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• W2023588586 abstract "J W Tomlinson and colleagues1Tomlinson JW Holden N Hills RK et al.Association between premature mortality and hypopituitarism.Lancet. 2001; 357: 425-431Summary Full Text Full Text PDF PubMed Scopus (842) Google Scholar confirm the previously reported increased mortality in adults with hypopituitarism, but their conclusions on the lack of contribution of GH deficiency to the adverse overall prognosis are not supported by their data. The study is prospective, but the investigators do not state how often pituitary function was reassessed; testing of pituitary reserve would need to be done repeatedly to uphold Tomlinson and colleagues' claim, since the patients probably had evolving endocrine deficiency patterns, especially if they had undergone radiotherapy. However, acceptable dynamic tests of GH reserve were done in only 10% of the 1014 patients; in an additional 1% the stimulus was clonidine, which is an inadequate test in adults.2Rahim A Toogood AA Shalet SM The assessment of growth hormone status in normal young adult males using a variety of provocative agents.Clin Endocrinol. 1996; 45: 557-562Crossref PubMed Scopus (143) Google Scholar In the admitted absence of data documenting GH status, Tomlinson and colleagues argue that the lack of a gradation in mortality across the range of severity of hypopituitarism, as reflected by number of additional hormone deficiencies, provides compelling evidence that GH deficiency is not a contributory mechanism to the increased overall mortality observed. This conclusion is clearly incorrect. Use of Toogood and colleagues' data3Toogood AA Beardwell CG Shalet SM The severity of growth hormone deficiency in adults with pituitary disease is related to the degree of hypopituitarism.Clin Endocrinol. 1994; 41: 511-516Crossref PubMed Scopus (202) Google Scholar to calculate the probability of severe GH deficiency (peak GH <9 mU/L) in patients with differing degrees of hypopituitarism, and application of this value to the data in Tomlinson and colleagues' table 5 shows that around 900 of the 1014 patients would have severe GH deficiency on testing. Therefore, only 69 of 1014 patients would have preservation of GH reserve but deficiency of one other pituitary hormone. The frequency of GH deficiency exceeds 95% in all patients with more than one additional deficiency. Thus the concept of gradation or cumulative risk of GH deficiency is incorrect and their argument is unsustainable. This finding should not be surprising, since the likely proportion of patients with intact GH secretion in the group with a single deficient axis is only 7%, and the power of the study falls substantially short of that required to draw conclusions on the contribution of GH deficiency to mortality. Formal power calculations done to test this hypothesis suggest that there would be only a 15% chance of observing a significant effect with this study design. We agree with Tomlinson and colleagues that previous studies have limitations that prevent clear conclusions about whether GH deficiency and increased mortality are linked. Unfortunately, their report has equal limitations and the question clearly remains open." @default.
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• W2023588586 date "2001-06-01" @default.
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• W2023588586 title "Premature mortality and hypopituitarism" @default.
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• W2023588586 doi "https://doi.org/10.1016/s0140-6736(00)05035-2" @default.
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