2017, Number 4
<< Back Next >>
Rev Fac Med UNAM 2017; 60 (4)
Multimodal treatment of non-functional recidivant hypophyseal adenomas. A case report and literature review
Balcázar-Hernández LJ, Benítez-Rodríguez FJ, Jandete-Medina MÁ, Murillo-Galindo KV, Sánchez-Mentado JA, Torres-Paniagua JL, González-Virla B, Mendoza-Zubieta V, Gregor-Gooch JM, Vargas-Ortega G
Language: Spanish
References: 34
Page: 19-26
PDF size: 792.42 Kb.
ABSTRACT
Background: Non-functional pituitary adenomas generally
have a benign and non-invasive nature, however, it may show
aggressiveness with invasion of surrounding tissues, high
mitotic index, an index of Ki67› 3% and extensive positive
staining for the cellular tumor antigen p53, differing from
the pituitary carcinomas by the absence of craniospinal dissemination
or systemic metastases. Aggressive adenomas
show resistance to surgical, medical and radiation therapy,
including chemotherapeutic agents such as temozolomide,
a promising therapeutic option according to reports in the
international literature.
Case presentation: This is a woman in her 6th decade of life
with a clinical presentation characterized by a progressive
chiasm syndrome and hypopituitarism in the presence of
non-functional pituitary macroadenoma, with initial resistance
of neurosurgical treatment, medical treatment with a
dopaminergic agonist plus a somatostatin receptor agonist
and conventional fractionated radiotherapy, meeting the
criteria of aggressive pituitary adenoma. After the treatment
with temozolomide as a chemotherapy regimen, the patient
showed clinical stability and absence of tumor progression
during her follow-up.
Conclusion: Defining aggressiveness is of crucial importance
for improving the management of patients by enhancing
prognostic predictions and effectiveness of treatment.
The treatment of nonfunctioning pituitary adenomas with
aggressiveness is a clinical challenge that involves a multidisciplinary
approach. Resistance to surgical, medical and
radiotherapeutic treatment have resulted in the investigation
of therapeutic options with chemotherapeutic agents such
as temozolomide, with promising response rates.
REFERENCES
Kaltsas GA, Nomikos P, Kontogeorgos G, Buchfelder M, Grossman AB. Clinical review: diagnosis and management of pituitary carcinomas. J Clin Endocrinol Metab. 2005;90:3089-99.
Ostrom QT, Gittleman H, Farah P, Ondracek A, Chen Y, Wolinsky Y, et al. CBTRUS statistical report: primary brain and central nervous system tumors diagnosed in the United States 2006-2010. Neuro Oncol. 2013;15 Suppl. 2:56.
Fernandez A, Karavitaki N, Wass JA. Prevalence of pituitary adenomas: a community based, cross-sectional study in Banbury (Ox- fordshire, UK). Clin Endocrinol. 2010;72:377-82.
Daly AF, Rixhon M, Adam C, Dempegioti A, Tichomirowa MA, Beckers A. High prevalence of pituitary ade- nomas: a cross-sectional study in the province of Liege, Belgium. J Clin Endocrinol Metab. 2006;91:4769-75.
Chatzellis E, Alexandraki KI, Androulakis II, Kaltsas G. Aggressive pituitary tumors. Neuroendocrinology. 2015; 101(2):87-104.
Scheithauer BW, Kurtkaya-Yapicier O, Kovacs KT, Young WF Jr, Lloyd RV. Pituitary carcinoma: a clinicopathological review. Neurosurgery. 2005;56:1066-74;discussion 1066-74.
Lloyd RV, Kovacs K, Young WF Jr, Farrel WE, Asa SL, Trouillas J, et al. Tumours of the pituitary gland. En: De- Lellis RA, Lloyd RV, Heitz PU, Eng C, eds. World Health Organization Classification of Tumours. Pathology and genetics of tumours of endocrine organs. Lyon: IARC Press; 2004. p. 9.
Yildirim AE, Divanlioglu D, Nacar OA, Dur- sun E, Sahinoglu M, Unal T, Belen AD. Incidence, hormonal distribution and postoperative follow up of atypical pituitary adenomas. Turk Neurosurg. 2013;23:226-31.
Raverot G, Jouanneau E, Trouillas J. Management of endocrine disease: clinicopathological classification and molecular markers of pituitary tumours for personalized therapeu- tic strategies. Eur J Endocrinol. 2014;170:R121– R132.
Mayson SE, Snyder PJ. Silent (clinically nonfunctioning) pituitary adenomas. Journal of neuro-oncology. 2014;117(3); 429-36.
Meij BP, Lopes MB, Ellegala DB, Alden TD, Laws ER Jr. The long-term significance of microscopic dural invasion in 354 patients with pituitary adenomas treated with transsphenoidal surgery. J Neurosurg. 2002;96:195-8.
Heaney A. Management of aggressive pituitary adenomas and pituitary carcinomas. J Neurooncol. 2014;117:459-68.
Kaltsas GA, Grossman AB. Malignant pituitary tumours. Pituitary. 1998;1:69-81.
Delgrange E, Trouillas J, Maiter D, Donckier J, Tourniaire J. Sex-related difference in the growth of prolactinomas: a clinical and proliferation marker study. J Clin Endocrinol Metab. 1997;82:2102-7.
Salehi F, Agur A, Scheithauer BW, Kovacs K, Lloyd RV, Cusimano M. Ki-67 in pituitary neoplasms: a review part I. Neurosurgery. 2009;65:429-37; discussion 437.
Middleton MR, Grob JJ, Aaronson N, Fierlbeck G, Tilgen W, Seiter S, et al. Randomized phase III study of temozolomide versus dacarbazine in the treatment of patients with advanced metastatic malignant melanoma. J Clin Oncol. 2000;18:158-66.
Friedman HS, Kerby T, Calvert H. Temozolomide and treatment of malignant glioma. Clin Cancer Res. 2000; 6:2585-97.
Syro LV, Uribe H, Penagos LC, et al. Antitumour effects of temozolomide in a man with a large, invasive prolactinproducing pituitary neoplasm. Clin Endocrinol (Oxf). 2006;65:552-3.
Lim S, Shahinian H, Maya MM, Yong W, Heaney AP. Temozolomide: a novel treatment for pituitary carcinoma. The Lancet Oncology. 2006;7:518-20.
Liu JK, Patel J, Eloy JA. The role of temozolomide in the treatment of aggressive pituitary tumors. Journal of clinical neuroscience: official journal of the Neurosurgical Society of Australasia. 2015:22(6):923-9.
Marchesi F, Turriziani M, Tortorelli G, Avvisati G, Torino F, De Vecchis L. Triazene compounds: mechanism of action and related DNA repair systems. Pharmacol Res. 2007;56:275-87.
Kaina B, Mühlhausen U, Piee-Staffa A, et al. Inhibition of O6-methylguanine-DNA methyltransferase by glucoseconjugated inhibitors: comparison with nonconjugated inhibitors and effect on fotemustine and temozolomide-induced cell death. J Pharmacol Exp Ther. 2004;311:585-93.
Bush ZM, Longtine JA, Cunningham T, et al. Temozolomide treatment for aggressive pituitary tumors: correlation of clinical outcome with O(6)-methylguanine methyltransferase (MGMT) promoter methylation and expression. J Clin Endocrinol Metab. 2010;95:E280-E290.
Raverot G, Sturm N, de Fraipont F, et al. Temozolomide treatment in aggressive pituitary tumors and pituitary carcinomas: a French multicenter experience. J Clin Endocrinol Metab. 2010;95:4592-9.
McCormack AI, Wass JA, Grossman AB. Aggressive pituitary tumours: the role of temozolomide and the assessment of MGMT status. Eur J Clin Invest. 2011;41:1133-48.
Heaney AP. Clinical review: pituitary carcinoma: difficult diagnosis and treatment. J. Clin Endocrinol Metab. 2011:96;3649-60.
Raverot G, et al. Pituitary carcinomas and aggressive pituitary tumours: merits and pitfalls of temozolomide treatment. Clin Endocrinol. 2012;76:769-75.
Ortiz LD, et al. Temozolomide in aggressive pituitary adenomas and carcinomas. Clinics. 2013;67 (Suppl. 1):119-23.
Bengtsson D, Schrøder HD, Andersen M, Maiter D, Berinder K, Feldt Rasmussen U, Petersson M. Long-term outcome and MGMT as a predictive marker in 24 patients with atypical pituitary adenomas and pituitary carcinomas given treatment with temozolomide. The Journal of Clinical Endocrinology & Metabolism. 2015;100(4):1689-98.
Kovacs K, Horvath E. Effects of medical therapy on pituitary tumors. Ultrastruct Pathol. 2005;29:163-7.
Jouanneau E, et al. New targeted therapies in pituitary carcinoma resistant to temozolomide. Pituitary. 2012;15:37-43.
Ortiz LD, et al. Anti‐VEGF therapy in pituitary carcinoma. Pituitary. 2012;15:445-9.
Fukuoka H, et al. EGFR as a therapeutic target for human, canine, and mouse ACTH‐secreting pituitary adenomas. J Clin Invest. 2011;121:4712-21.
Fukuoka H, et al. HER2/ErbB2 receptor signaling in rat and human prolactinoma cells: strategy for targeted prolactinoma therapy. Mol Endocrinol. 2011;25:92-103.