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Growth Hormone-Releasing Hormone Infusion in Patients with Active Acromegaly

Medizinische Klinik Innenstadt University of Munich, 8000 Munich 2, West Germany; Divisione di Endocrinologia, Ospedale Cà Granda Niguarda, Milan, Italy

Address requests for reprints to: Dr. K. von Werder, Medizinische Klinik Innenstadt, University of Munich, Ziernssenstr. 1,8000 Munich 2, West Germany.

To determine GH-releasing hormone (GHRH)- stimulated GH secretion in patients with active acromegaly, nine patients received a _*50-µg GHRH-(l-44) bolus dose followed by a 2-h infusion with 100 µg GHRH/h, after which a second 50-µg GHRH bolus dose was given. Serum GH, PRL, and immunoreactive GHRH levels were measured from 2 h before to 1 h after the end of the infusion and compared with hormone levels in six normal subjects subjected to the same protocol. In addition, seven of the nine acromegalic patients received 100 fig GHRH as an iv bolus dose, followed by a 2-h saline infusion on a different day.

After the 100-µg GHRH bolus dose, the mean GH level increased from 55.9 ± 18.0 (±SE) to 148.5 ± 40.0 ng/ml within 15 min. Thereafter, GH levels decreasedand were significantly lower at 90 and 120 min compared to the peak level 15 min after GHRH injection. After the 50-/ig GHRH bolus dose, all acromegalic patients except two also had a clear-cut rise of GH levels, with the mean GH level increasing from 37.5 ± 13.2 to 108.4 ± 55.0 ng/ml at 60 min. Thereafter, elevated GH levels were sustained in the acromegalic patients throughout the GHRH infusion. In contrast, normal subjects had a significant decrease in the initially elevated GH levels, despite continuous GHRH infusion. There were no significant differences between PRL secretion and immunoreactiveGHRH levels in either group.

These findings suggest that patients with active acromegaly not only have elevated basal GH levels, but also have a greater ready releasable GH pool and/or accelerated GH turnover compared to those of normal subjects, which cannot be exhausted by a 2-h GHRH infusion. (J Clin Endocrinol Metab63: 88, 1986)

^* Supported by the Deutsche Forschungsgemeinschaft (We 439/5-1).

Received April 26, 1985.

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