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D. T. den Ouden, M. Kroon, P. H. Hoogland, P. H. L. M. Geelhoed-Duijvestijn, J. M. Wit, Author’s Response: The Apparent Paradox of Tall Stature with Hypopituitarism: New Insights from an Old Story, The Journal of Clinical Endocrinology & Metabolism, Volume 88, Issue 8, 1 August 2003, Pages 4001–4004, https://doi.org/10.1210/jc.2003-030836
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To the editor:
The letter of Dr. Faustini-Fustini and colleagues (1) in response to our recent article (2) in JCEM makes three interesting points. First, some additional cases with similar phenotypes are mentioned, which illustrates that the pattern of continuing growth in adulthood—in some cases resulting in gigantism—in panhypopituitary patients may be not as rare as has been previously believed. Second, an additional hypothesis is put forward to explain why some untreated patients with multiple pituitary deficiency continue to grow, whereas others do not. In addition to variability in insulin secretion and sensitivity, and sex steroid sensitivity, the authors suggest that there may also be an interindividual variation of local aromatase activity and, thus, local availability of estrogen. We agree that, indeed, this is a plausible hypothesis; however, it will be virtually impossible to prove or disprove any of these hypotheses. The third point is the unexpected finding of a low bone mineral density, despite the known effects of sex steroid deficiency on bone mineral density. We believe that the patient’s recent humerus fracture and the thoracic kyphoscoliosis indicate a decreased bone strength, whereas the normal bone mineral density indicates a normal amount of calcified bone. We hypothesize that this apparent contradiction can be explained by a slow bone turnover and remodeling that has resulted in a bone with an apparently normal bone mineral density but with a decreased strength. This is consistent with the observations that, in patients with GH deficiency, bone mineral density is not far below the mean for age when corrected for body size (3), while both osteoclastic and osteoblastic activity are decreased (4, 5). The findings in our patient may suggest that sex hormone deficiency may only result in low bone density in the presence of a normal GH secretion.
