Endocrine Abstracts (2001) 2 P35

Medical therapy of macroprolactinomas in men: (1) prevalence of hypopituitarism at diagnosis and (2) proportion of cases exhibiting recovery of pituitary function

L Sibal1, P Ugwu2, P Kendall-Taylor2, S Ball1,2, RA James1,2 & R Quinton1,2

1Department of Endocrinology, Royal Victoria Infirmary, Newcastle-upon-Tyne, UK; 2Department of Medicine, School of Clinical Medical Sciences, University of Newcastle, UK.

INTRODUCTION: Hyperprolactinaemia frequently causes secondary hypogonadism through central suppression of gonadotropin secretion. Macroprolactinomas (>1cm diameter) may additionally cause more generalised hypopituitarism; a recent series finding the prevalence of TSH and ACTH deficiencies to be 35% and 9%, respectively. Recovery of the thyrotropic and/or corticotropic axes is well described following surgery to pituitary tumours, but remains poorly defined in relation to medical (dopamine-agonist) therapy of macroprolactinomas.

PATIENTS & METHODS: We retrospectively examined case records of 25 male patients who had received medical therapy alone for macroprolactinoma between 1979 - 2000. Mean prolactin level at baseline was 41,945U/L (range 4,329 - 332,000). Defects of the following pituitary hormone axes were evident at diagnosis: LH/FSH-testosterone (n=19; 76%), TSH-T4 (n=7; 28%) and ACTH-cortisol (n=3; 12%). Overall, 11 men (44%) were deficient in 1 axis, seven (28%) in 2 axes and two (8%) in 3 axes (growth hormone secretory status was not systematically evaluated). In all patients, tumour shrinkage was documented by interval cranial imaging and prolactin levels fell to normal or near-normal levels (mean 590U/L). Post-treatment, LH/FSH-testosterone deficiency persisted in seven (28%) patients, TSH-T4 deficiency in four (16%) and ACTH-cortisol deficiency in one patient (4%).

DISCUSSION: The prevalence of ACTH and/or TSH deficiency in men with macroprolactinomas is 32% at diagnosis. If interval reassessments are performed over several years of treatment, recovery of corticotropic and/or thyrotropic function is demonstrable in more than half of these patients. Without adequately reassessment, such patients might be unnecessarily maintained on long-term thyroxine and/or glucocorticoid therapy. Potential complications of glucocorticoid therapy include osteoporosis, weight gain, insulin resistance and adrenal suppression, so consigning a patient to indefinite therapy should not be undertaken lightly.

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