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Enhanced plasma GH responses to simultaneous administration of TRH and GHRH in patients with primary hypothyroidism
K Hanew1, A Utsumi, A Sugawara
1Second Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
The mechanism of aberrant GH responses to TRH was indirectly evaluated in 7 patients with primary hypothyroidism. All patients showed GH response to TRH. When TRH was administered together with GHRH, the plasma GH response was much greater than after a single administration of TRH or GHRH (TRH+GHRH vs. TRH or GHRH: max. delta GH, 16.4 +/- 3.2 vs. 5.4 +/- 1.3 or 6.0 +/- 0.8 microgram/L; AUC, 1282.7 +/- 234.7 vs. 384.0 +/- 95.0 or 441.8 +/- 66.2, both P < 0.01). The combined administration of TRH and GHRH caused an additive, but not a synergistic, GH response. In contrast, 8 normal subjects showed neither any plasma GH response to TRH nor enhancement by TRH of GHRH-induced GH response following combined administration. It is concluded that the sites of action of TRH seemed to be different from GHRH in patients with primary hypothyroidism.
The mechanism of aberrant GH responses to TRH was indirectly evaluated in 7 patients with primary hypothyroidism. All patients showed GH response to TRH. When TRH was administered together with GHRH, the plasma GH response was much greater than after a single administration of TRH or GHRH (TRH+GHRH vs. TRH or GHRH: max. delta GH, 16.4 +/- 3.2 vs. 5.4 +/- 1.3 or 6.0 +/- 0.8 microgram/L; AUC, 1282.7 +/- 234.7 vs. 384.0 +/- 95.0 or 441.8 +/- 66.2, both P < 0.01). The combined administration of TRH and GHRH caused an additive, but not a synergistic, GH response. In contrast, 8 normal subjects showed neither any plasma GH response to TRH nor enhancement by TRH of GHRH-induced GH response following combined administration. It is concluded that the sites of action of TRH seemed to be different from GHRH in patients with primary hypothyroidism.
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