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Am J Physiol Endocrinol Metab (September 23, 2003). doi:10.1152/ajpendo.00230.2003
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Submitted on May 21, 2003
Accepted on August 28, 2003

Octreotide Represses Secretory- Burst Mass and Nonpulsatile (Basal) Secretion but does not Restore Event Frequency or Orderly GH Secretion in Acromegaly

Nienke R. Biermasz1, Alberto M. Pereira1, Marijke Frolich2, Johannes A. Romijn1, Johannes D. Veldhuis3, and Ferdinand Roelfsema1*

1 Department of Metabolism and Endocrinology, Leiden University Medical Center, Leiden, The Netherlands
2 Department of Clinical Chemistry, Leiden University Medical Center, Leiden, The Netherlands
3 Department of Endocrinology/Metabolism and Internal Medicine, Mayo Medical School Mayo Clinic and Foundation, Rochester, MN, USA

* To whom correspondence should be addressed. E-mail: f.roelfsema{at}lumc.nl.

Octreotide is a potent somatostatin analog, which inhibits GH release and restricts somatotrope-cell growth. The long-acting octreotide formulation, Sandostatin LAR, is effective clinically in approximately 60% of patients with acromegaly. Tumoral GH secretion in this disorder is characterized by increases in pulse amplitude and frequency, nonpulsatile (basal) release and irregularity. Whether sustained blockade by octreotide can restore physiological secretion patterns in this setting is unknown. To address this question, we studied seven patients with GH-secreting tumors during chronic receptor agonism. Responses were monitored by sampling blood at 10 min intervals for 24 hr, followed by analyses of secretion and regularity by multiparameter deconvolution and approximate entropy (ApEn) analyses. The somatostatin agonist suppressed GH secretory-burst mass, nonpulsatile (basal) GH release and pulsatile secretion, thereby decreasing total GH secretion by 86 % (range 70-96 %). ApEn decreased from 1.203 ± 0.129 to 0.804 ± 0.141 (P=0.032), denoting greater regularity. None of GH pulse frequency, basal GH secretion rates or ApEn normalized. In summary, chronic somatostatin agonism is able to repress amplitude-dependent measures of excessive GH secretion in acromegaly. Presumptive tumoral autonomy is inferred by continued elevations of event frequency, overall pattern disruption (irregularity) and nonsuppressible basal GH secretion.




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