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Istituto Auxologico Italiano, IRCCS Milan, Italy
We read with great interest the paper by Ross et al. (1), concerning the absence of GH effects on cognitive function in girls with Turners syndrome. In our opinion, the statement that these results are in agreement with most of the previous studies that found no apparent GH treatment effects on cognitive function in patients with GH deficiency (GHD) needs a fair degree of caution.
In fact, although GH treatment is recommended worldwide for ameliorating the final height of girls with Turners syndrome, these patients are generally not classically GH-deficient. For this reason, we believe that the absence of GH effects on cognitive function, as clearly demonstrated by Ross et al. (1) in girls with Turners syndrome (without estrogen replacement treatment), is not easily comparable with the data obtained in GHD patients, in whom GH represents the "substitution" therapy.
Furthermore, the concern by Ross et al. (1) that the presence of multiple pituitary hormonal defects in adults with GHD could have a negative impact on brain development and could potentially interfere with the results of the psychological tests is not completely justified, as the majority of clinical studies [including the only mentioned (2)] have been performed in patients receiving stable and adequate hormonal replacement therapies.
As far as the effects of GH therapy on cognitive functions in adults with GHD are concerned, Degerblad et al. (3) actually found no significant effects of GH treatment; however, they suggested that the negative results could be tentatively explained by the difficulty in optimizing the measurement of subtle changes of mood and cognitive functions, rather than by a real lack of effects exerted by GH. In a short-term study (1 month) using GH treatment, Almqvist et al. (4) demonstrated that recombinant GH was able to improve cognitive psychometric testing, in particular the face recognition test, a test primarily for evaluating memory function.
Our experience in adults with childhood-onset GHD (5, 6) showed that 6 months of GH treatment caused an overall improvement in relation to intellectual tasks, accompanied by a lower level of stress during their performance. In particular, the scores of the tasks in the nonverbal Wechsler Adult Intelligence Scale (WAIS) and in the mental arithmetic test increased significantly, while those of "sensitivity," "thought," "impulsiveness," and "anxiety" scales (evaluated using the "Experiential-World Inventory"-EWI) reduced. The finding that the psychological characteristics of patients reverted to those before treatment after stopping recombinant GH supports the GH dependence of the effects observed during treatment.
In conclusion, as also stated by Ross et al. in their interesting paper (1), we agree that cognition in girls with Turners syndrome is more probably estrogen-dependent rather than GH-dependent, as the former actually represents the main feature of the syndrome. Further additional studies, aimed at correcting the real hormonal defects, are required to understand the potential reversibility (or not) of the neurocognitive deficits observed in Turners syndrome.
Footnotes
Address correspondence to: Alessandro Sartorio, M.D., Endocrine Unit, Italian Institute for Auxology, Via Ariosto 13, 20145 Milan, Italy.
Received October 21, 1997.
References
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