Public Defence: Anders Jensen Kolnes
MD Anders Jensen Kolnes at Institute of Clinical Medicine will be defending the thesis “Non-functioning pituitary adenomas: complications, prognostic factors and tumor behavior” for the degree of PhD (Philosophiae Doctor).
An electronic copy of the thesis may be ordered from the faculty up to 2 days prior to the public defence. Inquiries regarding the thesis after the public defence must be addressed to the candidate.
Trial Lecture – time and place
See Trial Lecture.
- First opponent: Professor Gérald Raverot, Fédération d'Endocrinologie, Groupement Hospitalier Est, Hôpital Louis Pradel
- Second opponent: Associate Professor Rupavathana Mahesparan, Universitetet i Bergen
- Third member and chair of the evaluation committee: Professor II Trond Melbye Michelsen, University of Oslo
Chair of the Defence
Associate Professor Are Martin Holm, Faculty of Medicine, University of Oslo
Senior Consultant Anders Palmstrøm Jørgensen, Oslo University Hospital
Pituitary adenomas are benign tumors of the pituitary gland and are among the most common intracranial neoplasms. Non-functioning pituitary adenomas (NFPA) do not cause clinical findings of hormone hypersecretion, however they can cause symptoms from compression of surrounding structures. The most common symptoms are headache, hypopituitarism, and visual disturbances.
Surgery is the main treatment for NFPAs, however some patients develops pituitary insufficiency after the operation. Failure of the hypothalamic-pituitary-adrenal (HPA) axis is life threatening and correct diagnosis of secondary adrenal insufficiency is important. The studies in the thesis were performed in the department of Endocrinology at Oslo University Hospital. Clinical data, blood samples, and NFPA tissue were examined.
In paper 1 we aimed to identify risk factors for developing secondary adrenal insufficiency after surgery, and to describe normal p-cortisol levels. We showed that pituitary apoplexy increased the risk of developing secondary adrenal insufficiency, and that traditional cut-off levels for p-cortisol should be revised.
In paper 2 we studied the relationship between gonadotropin (FSHβ and LHβ) staining and markers of aggressiveness in NFPAs. Tumors with high gonadotropin staining exhibited an aggressive phenotype. In addition, FSHβ staining correlated with circulating levels of plasma-FSH.
Paper 3 and 4 studied the newly discovered protein TGFBR3L. We showed that TGFBR3L was seen exclusively on gonadotroph cells, both in normal and neoplastic tissue. TGFBR3L correlated positively with LHβ and FSHβ in tumors, but inversely with circulating gonadotropins. Our findings suggested a role for TGFBR3L in gonadotropin regulation, but this needs further studies.
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