Abstract
The development of highly sensitive and specific GH assays has necessitated a critical re-evaluation of the biochemical criteria needed for the diagnosis of acromegaly. Use of these assays has revealed that GH levels after oral glucose in healthy subjects and postoperative patients with active acromegaly can be significantly less than previously recognized with older GH assays.
In order to assess GH criteria for newly diagnosed acromegaly with a modern assay we have evaluated GH levels in 25 patients referred to our Neuroendocrine Unit for evaluation of untreated acromegaly. All patients underwent measurement of basal GH and IGF-I levels and 15 of these patients also underwent oral glucose tolerance testing for GH suppression (OGTT).
Basal GH levels were <1.0 μg/L at diagnosis in 5 of these 25 patients. Nadir GH levels were less than 1 μg/L also in 5 of 15 patients, and as low as 0.42 μg/L. All patients had elevated IGF-I levels preoperatively and pathological confirmation of a GH secreting pituitary tumor at the time of transsphenoidal surgery. The clinical presentations of these patients was variable. Most patients presented with classical manifestations of acromegaly, but 3 of the 5 patients with low nadir GH values had only very subtle signs of acromegaly.
Although most newly diagnosed patients have classically elevated GH levels and obvious clinical features of acromegaly, early recognition of disease may uncover patients with milder biochemical and clinical abnormalities. The diagnosis should not be discounted in patients who have elevated IGF-I levels, but have basal or nadir GH levels less than 1 μg/L. Conventional GH criteria for the diagnosis of acromegaly cannot be applied to the use of modern sensitive and specific GH assays.
This is a preview of subscription content, log in via an institution to check access.
Similar content being viewed by others
References
Giustina A, Barkan A, Casanueva FF, Cavagnini F, Frohman L, Ho K, Veldhuis J, Wass J, Von Werder K, Melmed S. Criteria for cure of acromegaly: A consensus statement. J Clin Endocrinol Metab 2000; 85:526–529.
Dimaraki EV, Jaffe CA, DeMott-Friberg R, Chandler WF, Barkan AL. Acromegaly with apparently normal GH secretion: Implications for diagnosis and follow-up. J Clin Endocrinol Metab 2002;87:3537–3542.
Freda PU, Post KD, Powell JS, Wardlaw SL. Evaluation of disease status with sensitive measures of growth hormone secretion in 60 postoperative patients with acromegaly. J Clin Endocrinol Metab 1998;83:3808–3816.
Freda PU, Landman RE, Sundeen RE, Post KD. Gender and age in the biochemical assessment of cure of acromegaly. Pituitary 2001;4:163–171.
Freda PU. Current concepts in the biochemical assessment of the patient with acromegaly. Growth Hormone & IGF Research 2003;13:171–184.
Duncan E, Wass JA. Investigation protocol: Acromegaly and its investigation. Clin Endocrinol (Oxf) 1999;50:285–293.
Chang-DeMoranville BM, Jackson IM. Diagnosis and endocrine testing in acromegaly. Endocrinol Metab Clin North Am 1992;21:649–668.
Hartman ML, Veldhuis JD, Thorner MO. Normal control of growth hormone secretion. Horm Res 1993;40:37–47.
Bates AS, Evans AJ, Jones P, Clayton RN. Assessment of GH status in acromegaly using serum growth hormone, serum insulin-like growth factor-1 and urinary growth hormone excretion. Clin Endocrinol (Oxf) 1995;42:417–423.
Earll JM, Sparks LL, Forsham PH. Glucose suppression of serum growth hormone in the diagnosis of acromegaly. JAMA 1967;201:628–630.
Lawrence AM, Goldfine ID, Kirsteins L. Growth hormone dynamics in acromegaly. J Clin Endocrinol Metab 1970;31:239–247.
Stewart PM, Smith S, Seth J, Stewart SE, Cole D, Edwards CR. Normal growth hormone response to the 75 g oral glucose tolerance test measured by immunoradiometric assay. Ann Clin Biochem 1989;26(Pt 2):205–206.
Hattori N, Shimatsu A, Kato Y, Koshiyama H, Ishikawa Y, Assadian H, Tanoh T, Nagao M, Imura H. Growth hormone responses to oral glucose loading measured by highly sensitive enzyme immunoassay in normal subjects and patients with glucose intolerance and acromegaly. J Clin Endocrinol Metab 1990;70:771–776.
Costa AC, Rossi A, Martinelli CE Jr, Machado HR, Moreira AC. Assessment of disease activity in treated acromegalic patients using a sensitive GH assay: Should we achieve strict normal GH levels for a biochemical cure? J Clin Endocrinol Metab 2002;87:3142–3147.
Chapman IM, Hartman ML, Straume M, Johnson ML, Veldhuis JD, Thorner MO. Enhanced sensitivity growth hormone (GH) chemiluminescence assay reveals lower postglucose nadir GH concentrations in men than women. J Clin Endocrinol Metab 1994;78:1312–1319.
De Marinis L, Mancini A, Bianchi A, Gentilella R, Valle D, Giampietro A, Zuppi P, Anile C, Maira G, Giustina A, Preoperative growth hormone response to thyrotropin-releasing hormone and oral glucose tolerance test in acromegaly: A retrospective evaluation of 50 patients. Metabolism 2002;51:616–621.
Levin PA, Chalew SA, Martin L, Kowarski AA. Comparison of assays for growth hormone using monoclonal or polyclonal antibodies for diagnosis of growth disorders. J Lab Clin Med 1987;109:85–88.
Reiter EO, Morris AH, MacGillivray MH, Weber D. Variable estimates of serum growth hormone concentrations by different radioassay systems. J Clin Endocrinol Metab 1988;66:68–71.
Celniker AC, Chen AB, Wert RM Jr, Sherman BM. Variability in the quantitation of circulating growth hormone using commercial immunoassays. J Clin Endocrinol Metab 1989;68:469–476.
Ebdrup L, Fisker S, Sorensen HH, Ranke MB, Orskov H. Variety in growth hormone determinations due to use of different immunoassays and to the interference of growth hormone-binding protein. Horm Res 51 (Suppl 1) 1999;20–26.
Seth J, Ellis A, Al-Sadie R. Serum growth hormone measurements in clinical practice: An audit of performance from the UK National External Quality Assessment scheme. Horm Res 51 Suppl 1999;1:13–19.
Vinik A, Pimstone B, Buchanan-Lee B. Impairment of hyperglycemic induced growth hormone suppression in hyperthyroidism. J Clin Endocrinol Metab 1968;28:1534–1538.
Becker MD, Cook GC, Wright AD. Paradoxical elevation of growth hormone in active chronic hepatitis. Lancet 1969;2:1035–1039.
Pieters GF, Smals AG, Kloppenborg PW. Defective suppression of growth hormone after oral glucose loading in adolescence. J Clin Endocrinol Metab 1980;51:265–270.
Holl RW, Bucher P, Sorgo W, Heinze E, Homoki J, Debatin KM. Suppression of growth hormone by oral glucose in the evaluation of tall stature. Horm Res 1999;51:20–24.
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Freda, P.U., Reyes, C.M., Nuruzzaman, A.T. et al. Basal and Glucose-Suppressed GH Levels Less Than 1 μg/L in Newly Diagnosed Acromegaly. Pituitary 6, 175–180 (2003). https://doi.org/10.1023/B:PITU.0000023424.72021.e2
Issue Date:
DOI: https://doi.org/10.1023/B:PITU.0000023424.72021.e2