Kristin Astrid Øystese1,2, Manuela Zucknick3, Olivera Casar-Borota4,5,6, Geir Ringstad7,8, Jens Bollerslev7,9. 1. Section of Specialized Endocrinology, Department of Endocrinology, Oslo University Hospital Rikshospitalet, P.b.4950 Nydalen, Oslo, 0424, Norway. k.a.b.oystese@medisin.uio.no. 2. Faculty of Medicine, University of Oslo, Oslo, Norway. k.a.b.oystese@medisin.uio.no. 3. Oslo Centre for Biostatistics and Epidemiology, Department of Biostatistics, Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway. 4. Department of Immunology, Genetics and Pathology, Uppsala University, Rudbeck Laboratory, Dag Hammarskjölds väg 20, Uppsala, 751 85, Sweden. 5. Department of Clinical Pathology and Cytology, Uppsala University Hospital, Rudbeck Laboratory, Dag Hammarskjölds väg 20, Uppsala, 751 85, Sweden. 6. Department of Pathology, Oslo University Hospital, Sognsvannsveien 20, Oslo, 0372, Norway. 7. Faculty of Medicine, University of Oslo, Oslo, Norway. 8. Department of Radiology and Nuclear Medicine, Oslo University Hospital- Rikshospitalet, Oslo, Norway. 9. Section of Specialized Endocrinology, Department of Endocrinology, Oslo University Hospital Rikshospitalet, Oslo, Norway.
Abstract
PURPOSE: Non-functioning pituitary adenomas are common, and the treatment and follow-up of these patients represent a multidisciplinary challenge. First line treatment is transphenoidal surgery, with debulking or total removal of tumour. A substantial portion of the tumours relapse after surgery, and there is no consensus of how to follow these patients postoperatively. Our aim was to characterize the postoperative growth of non-functioning pituitary adenomas and correlate it to clinical and paraclinical data. METHODS: We retrospectively registered 52 patients operated for non-functioning pituitary adenomas, with four or more consecutive MR-investigations not interrupted by secondary treatment. Adenoma volumes were estimated by the Cavalieri principle with summation of manually drawn areas multiplied by slice interval. Growth curves were modelled and tumour volume doubling time was calculated for 39 tumours with regrowth after surgery. RESULTS: A total of 13 tumours showed exponential growth, 10 linear growth and 16 logistic growth after surgery. The remaining 13 did not show regrowth of tumour. Seven of the exponential growing tumours underwent secondary surgery, compared to one and two of linear and logistic growing tumours (p = 0.03), respectively. Initial tumour volume doubling time was significantly lower in logistic growing tumours than in exponential growing tumours (p < 0.01). Men had tumours with lower tumour volume doubling time than women (p = 0.03). None of the tumours demonstrated signs of accelerated growth. CONCLUSION: Residual tumours following surgery frequently grow. The logistic growing tumours had the fastest initial growth in our cohort. We found no indication of accelerated growth, whereby the tumour volume doubling time might be used to predict a "worst-case" scenario when planning follow-up of these patients.
PURPOSE: Non-functioning pituitary adenomas are common, and the treatment and follow-up of these patients represent a multidisciplinary challenge. First line treatment is transphenoidal surgery, with debulking or total removal of tumour. A substantial portion of the tumours relapse after surgery, and there is no consensus of how to follow these patients postoperatively. Our aim was to characterize the postoperative growth of non-functioning pituitary adenomas and correlate it to clinical and paraclinical data. METHODS: We retrospectively registered 52 patients operated for non-functioning pituitary adenomas, with four or more consecutive MR-investigations not interrupted by secondary treatment. Adenoma volumes were estimated by the Cavalieri principle with summation of manually drawn areas multiplied by slice interval. Growth curves were modelled and tumour volume doubling time was calculated for 39 tumours with regrowth after surgery. RESULTS: A total of 13 tumours showed exponential growth, 10 linear growth and 16 logistic growth after surgery. The remaining 13 did not show regrowth of tumour. Seven of the exponential growing tumours underwent secondary surgery, compared to one and two of linear and logistic growing tumours (p = 0.03), respectively. Initial tumour volume doubling time was significantly lower in logistic growing tumours than in exponential growing tumours (p < 0.01). Men had tumours with lower tumour volume doubling time than women (p = 0.03). None of the tumours demonstrated signs of accelerated growth. CONCLUSION: Residual tumours following surgery frequently grow. The logistic growing tumours had the fastest initial growth in our cohort. We found no indication of accelerated growth, whereby the tumour volume doubling time might be used to predict a "worst-case" scenario when planning follow-up of these patients.
Authors: Michael A Mooney; Douglas A Hardesty; John P Sheehy; Robert Bird; Kristina Chapple; William L White; Andrew S Little Journal: J Neurosurg Date: 2016-07-01 Impact factor: 5.115
Authors: Anne Line Stensjøen; Ole Solheim; Kjell Arne Kvistad; Asta K Håberg; Øyvind Salvesen; Erik Magnus Berntsen Journal: Neuro Oncol Date: 2015-03-10 Impact factor: 12.300
Authors: Geir Andre Ringstad; Kyrre Eeg Emblem; Dominic Holland; Anders M Dale; Atle Bjornerud; John K Hald Journal: Neuroradiology Date: 2011-06-07 Impact factor: 2.804
Authors: Anders J Kolnes; Kristin A B Øystese; Nicoleta C Olarescu; Geir Ringstad; Jon Berg-Johnsen; Olivera Casar-Borota; Jens Bollerslev; Anders P Jørgensen Journal: J Clin Endocrinol Metab Date: 2020-08-01 Impact factor: 5.958