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By H. Jick (auth.), E. Grundmann (eds.)

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The development of de- 46 pendence and the appearance of withdrawal symptoms can be explained often on the basis of modified post-synaptic sensitivity not adequately compensated by pre-synaptic sensitivity. The recent discovery of enkephalin receptors on catecholaminergic nerve endings in the CNS may greatly contribute to an improved understanding of the mechanisms involved in the manifestations of the narcotic abstinence syndrome. Schwartz and associates (1978) have proposed that tolerance and dependence to opi ate drugs develop as a consequence of post-synaptic super sensitivity secondary to presynaptic inhibition of transmitter (including catecholamines) release in different area of the brain.

Disturbances of sex hormone metabolism High incidence of impotence, loss of libido and reduced fertility in drug-treated epileptic patients. Enhanced biodegradation cholecalciferol to inactive metabolites. of androgen steroids. metabolism. Induction of the biotransformation of these compounds is probably responsible for certain aspects of the chronic toxicity of antiepileptic drugs (Table 5) (Perucca 1978). In some cases enzyme-induction results in enhancement of the pharmacological effect, due to increased rate of formation of active metabolites.

Patients sensitive to the taste of quinine developed extrapyramidal signs at an average cumulative dose of prochlorperazine significantly lower than that required to produce the same effects in non-sensitive tasters (97 versus 225 mg respectively). Although no attempt was made to ascertain possible differences in drug disposition between the two groups, these and other fmdings by the same authors (Fischer et al. 1965) were interpreted as indicative of a relationship between drug responses at different sites of action.

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