{'fraction_non_alphanumeric': 0.01732283464566929, 'fraction_numerical': 0.0015748031496062992, 'mean_word_length': 5.517948717948718, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Pharmacokinetic and pharmacodynamic drug interactions during treatment with vigabatrin

Pharmacokinetic drug interactions take place when one drug interacts with another at the level of metabolism, absorption or excretion. Pharmacodynamic interactions take place at the level of receptor sites, where they may have additive or potentiating effects. Vigabatrin is relatively free of pharmacokinetic interactions, and though it is associated with about a 20% decrease in serum levels of concomitantly administered phenytoin, the reduction is of little clinical significance. The mechanism underlying this effect is unknown. Because vigabatrin increases GABA‐mediated inhibition in the brain (an action that is believed to account for its anticonvulsant effects), it might be expected to potentiate the CNS effects of benzodiazepines and alcohol. However, very sensitive eye movement studies have failed to detect any evidence of such an interaction. Overall, vigabatrin appears to be remarkably free of drug interactions. As a result, it is easier to use in clinical practice than older anti‐epilepsy agents. Perhaps the most important finding of the interaction studies with vigabatrin is that there is no need for patients receiving the drug to be told to avoid alcohol.