Abstract
The alterations in thyroid function during recombinant human growth hormone (rhGH) treatment have been reported by many authors since this therapy became widely available for patients with growth hormone deficiency (GHD). Decrease of thyroxine level is the most frequent observation in patients treated with rhGH. This paper presents literature data describing changes in thyroid function related to rhGH therapy and a current explanation of mechanisms involved in this phenomenon. The effect of GH on the hypothalamic-pituitary-thyroid (HPT) axis is dependent on a multilevel regulation beginning from influence on the central axis, thyroid, and extra-thyroidal deiodinases activity as well as the impact on thyroid hormone receptors on the end. Changes in central and peripheral regulation could overlap during rhGH therapy, resulting in central hypothyroidism or an isolated slight deficiency of thyroxine. The regular monitoring of thyroid function is recommended in patients treated with rhGH and the decision of levothyroxine (L-thyroxine) supplementation should be made in the clinical context, taking into account thyroid hormone levels, as well as the chance for satisfactory growth improvement.
Highlights
The alterations in thyroid function during growth hormone (GH) therapy have been reported by many authors since the treatment with recombinant human GH became widely available for GH-deficient patients
The initial number of papers was 559, and we found 30 papers that reported thyroid hormones changes in growth hormone deficiency (GHD) patients treated with recombinant human GH (rhGH) (Table 1) [1–30]
An interesting idea was postulated recently by Ebuchi et al [29], who reported that a thyrotropin-releasing hormone (TRH) stimulation test, conducted before the initiation of growth promoting treatment, could help to identify individuals who are at risk of central hypothyroidism due to rhGH therapy and could require L-thyroxine replacement therapy
Summary
The alterations in thyroid function during growth hormone (GH) therapy have been reported by many authors since the treatment with recombinant human GH (rhGH) became widely available for GH-deficient patients. Porretti et al [13], who studied the effects of six-month rhGH replacement therapy in adults with severe GHD, both isolated and in association with other multiple deficiencies, found that GH deficit, and low IGF-1 levels, could mask central hypothyroidism in those patients They reported that in 47% of the initially euthyroid individuals without any history of thyroid dysfunction, and in 18.3% of patients diagnosed earlier with central hypothyroidism with adequate baseline L-thyroxine substitution, fT4 levels significantly decreased below the reference values. An interesting idea was postulated recently by Ebuchi et al [29], who reported that a thyrotropin-releasing hormone (TRH) stimulation test, conducted before the initiation of growth promoting treatment, could help to identify individuals who are at risk of central hypothyroidism due to rhGH therapy and could require L-thyroxine replacement therapy This method of prediction seems to be relatively expensive and not widely available. In patients with supraphysiological level of GH, goiter is reported in 55–87% [39,40] and thyroid cancer in 8.7–10.6% [41–43]
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