title: The pituitary as a target of antalgic treatment of chronic cancer pain: a possible mechanism of pain relief through pituitary neuroadenolysis.
abstract: Surgical hypophysectomy performed in 18 cases with hormone-dependent carcinoma resulted in tumour regression in 38.8% of the cases, and pain relief in 88%. Neuroadenolysis performed 170 times on 130 cases resulted in pain relief in 94% with hormone-dependent carcinoma, and 70% with non-dependent carcinoma. The clinical investigations, following performance of neuroadenolysis, indicate suppressed pituitary function, significant increase of ACTH, thyrotropin-releasing hormone and vasopressin in the cerebrospinal fluid (CSF), delay of long latencies in somatosensory evoked potential and increased pain threshold of C-fibres. Increase of beta-endorphin in CSF was very brief. Though the exact physiological activity in pain sensation of those peptides other than endorphins still remains obscure, increase of the peptides which are mainly synthesized in the hypothalamopituitary axis, along with suppressed pituitary function, is considered to exert a long-lasting suppressive effect on the mediation and perception of cancer pain through C-fibres and the central nervous system.
mesh_terms: D004723:Endorphins / Q000378:metabolism; D000431:Ethanol / Q000627:therapeutic use*; D005073:Evoked Potentials, Somatosensory; D005260:Female; D006801:Humans; D007016:Hypophysectomy; D008297:Male; D009369:Neoplasms / Q000628:therapy*; D009376:Neoplasms, Hormone-Dependent / Q000628:therapy*; D010147:Pain Measurement; D010166:Palliative Care; D010903:Pituitary Gland, Anterior / Q000187:drug effects*; D010907:Pituitary Hormones / Q000378:metabolism; D013973:Thyrotropin-Releasing Hormone / Q000378:metabolism; D001615:beta-Endorphin
chemical_list: D004723:Endorphins; D010907:Pituitary Hormones; D000431:Ethanol; D013973:Thyrotropin-Releasing Hormone; D001615:beta-Endorphin