By Silvio Garattini
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Metabolism of Dilantin proceeds by parahydroxylation of one of the phenyl groups to yield 5-phenyl-5'-parahydroxyphenylhydantoin,HPPH, which is conjugated with glucuronic acid and then eliminated in urine (Butler, 1957; Woodbury and Esplin, 1959; Maynert, 1960). Kutt et al. 4 nig/kg. Their investigations established high blood levels of unchanged Dilantin and low urine levels of HPPH. Astudy of the family of W. J. (Fig. 10)showed 2 30 ELLIOT 9. VESELL affectedand 3 unaffected individuals. These results suggest that low activity of Dilantin hydroxylase exhibits dominant transmission.
VI. Genetic Conditions, Probably Transmitted as Single Factors, Altering the W a y Drugs Act on the Body A. WARFARIN RESISTANCE O’Reilly et al. (1964) reported resistance to warfarin in a man who a t age 7 1 received anticoagulants for a myocardial infarction. Other than for a reproducible reduction in his one-stage prothrombin concentration to approximately 60% of normal, the patient exhibited no abnormalities by physical or laboratory examination. Because of the patient’s low prothrombin time, anticoagulants were initially withheld, but 1 month later were administered.
Decreased toxicity in rapid as opposed to slow acetylators of a polymorphically acetylated drug may explain why toxic effects of the hydrazine drug phtivazid occurred infrequently in those patients who excreted the acetylated form in high concentrations (Smirnov and Kozulitzina, 1962). , 1967). 23 RECENT PROGRESS IN PHARMACOGENETICS TABLE I V ISONIAZID INACTIVATION IN DIFFERENT POPULATIONS‘ ~ Percent slow inactivators Gene frequency No. 87 Population Asiatic origin Eskimosb Japanese‘ Japanesed Ainud Koreand Ryukyuand Chinese’ Thaisd American Indians’ Hindu Indians# Hindu Indians* (I From Motulsky (1964).
Advances in Pharmacology and Chemotherapy Volume 7 by Silvio Garattini