| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
REVIEW |
Department of Endocrinology, St Bartholomew’s Hospital, London EC1A 7BE, UK, 1 Department of Medical Sciences, University Hospital, Uppsala, Sweden and 2 Department of Endocrinology, CHU de Liège, Domaine Universitaire Sart-Tilman, 4000 Liege, Belgium
(Correspondence should be addressed to G M Besser; Email: endo{at}thelondonclinic.co.uk)
Abstract
Background: Multimodal therapy for acromegaly affords adequate disease control for many patients; however, there remains a subset of individuals that exhibit treatment-resistant disease. The issue of treatment-resistant pituitary tumor growth remains relatively under-explored.
Methods: We assessed the literature for relevant data regarding the surgical, medical and radiotherapeutic treatment of acromegaly in order to identify the factors that were predictive of aggressive or treatment-resistant pituitary tumor behavior in acromegaly and undertook an assessment of the rates of failure to control tumor progression with available treatment modalities.
Results: Young age at diagnosis, large tumor size, high growth hormone secretion and certain histological markers are predictors of future aggressive tumor behavior in acromegaly. Significant tumor regrowth occurs in less than 10% of cases thought to be cured surgically, whereas failure to control tumor growth is seen in less than 1% of patients receiving radiotherapy. Somatostatin analogs induce a variable degree of tumor shrinkage in acromegaly but up to 2.2% of somatostatin analog-treated tumors continue to grow. Relative to other therapies, limited data are available for pegvisomant, but these indicate that persistent tumor growth occurs in 1.6–2.9% of cases followed up regularly with serial magnetic resonance imaging scans.
Conclusions: Treatment-resistant tumor progression occurs in a small minority of patients with acromegaly, regardless of treatment modality. Young patients with large tumors or those with high pre-treatment levels of growth hormone particularly warrant close monitoring for continued tumor progression during treatment for acromegaly.
This article has been cited by other articles:
|
|
 |
|
  A. Beckers and A. F Daly The clinical, pathological, and genetic features of familial isolated pituitary adenomas Eur. J. Endocrinol., October 1, 2007; 157(4): 371 - 382. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Georgitsi, A. Raitila, A. Karhu, K. Tuppurainen, M. J. Makinen, O. Vierimaa, R. Paschke, W. Saeger, R. B. van der Luijt, T. Sane, et al. Molecular diagnosis of pituitary adenoma predisposition caused by aryl hydrocarbon receptor-interacting protein gene mutations PNAS, March 6, 2007; 104(10): 4101 - 4105. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
I Schreiber, M Buchfelder, M Droste, K Forssmann, K Mann, B Saller, and C J Strasburger Treatment of acromegaly with the GH receptor antagonist pegvisomant in clinical practice: Safety and efficacy evaluation from the German Pegvisomant Observational Study Eur. J. Endocrinol., January 1, 2007; 156(1): 75 - 82. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. F. Daly, M.-L. Jaffrain-Rea, A. Ciccarelli, H. Valdes-Socin, V. Rohmer, G. Tamburrano, C. Borson-Chazot, B. Estour, E. Ciccarelli, T. Brue, et al. Clinical Characterization of Familial Isolated Pituitary Adenomas J. Clin. Endocrinol. Metab., September 1, 2006; 91(9): 3316 - 3323. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Colao, R. Pivonello, R. S Auriemma, M. C. De Martino, M. Bidlingmaier, F. Briganti, F. Tortora, P. Burman, I. A Kourides, C. J Strasburger, et al. Efficacy of 12-month treatment with the GH receptor antagonist pegvisomant in patients with acromegaly resistant to long-term, high-dose somatostatin analog treatment: effect on IGF-I levels, tumor mass, hypertension and glucose tolerance. Eur. J. Endocrinol., March 1, 2006; 154(3): 467 - 477. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
