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Letter to the Editor |
Division of Medical Sciences (J.A., M.C.S., P.M.S.), University of Birmingham, Queen Elizabeth Hospital, Birmingham B15 2TH, United Kingdom; and Department of Diabetes and Endocrinology (A.S.B.), Birmingham Heartlands and Solihull, National Health Service Trust, Birmingham B9 5SS, United Kingdom
Address all correspondence to: Professor P. M. Stewart, Division of Medical Sciences, Queen Elizabeth Hospital, Edgbaston, Birmingham, B15 2TH, United Kingdom. E-mail: p.m.stewart{at}bham.ac.uk.
To the editor:
We write in response to the commentary by Clemmons and Strasburger in the November 2004 edition of JCEM with its preference for IGF-I over GH in monitoring the response to treatment in acromegaly (1). We believe this stance contradicts the current literature. We also disagree with certain points in their critique of our recent study reporting on outcome in over 400 patients with acromegaly (2).
The criticism focuses on the lack of age-related normative data for IGF-I and the omission of IGF-I values in 59 of our 419 subjects. We believe this is preferable to relying on underpowered studies having less than half the numbers of patients and fewer deaths and employing multiple IGF-I assays (3, 4). We were quoted as saying "the use of IGF-I as a marker of effective treatment is not justified." This is incorrect; our paper merely highlighted that at present GH remains superior to IGF-I, and IGF-I should not be used as the sole marker of efficacy.
In biochemically proven, severe GH deficiency, a significant proportion of patients have IGF-I values within a normal age-related reference range (5); in addition, other non-GH dependent factors impact on IGF-I concentrations. Consequently, the presence of discordances between GH and IGF-I, particularly at cut-off values used to define "cure" in acromegaly, is no surprise.
Every large outcome study has confirmed the importance of GH excess in predicting mortality; some have reported an association with IGF-I, which is to be expected, bearing in mind its dependency in part upon underlying GH secretion, but these associations are weaker than for GH and in most cases not independent (3, 4). In the study by Holdaway et al. (4), when included in a multivariate analysis with GH, IGF-I at last follow-up was not an independent predictor of mortality.
We disagree that our results may have been biased by a difference in the proportion of patients with IGF-I measurements treated with radiotherapy vs. the entire cohort, 57% vs. 50% (P = not significant). All patients had serial GH and IGF-I measurements.
The introduction of GH receptor antagonists and advances in IGF-I assays may negate the use of GH for monitoring some patients. It is important, however, that clinicians fully appreciate the evidence base on which they treat their patients. We believe the evidence for monitoring outcome in acromegaly is currently stronger for GH than IGF-I, and the sole use of IGF-I as a marker for effective treatment is not justified.
Footnotes
A response to this letter was invited, but the authors of the original article chose not to provide one.
Received February 13, 2005.
References
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