Аннотация:FP-08-2
Compression or surgically transcection of pituitary stalk
Ludmila Astafyeva, Boris Kadashev, Aleksander Konovalov, Pavel Kalinin, Maxim Kutin, Oleg Sharipov, Irina Klochkova, Dmitri Fomichev, Yuliya Sidneva
Objective: Study of pre- and post-operative endocrinological disorders in patients with cellar and paracellar region tumors with compressed and surgically transected of Pituitary Stalk(PS).
Methods: In 82 patients the compressed PS was possible to preserve (41 endosuprasellar non-functioning pituitary adenomas (РА)and 41 suprasellar meningiomas); In 57 patients PS was transected during the surgery(46 suprasellar craniopharyngiomas (these tumors seemed to completely destroy transected PS) and 11 endosuprasellar non-functioning PA(these tumors compressed the PS, which later was transected during the resection of suprasellar capsule of adenoma). In follow up and pre-op observation period of 6 month all patients demonstrated levels of prolactin(PRL),TSH,LH,FSH, free T4, cortisol, testosterone or estradiol.
Results: Compression of the PS has resulted in hyperprolactinemia in 37,4% of patients. Removal of meningiomas and non-functioning РА was accompanied by normal PRL concentration in the majority of patients with no presence of hypopituitarism. PS transection during surgery did not result in rise of PRL level in 58,7% of patients with craniopharyngiomas and 81,9% with РА.
Conclusion: Considering differentiation of symptoms when PS is compressed or transected we have developed 2 definitions: PS compression syndrome and PS transection syndrome. PS compression syndrome is caused by compression with tumor and majorly included hyperprolactinemia(37,4% cases); releasing of the pressure by surgically removing tumors lead to normalization of PRL levels in majority of patients and was not accompanied by rise of hypopituitary symptoms. PS transection syndrome in patients with craniopharyngiomas and non-functioning PA lead to appearance of panhypopituitarism in all the patients and permanent diabetes insipidus in majority of cases. Reasons of hyperprolactinemia absence in many patients with transected PS require further investigation–2 different possible mechanisms cannot be excluded: development of adenopituitary ischemia as a result of blood supply disorder resulting in partial or full atrophy of hormone-producing cells(e.g. lactotroph) or revascularization of portal veins with dopamine transportation restored.