In 2011 is the 40th anniversary of prolactin (PRL) characterisation as a distinct hormone. Only 30 years ago most patients with large pituitary tumours received primary surgery (often transcranial) followed by routine radiotherapy treatments associated with significant morbidity and hypopituitarism. Much therapeutic progress has been made; effective medical treatments now exist for many pituitary tumour subtypes, particularly the use of long-acting dopamine agonists (DA) and somatostatin analogues (SA), with potential for growth control and tumour shrinkage (TS). Typical DA responses of a macroprolactinoma include rapid PRL reduction, TS (within days/weeks), visual improvement (often within hours/days) and recovery of normal pituitary function. Up to 90% of patients show these responses and most tumours shrink by at least 50%. Lactotroph cells shrink by over 50% with notable reductions in the cytoplasmic and RER components. In acromegaly, SAs control tumour growth in the majority and induce significant TS in ~75% of de novo patients, with an average tumour volume reduction of ~50%, but there is a wide range of TS in unselected GH-tumours. Somatotroph cell size reduction is modest, but diminished proliferation and angiogenesis have been demonstrated. SA are also effective in de novo patients with TSH-secreting adenomas with significant TS in the majority. Many non-functioning pituitary tumours express D2 dopamine receptors (albeit fewer than in prolactinomas) and DA therapy restrains tumour growth in up to 70%, although only a minority show marked shrinkage. Increasingly, dopamine and somatostatin receptor subtype analysis will guide specific medical therapies for individual tumours, not only with the agents currently available, but also with multiligand SA (such as pasireotide) and chimeric molecules (such as dopastatin). Despite their frequent clinical effectiveness, issues of drug safety, value for money and long-term cure rates associated with medical treatments for pituitary tumours continue to be evaluated and debated.
Generously supported by the Clinical Endocrinology Trust.