PITUITARY RESPONSIVENESS TO GONADOTROPHIN-RELEASING AND THYROTROPHIN-RELEASING HORMONES IN EPILEPTIC PATIENTS RECEIVING CARBAMAZEPINE OR PHENYTOIN

Authors

  • J. DANA-HAERI,

    1. Institute of Neurology, National Hospital, Queen Square, London WC1N 3BG, Chalfont Centre for Epilepsy, Chalfont St. Peter, Buckinghamshire SL9 0RJ and Department of Pharmacology & Therapeutics, Welsh National School of Medicine, Cardiff CF4 4XN
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  • J. OXLEY,

    1. Institute of Neurology, National Hospital, Queen Square, London WC1N 3BG, Chalfont Centre for Epilepsy, Chalfont St. Peter, Buckinghamshire SL9 0RJ and Department of Pharmacology & Therapeutics, Welsh National School of Medicine, Cardiff CF4 4XN
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  • A. RICHENS

    Corresponding author
    1. Institute of Neurology, National Hospital, Queen Square, London WC1N 3BG, Chalfont Centre for Epilepsy, Chalfont St. Peter, Buckinghamshire SL9 0RJ and Department of Pharmacology & Therapeutics, Welsh National School of Medicine, Cardiff CF4 4XN
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Professor A. Richens, Department of Pharmacology and Therapeutics, Welsh National School of Medicine, Cardiff CF4 4XN, Wales.

SUMMARY

Pituitary responsiveness to gonadotrophin-releasing (LHRH) and thyrotrophin-releasing (TRH) hormones was studied in 19 epileptic patients receiving long-term carbamazepine or phenytoin therapy and 14 normal control subjects. Baseline prolactin levels were normal in the patients; 2 h after LHRH-TRH the prolactin levels in women on carbamazepine were significantly higher than in the controls, but apart from this, no other differences were found. Baseline LH levels were raised in male patients and the response to LHRH-TRH was exaggerated in all patients on carbamazepine. FSH levels were normal throughout. The exaggerated LH response is consistent with primary hypogonadism caused by enhanced sex hormone metabolism, secondary to hepatic enzyme induction by the antiepileptic drugs.

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