{'fraction_non_alphanumeric': 0.04316546762589928, 'fraction_numerical': 0.039568345323741004, 'mean_word_length': 4.734020618556701, 'pattern_counts': {'":': 0, '<': 5, '<?xml version=': 0, '>': 1, '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}}
Lack of interaction between ranitidine and phenytoin.

Cimetidine inhibits the hepatic microsomal oxidation system and reduces the clearance of a number of drugs metabolized by these enzymes (Somogyi & Gugler, 1982). Adverse effects resulting from the interaction of cimetidine with warfarin (Hetzel et al., 1979; Serlin et al., 1979) and phenytoin (Hetzel et al., 1981) have been reported. Ranitidine, a newer histamine H2-receptor antagonist, has a different chemical structure from cimetidine; the imidazole ring of cimetidine has been replaced by a furan ring and the side chain has been modified. Ranitidine does not impair the metabolism of antipyrine (Henry et al., 1980), warfarin (Serlin et al., 1981) or propranolol (Heagarty et al., 1982). We therefore compared the effect of ranitidine and cimetidine on steady state plasma phenytoin levels in epileptic patients. Plasma phenytoin concentrations were measured in four well motivated chronic epileptic outpatients by EMIT (Syva, Palo Alto, California) twice a week at 15.00 h over a period of 7 weeks. Each patient gave informed consent to the study which was approved by the Research Review Committee of the Royal Adelaide Hospital. Week 1 established the steady state values. In weeks 2 and 3, the patients were given ranitidine 150 mg twice daily. During week 4 no ranitidine or cimetidine was taken and during weeks 5 and 6, patients were given cimetidine 200 mg thrice daily with meals and 400 mg at night. Concentrations were then measured in week 7 after cimetidine had been ceased. All patients were non-smokers, and two were receiving multiple anticonvulsants (Table 1). Renal function as judged by serum creatinine was normal in all patients. The y-glutamyl transferase was slightly elevated in all patients and thought to be consistent with long term anticonvulsant treatment. Table 1 shows the effect of ranitidine and cimetidine on the mean plasma phenytoin concentrations in each of the treatment periods. Analysis of variance showed that there was significant variation in mean plasma phenytoin concentrations between different weeks of the study (F6,23 = 28.4, P < 0.001) and between patients (F323 = 63.5, P < 0.001). Ranitidine produced no significant increase in plasma phenytoin concentrations, when compared with the pretreatment values (week 2 mean-week 1 mean, t23 = 1.2, P > 0.2). In contrast, plasma phenytoin concentrations during cimetidine administration were significantly higher than during the pretreatment period (week 5 mean-week 1 mean, t23 = 4.6, P < 0.001), the ranitidine treatment period (week 5 mean-week 2 mean, t23 = 3.4, P < 0.01) and the 'washout' 4th week (week 5 mean-week 4 mean, t23 = 5.9, P < 0.001). During the second week of cimetidine treatment plasma phenytoin conC._