The Response of Thyrotropin and Triiodothyronine to Various Doses of Thyrotropin Releasing Hormone in Normal Man
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Abstract. The relationship between serum thyrotropin (TSH) and serum triiodothyronine (T 3 ) before and after injection of different doses of thyrotropin releasing hormone (TRH), given as single injections or as multiple injections with short intervals, was investigated in normal men. A positive correlation between prestimulated serum TSH and serum T 3 levels and between the increase in the serum TSH and the serum T 3 levels after TRH was found when repeated tests were performed in the same individual. There was a dose dependent TSH and T 3 response to TRH. The smallest dose that produced a maximal response of both TSH and T 3 was only 30 μg TRH. After six injections of 30 μg TRH with an interval of 30 minutes the increase in TSH was two times and the increase in T 3 was three times as high as the maximal increase after single injections of TRH. This test with multiple injections of TRH may prove to be of clinical value in the measurement of both pituitary and thyroid function in selected patients. The close positive correlation between the serum TSH and serum T 3 levels in basal conditions, demonstrated in four normal subjects in this study, probably reflects the steady state level determined by the hypothalamus from which the feedback control of TSH secretion operates.Keywords:
TRH stimulation test
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Abstract. The relationship between serum thyrotropin (TSH) and serum triiodothyronine (T 3 ) before and after injection of different doses of thyrotropin releasing hormone (TRH), given as single injections or as multiple injections with short intervals, was investigated in normal men. A positive correlation between prestimulated serum TSH and serum T 3 levels and between the increase in the serum TSH and the serum T 3 levels after TRH was found when repeated tests were performed in the same individual. There was a dose dependent TSH and T 3 response to TRH. The smallest dose that produced a maximal response of both TSH and T 3 was only 30 μg TRH. After six injections of 30 μg TRH with an interval of 30 minutes the increase in TSH was two times and the increase in T 3 was three times as high as the maximal increase after single injections of TRH. This test with multiple injections of TRH may prove to be of clinical value in the measurement of both pituitary and thyroid function in selected patients. The close positive correlation between the serum TSH and serum T 3 levels in basal conditions, demonstrated in four normal subjects in this study, probably reflects the steady state level determined by the hypothalamus from which the feedback control of TSH secretion operates.
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TRH stimulation tests (n = 1109) were performed on 1061 ambulatory and 43 hospitalized patients with varying thyroid status, using a TSH immunochemiluminometric assay with third and fourth generation sensitivity characteristics (functional sensitivity, 0.01 and 0.001 mU/L, respectively). TRH test results were analyzed as both absolute (stimulated minus basal TSH) and fold (stimulated/basal TSH) responses. The absolute TRH response varied 8-fold across the physiological TSH range, whereas the mean fold response remained almost constant (mean +/- SEM, 8.5 +/- 0.2). The fold response became progressively attenuated as basal TSH values declined below physiological levels, becoming essentially absent in clinically thyrotoxic patients with markedly depressed basal serum TSH levels (0.007 +/- 0.002 mU/L). Progressive attenuation also occurred at hypothyroid TSH levels; a markedly impaired fold response (2.5 +/- 0.4) was characteristic of primary hypothyroid patients with basal TSH values greater than 50 mU/L. In untreated central hypothyroid patients with near-normal basal TSH levels, the TRH fold response was impaired (1.7 +/- 0.2), whereas in T4-replaced central hypothyroid patients, fold responses were near normal (5.6 +/- 1.2). Neither nonthyroidal illness, age, or sex appeared to influence the pattern of fold TRH response in the populations evaluated. When using third and fourth generation TSH methodology, the TRH-stimulated TSH fold response is more diagnostically useful than the absolute TRH response. However, if patients have an intact hypothalamic-pituitary axis, there appears to be no diagnostic advantage gained by TRH testing over an accurately measured basal TSH value.
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Twenty-three euthymic alcoholics in medium- and long-term abstinence were studied as were 20 healthy controls. All underwent a Thyrotropin Releasing Hormone/Thyrotropin Stimulating Hormone (TRH/TSH) stimulation test. Ninety per cent of medium-term abstinent and 100 per cent of long-term abstinent alcoholics had a response within the normal range. However, overall, the TSH responses to TRH were significantly less than in controls. Our study suggests that while there is some improvement in TRH/TSH responses in long-term abstinent patients, there is still evidence of hypo function in those over 1 year alcohol-free.
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In order to gain insight into the neuroendocrine mechanism underlying the paradoxical GH response to TRH in acromegalic patients, we have investigated the effect of an infusion of Naloxone (Nal, 1.6 mg/hr for two hours), on a TRH test performed both in responder (n = 9) and non-responder (n = 5) acromegalic patients. The response of GH, PRL and TSH to TRH injection were evaluated. NAL did not exert significant variations in the GH response, even if different patterns of GH response during NAL were observed in the group of TRH-responder patients. Similarly, TRH-induced PRL response was not significantly affected by the infusion of an opiate antagonist. On the contrary, a significant inhibition of the TSH response was observed in the group of TRH-responder patients (delta TSH after TRH 4.76 +/- 1.11 microU/ml, after NAL + TRH 2.81 +/- 0.99 microU/ml, p < 0.05). No significant effects were observed in the TRH non-responder patients (delta TSH after TRH 4.58 +/- 1.44 microU/ml, after NAL + TRH 6.26 +/- 3.27 microU/ml). The differences observed in the two groups of patients could be ascribed to a different endogenous somatostatinergic tone and could furnish a prognostic indication in acromegalic patients.
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Effects of growth hormone-releasing hormone (GRH) and corticotropin-releasing hormone (CRH) on the release of immunoreactive thyrotropin-releasing hormone (ir-TRH) from the rat hypothalamus in vitro were studied. The rat hypothalamus was incubated in medium 199 with 1.0 mg/ml of bacitracin (pH 7.4) for 20 min. The amount of ir-TRH release into the medium was measured by radioimmunoassay. The ir-TRH release from the rat hypothalamus was inhibited significantly in a dose-related manner with the addition of GRH or CRH. These findings suggest that GRH and CRH inhibit ir-TRH release from the rat hypothalamus in vitro.
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Abstract. The relationship between serum thyrotropin (TSH) and serum triiodothyronine (T3) before and after injection of different doses of thyrotropin releasing hormone (TRH), given as single injections or as multiple injections with short intervals, was investigated in normal men. A positive correlation between prestimulated serum TSH and serum T 3 levels and between the increase in the serum TSH and the serum T3 levels after TRH was found when repeated tests were performed in the same individual. There was a dose dependent TSH and T3 response to TRH. The smallest dose that produced a maximal response of both TSH and T3 was only 30 ug TRH. After six injections of 30 ug TRH with an interval of 30 minutes the increase in TSH was two times and the increase in T3 was three times as high as the maximal increase after single injections of TRH. This test with multiple injections of TRH may prove to be of clinical value in the measurement of both pituitary and thyroid function in selected patients. The close positive correlation between the serum TSH and serum T3 levels in basal conditions, demonstrated in four normal subjects in this study, probably reflects the steady state level determined by the hypothalamus from which the feedback control of TSH secretion operates.
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Different variants of a solid phase TSH radioimmunoassay method (having optimal precision at different S-TSH levels) were investigated for their capability in predicting an S-TSH response to TRH from the basal S-TSH levels. Sera from 283 patients with, or suspected of having a thyroid disorder, were tested. There was a highly significant correlation between the basal S-TSH level and the increase of S-TSH after TRH for a group of individuals with normal S-TSH levels. The best discrimination of responders to TRH from non-responders was obtained with a TSH assay method with prolonged preincubation (144 h) of serum specimens and antibody. With this method assay of the basal S-TSH level was found to be useful in predicting an S-TSH response to TRH in untreated patients suspected of having hyperthyroidism.The assay offers a less expensive diagnostic alternative to the TRH test in this clinical situation. We demonstrated the effect of varying the weight of the ratio of false positive to false negative results on the optimal decision level.The basal S-TSH level should be measured by different variants of the assay method whether this is used in the diagnosis of hyper- or hypothyroidism.
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A study was carried out in 10 patients with multiple pituitary hormone deficiencies to determine the response of thyroid-stimulating hormone (TSH) and prolactin (PRL) to thyrotropin-releasing hormone (TRH) and their suppressibility by treatment with triiodothyronine (T3) given at a dose of 60 µg/day for 1 week. In 3 patients the basal TSH values were normal and in 7 patients, 2 of whom had not received regular thyroid replacement therapy, they were elevated. The response of TSH to TRH was normal in 6 patients and exaggerated in 4 (of these, 1 patient had not received previous substitution therapy and 2 had received only irregular treatment). The basal and stimulated levels of TSH were markedly suppressed by the treatment with T3. The basal PRL levels were normal in 7 and slightly elevated in 3 patients. The response of PRL to TRH stimulation was exaggerated in 2, normal in 6 and absent in 2 patients. The basal PRL levels were not suppressible by T3 treatment but in 4 patients this treatment reduced the PRL response to TRH stimulation. From these findings the following conclusions are drawn: (1) T3 suppresses TSH at the pituitary level, and (2) the hyperreactivity of TSH to TRH and the low set point of suppressibility are probably due to a lack of TRH in the type of patients studied.
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Abstract Serum free T4, free T3 and TSH (IRMA), along with TSH responsiveness to TRH (500 μg i.v.), were investigated in 12 patients, initially when severely depressed and again upon recovery, and in a group of age‐matched controls. The TSH response to TRH did not differ significantly between patients and controls, nor did it alter with treatment of depression. There were no significant differences in basal TSH levels. Free T3 levels were very significantly lower in untreated patients than in controls ( p = 0·004), as were free T4 levels ( p = 0·02), and had not improved significantly at recovery. Basal TSH levels showed a strong association with the integrated TSH response to TRH ( p < 0·001) in both patients and controls. Thus in depression, as in thyoid dysfunction, the TRH test can be abandoned in favour of sensitive basal TSH measurement but, more importantly, the TRH test has no value in the diagnosis of endogenous depression or in monitoring treatment response. However, there is a reduction in free thyroid hormone levels in depression which has not been rectified by the time of clinical recovery.
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The clinical usefulness of the measurement of basal TSH by an ultrasensitive assay (IRMA) versus the TRH test has been challenged in 49 children treated with L-thyroxine. They were given suppressive or replacement therapy depending on the underlying disease. An absent response of TSH to TRH could be predicted from a basal TSH value less than 0.1 mU/l in 88.8% of the cases, while only in 77.7% from a basal TSH value = 0.1 mU/l. A basal TSH value found in the range of the normal children always predicted a normal TRH test. We conclude that a sensitive TSH assay has some clinical application in monitoring L-thyroxine therapy, but can not absolutely replace the TRH test.
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