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Departments of Endocrinology and Metabolism (F.B., C.C., C.S., L.M., M.G., E.M.) and Oncology (A.C.), University of Pisa, 56124 Pisa, Italy; Unit of Epidemiology and Biostatistics (G.R.), Institute of Clinical Physiology, National Research Council, 56124 Pisa, Italy; and Department of Clinical Medicine (L.B.), University of Insubria, 21100 Varese, Italy
Address all correspondence and requests for reprints to: Fausto Bogazzi, M.D., Dipartimento di Endocrinologia e Metabolismo, Università di Pisa, Ospedale Cisanello, Via Paradisa 2, 56124 Pisa, Italy. E-mail: f.bogazzi{at}endoc.med.unipi.it; or fbogazzi{at}hotmail.com.
Background: Acromegaly seems to be associated with an increased prevalence of colonic adenomas, although factors affecting their development and recurrence of the latter are not fully known.
Subjects and Methods: Seventy-nine patients with active acromegaly were prospectively followed up for 5 yr. Two hundred eighty healthy subjects served as controls. Colonoscopy and assessment of acromegaly activity were performed at 1-yr intervals. Acromegaly was defined as controlled if serum IGF-I levels were within the normal age-adjusted range.
Results: Colonic adenomas were found in 26 of 79 acromegalic patients (32.9%) and 60 of 280 controls (21.4%) at baseline (P = 0.035, adjusted for age and sex, odds ratio 1.82, 95% confidence interval, 1.023.25). Seven patients had hyperplastic polyps; the remaining 46 acromegalic patients had no detectable lesions at baseline and did not develop adenomas during the study period. Of the 26 patients with colonic adenomas at baseline, 16 (61.5%) had at least one recurrence of colonic adenomas (P < 0.0001 vs. patients without colonic lesions at baseline), and multiple recurrences were more frequent in patients with uncontrolled acromegaly (66.7% vs. 17.6% in patients with controlled acromegaly, P = 0.028).
Conclusions: The first colonoscopy helps to identify acromegalic patients at high risk of developing colonic adenomas. If colonic adenomas are not present initially, it is unlikely that they develop thereafter, independently of metabolic control of acromegaly. Conversely, new lesions are frequent (and often multiple) in patients who already have colonic adenomas at baseline, particularly if acromegalic disease is poorly controlled by treatment.
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