ECE2010 Poster Presentations Neuroendocrinology and Pituitary (<emphasis role="italic">Generously supported by Novartis</emphasis>) (125 abstracts)
Biochemical control of acromegaly is currently defined by the achievement of GH suppression after oral glucose tolerance test (OGTT) and of normal age- and gender-matched IGF1 levels. OGTT is believed to inhibit somatotropin secretion by enhancing central somatostatinergic tone; thus, the use of this test in evaluating biochemical control in acromegalic patients on somatostatin analogues (SSA) is questionable. To gain further insights into this topic, we analyzed basal and nadir GH levels during OGTT in acromegalic patients on SSA.
Patients and methods: Basal IGF1 and GH values, as well as GH levels along the test, were analyzed in 115 standard OGTTs performed in 33 acromegalic patients (16 males and 17 females, aged 55.61±14.48 years), followed between 1993 and 2009. All patients were on SSA at the time of the study: in particular, 36 OGTTs were performed during lanreotide, 52 during octreotide, 27 during combined therapy with SSA and dopamine agonists. Seventy OGTTs were performed after unsuccessful surgery in 22 patients. No patient had undergone radiotherapy. GH suppression was considered normal when the hormonal value fell to <1 μg/l during OGTT. Diagnostic accuracy was analyzed by receiver-operator characteristic (ROC).
Results: ROC analysis showed that the GH basal value yielding the best specificity (100%) was 3.9 μg/l. All patients with basal GH>3.9 μg/l displayed lack of GH suppression after OGTT and 80% also displayed high IGF1. Conversely, patients with basal GH<3.9 μg/l presented a variable biochemical pattern with half failing to suppress GH after OGTT and over 35% displaying high IGF1 levels.
Conclusion: Our results show that baseline GH levels >3.9 μg/l are predictive of absent OGTT-dependent GH suppression; however, 20% of these patients display partial biochemical control (normal IGF levels). On the other hand, basal GH values <3.9 μg/l, such as those suggested by Jayasena et al. (Clin Endocrinol 2007), are not predictive of the GH suppressibility by glucose and are often discordant with IGF1 levels.