University of Gothenburg
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  4. Gudmundur Johannsson

Gudmundur Johannsson

Professor/ Chief Physician

Department of Internal Medicine and Clinical Nutrition
Telephone
+46 31-342 70 52
Mail
gudmundur.johannsson@medic.gu.se
Visiting address
Vita stråket SU
41345 Göteborg
Postal address
SU Sahlgrenska
41345 Göteborg

About Gudmundur Johannsson

The pituitary gland is a master regulator of growth, sexual development, fertility and energy metabolism. Pituitary tumours cause loss of pituitary function, but also obesity and cognitive dysfunction due to hypothalamic injury.

The overall aim is to develop individualised management and care of patients with pituitary tumours from time of primary tumour treatment to the life-long endocrine/metabolic treatment and tumour surveillance. A person centred care approach for these patients will be developed in order to strengthen their own role in the management of their disease.

The studies depend on access to unique study population made possible by centre of excellence standard of care, long-standing prospective collection of data in patients with pituitary tumour, novel study design and a multidisciplinary study team, the Gothenburg Pituitary Tomour (GoPT) study.

At least one-third of pituitary tumours continue to grow or recur during follow. This may occur more than 10 years after primary surgery. Re-operation or radiotherapy is associated with increased risk of death. Identifying a tumour biomarker that early predicts tumour progression and improved post-operative tumour surveillance may allow an early individualised patient selection to second line tumour treatment.

Hypothalamic injury occurs in as many as 50 % of patients with pituitary tumours. This leads to obesity and cognitive impairment. By measuring brain injury biomarkers in serum in relation to surgery, we aim to early identify patients with hypothalamic injury. This allows early preventive measures for obesity and support for the cognitive dysfunction.

The excess risk of death in patients with pituitary insufficiency is strongly related to their cortisol replacement therapy. Individualised treatment is almost impossible since markers of response to cortisol are currently lacking. In an experimental approach using patients with severe cortisol deficiency we aim to identify a marker for the action of cortisol.