Hostname: page-component-848d4c4894-hfldf Total loading time: 0 Render date: 2024-06-02T16:22:37.963Z Has data issue: false hasContentIssue false
  • English
  • Français

Acromegaly with Normal Basal Growth Hormone Levels

Published online by Cambridge University Press:  18 September 2015

Rights & Permissions [Opens in a new window]

Abstract:

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.
Background:

The most common cause of acromegaly is excess of growth hormone (GH) secretion.

Methods:

We report a 42-year-old male patient, who had become acromegalic over the past 5 years. There were no visual changes or change in sexual function, no gynaecomastia or galactorrhoea. Both CT and MRI scans showed a large mass measuring 2.5 x 2.5 x 3.5 cm, originating from the sella turcica and extending into and totally filling up the sphenoid sinus with diffusely invasive features.

Results:

Basal serum GH level was within normal range, but insulin-like growth factor 1 (IGF-1) was elevated with slightly increased prolactin (PRL) and impaired GH secretory regulation as well. A pituitary adenoma was partially removed through transsphenoidal microsurgery. Pathology confirmed a mammo-somatotrophic adenoma but immunocytochemistry study of the tumour showed only positivity for PRL but not GH.

Conclusions:

When acromegaly occurs without GH level elevation, one should pay attention that: 1) IGF-1 might be the cause of the clinical feature of acromegaly; 2) The tumour might undergo morphological transformation; and 3) Hyperinsulinemia or GH receptor antibody formation could also be the cause of the acromegalic appearance.

Type
Original Articles
Information
Canadian Journal of Neurological Sciences , Volume 24 , Issue 3 , August 1997 , pp. 250 - 253
Copyright
Copyright © Canadian Neurological Sciences Federation 1997

References

REFERENCES

1.Marie, P. Sur deux cas d’acromégalie: hypertrophie singulière non congénitale des extrémités supérieures, inférieures et céphalique. Rev Med 1886; 297–333.Google Scholar
2.Cushing, H. Partial hypophysectomy for acromegaly: with remarks on the function of the hypophysis. Ann Surg 1909; 50: 1002–1017.Google Scholar
3.Melmed, S, Braunstein, GD, Horvath, E, Ezrin, C, Kovacs, K. Pathophysiology of acromegaly. EndocrRev 1983; 4: 271–290.Google Scholar
4.Melmed, S. Acromegaly. N Engl J Med 1990; 5: 966–977.Google Scholar
5.Mims, RB, Bethune, JE. Acromegaly with normal fasting growth hormone concentrations but abnormal growth hormone regulation. Ann Intern Med 1974; 81: 781–784.Google Scholar
6.Brockmeier, SJ, Buchfelder, M, Adams, EF, Schott, W, Fahlbusch, R. Acromegaly with “normal” serum growth hormone levels: clinical features, diagnosis and results of transsphenoidal microsurgery. Horm Metab Res 1992; 24: 392–396.Google Scholar
7.Flier, JS, Moller, DE, Moses, AC, et al. Insulin-mediated pseudoacromegaly: clinical and biochemical characterization of a syndrome of selective insulin resistance. J Clin Endocrinol Metab 1993; 76: 1533–1541.Google ScholarPubMed
8.Ashcraft, MW, Hartzband, PI, Van Herle, AJ, Bersch, N, Golde, DW. A unique growth factor in patients with acromegaloidism. J Clin Endocrinol Metab 1983; 57: 272–276.Google Scholar
9.Mahy, IR, Wiggins, J. Pachydermoperiotosis mimicking acromegaly. J R S Med 1992; 85: 46–47.Google Scholar
10.Comtois, R, Robert, F, Hardy, J. Immunoradiometric assays may miss high prolactin levels. Ann Intern Med 1993; 119: 173.CrossRefGoogle ScholarPubMed
11.Mathews, LS, Hammer, RE, Behringer, RR, et al. Growth enhancement of transgenic mice expressing human insulin-like growth factor I. Endocrinology 1988; 123: 2827–2833.Google Scholar
12.Pagesy, PJ, LI, Y, Rentier-Delrue, F, et al. Growth hormone and somatostatin gene expression in pituitary adenomas with active acromegaly and minimal plasma growth hormone elevation. Acta Endocrinol 1990; 122: 745–752.Google Scholar
13.Nicoll, CS. Prolactin and growth hormone: specialists on one hand and mutual mimic on the other. Perspect Biol Med 1982; 25: 369–381.Google Scholar
14.Ferreira, MF, Pires, JS, Sobrinho, LG. Prolactin, weight gain and psychgeny. In: Melmed, S, ed. Molecular and Clinical Advances in Pituitary Disorders: Proceedings of the 3rd International Pituitary Congress. Endocrine Research and Education, INC. 1993: 243–248.Google Scholar
15.Furuhata, S, Kameya, T, Otani, M, Toya, S. Prolactin presents in all pituitary tumours of acromegalic patients. Hum Pathol 1993; 24: 10–15.Google Scholar
16.Lloyd, RV, Can, M, Chandler, WF, et al. Human growth hormone and prolactin secreting pituitary adenomas analyzed by in situ hybridization. Am J Pathol 1989; 134: 605–613.Google Scholar
17.Baker, BL, Jaffe, RB. The genesis of cell types in the adenohypophysis of the human fetus as observed with immunocytochemistry. Am J Anat l975; 143: 137–162.Google Scholar
18.Joseph D’ercole, A, Underwood, LE, Groelke, J, Plet, A. Leprechaunism: studies of the relationship among hyperinsulinism, insulin resistance and growth retardation. J Clin Endocrinol Metab 1979; 48: 495–502.Google Scholar
19.Moller, DE, Flier, JS. Insulin resistance: mechanisms, syndromes and implications. N Engl J Med 1991; 325: 938–948.Google Scholar
20.Campino, C, Szecowka, J, Lopez, JM, Mulchahey, J, Seron-Ferre, M. Growth hormone (GH) receptor antibodies with GH-like activity occur spontaneously in acromegaly. J Clin Endocrinol Metab 1992;74:751–756.Google Scholar
21.Stolar, MW, Amburn, K, Baumann, G. Plasma “big” and “big-big” growth hormone (GH) in man: an oligomeric series composed of structurally diverse GH monomers. J Clin Endocrinol Metab 1984;59:212–218.Google Scholar