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We are accustomed to viewing drug reacactions as representing toxic, allergic, or idiosyncratic responses to the chemical administered; yet a drug may perform its normal action in an undesired tissue site and so give notable side-effects. Triparanol (MER 29) can produce such effects. It blocks synthesis of plasma cholesterol in the liver, but in certain individuals it also causes a slowly progressive, noninflammatory degeneration of the skin provisionally attributed to depression of cutaneous cholesterol synthesis. A few years ago Parsons and Flinn¹reported that dryness of the skin and a picture of pseudoacanthosis nigricans were produced by nicotinic acid administered in large quantities to patients for hypercholesterolemia. Ruiter and Meyler²confirmed this observation. Consequently, it was logical to look for such changes in patients taking a different medication but for a similar purpose, namely, to decrease plasma cholesterol. Six months after we started administration of triparanol to patients
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R.K. Winkelmann (1963) studied this question.
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