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Letters to the Editor |
Departments of Surgery (A.G.R.) and Endocrinology (S.M.S.), Christie Hospital NHS Trust, Manchester M20 4BX, United Kingdom
To the editor:
The question of whether acromegaly is a problem or not a problem has been passionately debated in a recent issue (1, 2). In the context of colorectal cancer, however, Jenkins and Besser (1) have perpetuated a mistaken calculation that acromegaly constitutes a high-risk group for the development of this neoplasia. It is a falsehood to believe that relative risk can be assessed by comparison with published series of screened asymptomatic nonacromeglaic patients, because there are major problems arising from lack of matched age-sex comparisons, the variability in colonoscopy completion rates, and the healthy-user factor in screened controls that underestimates disease prevalence. Moreover, the prevalence of occult cancer at screening colonoscopy is very low (less than 2%) such that calculations of relative risk in acromegaly (6- to 18-fold) are overinflated and associated with wide confidence intervals. This is simply bad comparative epidemiology. Instead, risk should be determined from population-based studies, the methodology used in all other at-risk group studies (e.g. positive family history).
There have been three population-based studies on acromegaly and cancer risk (3, 4, 5). For colon and rectal cancers combined, a meta-analysis (fixed-effect method) of these data demonstrates a pooled estimate risk ratio of 2.0 (95% confidence interval, 1.4–2.9) (full details available from authors). This is a modest risk that should be duly considered when formulating a screening colonoscopy policy for acromegalic patients. Colonoscopy is an invasive and potentially harmful investigation, and an aggressive screening strategy may be associated with escalating risks of morbidity and mortality, although potential benefits seem modest (6). Among clinical endocrinologists, we hope that Melmed’s (2) moderate position prevails and that the exaggerated risk estimates portrayed by Jenkins and Besser (1) are rapidly rejected.
Footnotes
c Address all correspondence to: Prof. Stephen M. Shalet, Department of Endocrinology, Christie Hospital NHS Trust, Wilmslow Road, Manchester M20 4BX, United Kingdom.
Received October 12, 2001.
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