title: A human TSH-secreting adenoma: endocrine, biochemical and morphological studies. Evidence of somatostatin receptors by using quantitative autoradiography. Clinical and biological improvement by SMS 201-995 treatment.
abstract: An invasive TSH-secreting adenoma inducing mild hyperthyroidism was diagnosed in a 16-year-old male. Initial surgical treatment led to a temporary clinical and biological improvement. Recurrence of the thyrotoxicosis was treated with the somatostatin analogue, SMS 201-995 (octreotide) with normalization of the serum thyroid hormone levels with a dose of 200 micrograms per day. With immunoelectron microscopy, the tumour cells appeared poorly granulated with small secretory granules located at the periphery of the cells; only part of those were immunoreactive with an anti-TSH beta monoclonal antibody. No specific TRH binding site was found in a tumour membrane preparation. By quantitative autoradiography, somatostatin specific binding sites were as numerous in the TSH-secreting tumour as in control GH-secreting tumours. Binding kinetics and guanosine triphosphate dependency of the binding were equivalent in the TSH and GH tumours tested. Although all of the tumour cells displayed the same ultrastructural features, some were non-immunoreactive, suggesting that they could secrete an altered form of TSH. The absence of TRH receptors in the tumour cells is in accordance with previous reports on this type of tumour. We confirm the efficiency of octreotide treatment in this case of neoplastic TSH inappropriate secretion. The therapeutic effect of octreotide goes along with the presence of a high density of guanine nucleotide-dependent somatostatin binding sites in the tumour cells.
authors.affiliation: Hôpital de la Pitié, Paris, France.
authors.forename: M
authors.initials: M
authors.lastname: Polak
authors.forename: J
authors.initials: J
authors.lastname: Bertherat
authors.forename: J Y
authors.initials: JY
authors.lastname: Li
authors.forename: M
authors.initials: M
authors.lastname: Kujas
authors.forename: M
authors.initials: M
authors.lastname: Le Dafniet
authors.forename: H
authors.initials: H
authors.lastname: Weizani
authors.forename: R
authors.initials: R
authors.lastname: Van Effenterre
authors.forename: J
authors.initials: J
authors.lastname: Epelbaum
authors.forename: G
authors.initials: G
authors.lastname: Turpin
mesh_terms: D000236:Adenoma / Q000188:drug therapy / Q000378:metabolism* / Q000648:ultrastructure; D000293:Adolescent; D000911:Antibodies, Monoclonal; D001345:Autoradiography; D013006:Growth Hormone / Q000378:metabolism; D006160:Guanosine Triphosphate / Q000502:physiology; D006801:Humans; D006980:Hyperthyroidism / Q000188:drug therapy / Q000209:etiology / Q000473:pathology; D008297:Male; D008854:Microscopy, Electron; D015282:Octreotide / Q000627:therapeutic use*; D010911:Pituitary Neoplasms / Q000188:drug therapy / Q000378:metabolism* / Q000648:ultrastructure; D017981:Receptors, Neurotransmitter / Q000032:analysis / Q000378:metabolism*; D017481:Receptors, Somatostatin; D013972:Thyrotropin / Q000276:immunology / Q000378:metabolism*; D013973:Thyrotropin-Releasing Hormone / Q000378:metabolism
chemical_list: D000911:Antibodies, Monoclonal; D017981:Receptors, Neurotransmitter; D017481:Receptors, Somatostatin; D013973:Thyrotropin-Releasing Hormone; D006160:Guanosine Triphosphate; D013972:Thyrotropin; D013006:Growth Hormone; D015282:Octreotide