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Comparison of the Sensitivity of Growth Hormone Secretion to Somatostatin in Vivo and in Vitro in Acromegaly^*

Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Cincinnati College of Medicine Cincinnati, Ohio 45267

Address requests for reprints to: Dr. Lawrence A. Frohman, Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267.

Somatostatin (SRIH) sensitivity in acromegaly was evaluated in vivo by comparing the inhibition of GHRH (1 µg/kg, iv)-stimulated GH secretion in eight acromegalic and six normal subjects. A SRIH infusion (50 µg/h) that inhibited the mean plasma GH response to GHRH by 74 ± 5% (±SE) in normal subjects had no significant effect in the acromegalic patients. However, when two acromegalic patients in whom SRIH had no suppressive effect were excluded from the analysis, the effect of SRIH in the other six (82 ± 7%) was comparable to that in the normal subjects. Within the acromegalic group, the percent suppression of basal and GHRH-stimulated GH secretion was inversely correlated with both basal plasma GH (r = –0.751; P = 0.03 and r = –0.727; P = 0.04, respectively) and insulin-like growth factor I (r = –0.800; P = 0.02 and r = –0.727; P = 0.04, respectively) concentrations. The in vitro sensitivity to SRIH was studied in pituitary adenomas from five of the acromegalic patients in 3- to 4-day monolayer cultures of dispersed cells. The SRIH IC₅₀ values were lowest in the tumors (8.6–44 pmol/L) from the three patients who had in vivo SRIH sensitivity (suppression of GHRH-stimulated GH secretion) comparable to that in the normal subjects. The IC₅₀ values were higher in the tumors (150 and 21,000 pmol/L) from the two patients that were least responsive to SRIH in vivo. These results indicate that there is considerable variability of SRIH sensitivity in patients with acromegaly. Although the role of this defect in the pathogenesis of acromegaly is uncertain, it may be an important determinant in the degree of elevation of plasma GH levels.

^* This work was supported in part by USPHS Grants DK-30667 and RR-00068.

Received April 11, 1988.

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