixture of caffeine, taurine, and inositol, affects mental performance and mood.
© 2003 Elsevier Science B.V. All rights reserved. Side Effects of Drugs, Annual 26 J.K. Aronson, ed.
• A 36-year-old man with bipolar I disorder had a second manic episode, after having been in remission for 5 years while taking lithium to maintain a serum lithium concentration of 0.8-1.1 mmol/l (2A ). One week before this episode he drank three cans of Red Bull at night and needed less sleep. Three days later he drank three more cans. After 4 days he was feeling euphoric, hyperactive, and insomniac. He gradually became more hyperactive and had increased libido and irritability. He took no more Red Bull and improved within 7 days.
Based on this report the authors suggested that stimulant beverages containing caffeine might cause cognitive and behavioral changes, especially in vulnerable patients with bipolar illness.
Musculoskeletal Caffeine toxicity is an uncommon cause of myopathy, but a history of excessive dietary and pharmaceutical consumption of caffeine should be sought in any patient with unexplained myopathy, particularly if there is concomitant hypokalemia (3A).
• A 21-year-old woman with a 12-month history of progressive muscle weakness, nausea, vomiting, diarrhea, and weight loss had significant worsening of muscle weakness over 2 weeks, associated with exercise-induced muscle stiffness and pain. She had severe hypokalemia and a metabolic aci-dosis. For the past 1-2 years she had been consuming about 8 liters of cola every day. She stopped drinking the cola and took potassium supplements, after which her hypokalemia and muscle weakness resolved and the serum creatine kinase activity fell. Based on the concentration of caffeine in the cola, it was estimated that she had been consuming at least 1 g/day of caffeine for more than 12 months.
Hypokalemia and myopathy are known effects of caffeine toxicity, and severe hy-pokalemia and fatigue and hypokalemia with myopathy have been described before (4R).
Consumption of methylxanthine-containing products can aggravate the neurological symptoms associated with the glucose transporter type 1 (Glut 1) deficiency syndrome. The human erythrocyte and brain glucose transporters are identical, and the erythrocyte transporter has been used in four patients with individual mutations in the Glut 1 gene to demonstrate that caffeine and theophylline inhibit glucose transport (5E). The Glut 1 deficiency syndrome represents impaired glucose transport across the blood-brain barrier caused by partial Glut 1 deficiency, which results in hypoglycorrhachia, seizures, and developmental delay. Identifying potential inhibitors of Glut 1 is essential in preventing further impairment of glucose transport in these patients. In addition to phospho-diesterase inhibition and adenosine A1 receptor antagonism by methylxanthines, it is likely that inhibition of glucose transport also contributes to the convulsive effects of methylxanthines in high doses.
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