Serum Thyrotropin Responses to Synthetic Thyrotropin-Releasing Hormone in Normal Children and Hypopituitary Patients. A NEW TEST TO DISTINGUISH PRIMARY RELEASING HORMONE DEFICIENCY FROM PRIMARY PITUITARY HORMONE DEFICIENCY

Foley, Thomas P.; Owings, Janice; Hayford, John T.; Blizzard, Robert M.

doi:10.1172/jci106829

Cited by 95 publications

(14 citation statements)

References 15 publications

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“…Hypothalamic lesions depleting TRH or administration of anti-TRH serum cause thyrotropin deficiency and hypothyroidism (33,34). The ontogenesis of rat hypothalamic TRH-LM is in agreement with the pattern of development of pituitary and thyroid gland activity for the secretion of thyrotropin and thyroid hormone (27).…”

Section: Methodssupporting

confidence: 61%

Ontogenetic patterns of thyrotropin-releasing hormone-like material in rat hypothalamus, pancreas, and retina: selective effect of light deprivation.

Martino¹,

Seo²,

Lernmark³

et al. 1980

Proc. Natl. Acad. Sci. U.S.A.

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ABSTRACr Recent observations have shown the presence of thyrotropin-releasing hormone-like material (TRH-LM) in rat pancreatic islets and in retina. Its immunological and biological properties are identical to those of synthetic thyrotropin-releasing hormone (thyroliberin) This communication deals with the ontogenesis of TRH-LM in rat pancreas and retina as compared to that of rat hypothalamus. Effects of sex and exposure to constant dark were also studied. Results show that asynchronous changes in the concentration of TRH-LM occur during the postnatal maturation of these tissues, presumably mediated by organ-specific control mechanisms-e.g., light affects only the accumulation of TRH-LM in the retina. TRH-LM may act as neurotransmitter in the regulation of pancreatic islet cell function and in the development of photoreception in the retina. Increases in hypothalamic TRH-LM seem to parallel the development of the pituitary-thyroid secretory activity, but the function of extrahypothalamic TRH-LM remains speculative.Thyrotropin-releasing hormone (TRH, thyroliberin) is a tripeptide that was isolated from mammalian hypothalami and characterized as pyroglutamylhistidylproline amide (1, 2). As evidenced by its name, TRH was initially considered to play a specific role in the regulation of pituitary thyrotropin secretion. Subsequently, it has been shown that TRH also stimulates pituitary prolactin and growth hormone secretion (3-5). Effects unrelated to the control of adenohypophyseal function have also been reported. These include: potentiation of behavioral excitation (6), mood elevation (7-9), stimulation of muscular activity of the intestine (10), induction of hypothermia (11), enhancement of cerebral noradrenaline turnover (12), inhibition of the electrical activity of some brain neurones (13), and potentiation of the excitatory action of acetylcholine (14). Thus, it is not surprising that significant amounts of TRH-like material (TRH-LM) have been found in areas of the central nervous system other than the hypothalamus (15)(16)(17)(18). The presence of immunoreactive (IR) and bioreactive TRH-LM has also been reported outside the central nervous system in human placenta (19,20), rat retina (21-23), frog skin (22), and rat gastrointestinal tract, including the pancreas (24-26). In the latter, the main source of TRH appears to be the islets of Langerhans (26).Although it has been speculated that TRH may act as neurotransmitter or modulator of synaptic function, its function in extrahypothalamic tissues remains unknown, as is the precise cell of origin. Because there appears to be a good correlation between the postnatal changes in hypothalamic IR-TRH content and in pituitary and serum thyrotropin concentrations (27) and because exposure to dark has been shown to reduce the METHODSAll rats were of the CD strain obtained from Charles River Breeding Laboratories. They were housed in individual cages in a temperature-controlled (19-210C) and artifically illuminated (light from 0700 to 1900) room and allowed free acces...

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Section: Methodssupporting

confidence: 61%

Ontogenetic patterns of thyrotropin-releasing hormone-like material in rat hypothalamus, pancreas, and retina: selective effect of light deprivation.

Martino¹,

Seo²,

Lernmark³

et al. 1980

Proc. Natl. Acad. Sci. U.S.A.

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“…We have reported (11) that 13 of 13 children with growth hormone (GH) deficiency without apparent TSH deficiency, 10 of 13 children with idiopathic GH deficiency plus TSH deficiency, and 1 of 5 children with GH and TSH deficiency secondary to operative procedures for craniopharyngiomas released TSH to a comparable extent as normal children after TRH injection. The interpretation of these data by our group (11) and similar data by Costom, Grumbach, and Kaplan (12) was that at least some children with apparent TSH deficiency had idiopathic hypopituitarism because an apparently normal pituitary gland was not receiving the appropriate releasing stimulus for TSH.…”

Section: Introductionsupporting

confidence: 68%

“…By (Table II). As previously reported (11) and as demonstrated in Fig. 1 Table III are obviously different than the others in respect to HPr, the data of these three were not used to calculate the mean values at each time for reasons cited above for patient S. C.…”

Section: Methodsmentioning

confidence: 99%

“…Thyrotropin-releasing hormone (TRH)1 releases thyrotropin (TSH) in vivo from the pituitaries of normal adults (1-10) and children (11,12), and most patients with idiopathic hypopituitarism (11)(12). We have reported (11) that 13 of 13 children with growth hormone (GH) deficiency without apparent TSH deficiency, 10 of 13 children with idiopathic GH deficiency plus TSH deficiency, and 1 of 5 children with GH and TSH deficiency secondary to operative procedures for craniopharyngiomas released TSH to a comparable extent as normal children after TRH injection.…”

Section: Introductionmentioning

confidence: 99%

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Human prolactin and thyrotropin concentrations in the serums of normal and hypopituitary children before and after the administration of synthetic thyrotropin-releasing hormone

Foley¹,

Jacobs²,

Hoffman³

et al. 1972

J. Clin. Invest.

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A B S T R A C T Synthetic thyrotropin-releasing hormone (TRH) was administered to normal children and hypopituitary patients in a dose of 7 jg/kg i.v. over 30-60 sec. Serum thyrotropin (TSH) and prolactin (HPr) concentrations were measured by radioimmunoassay before and at 15-min intervals for 2 hr after TRH. In 20 normal children HPr rose from a mean baseline value of 7.0±1.2 (SEM) ng/ml to a mean peak value of 39.5±5 ng/ml.In 11 patients with growth hormone (GH) deficiency without TSH deficiency, HPr values rose from a mean baseline of 3.6±0.8 ng/ml to a mean peak value of 13.9+-2.8, a significantly less peak response as compared with normal children (P < 0.005). The TSH responses to TRH, however, were statistically indistinguishable from those of normal children.In 10 patients with GH and TSH deficiency both the mean baseline HPr levels (25.0+5 ng/ml) and the mean peak HPr levels after TRH (68.5+10 ng/ml) were significantly higher (P < 0.005 and < 0.025) than those of normal children. Similar comparisons were also true for the peak TSH responses (P < 0.05). Two panhypopituitary patients released no TSH and only small amounts of HPr after TRH. After thyroid replacement therapy in eight of the patients with GH and TSH deficiency, the mean HPr baseline levels (7.6+1.0 ng/ml) and peak levels (23.3+4.6 ng/ml) after the same dose of TRH were significantly less than their pretreatment levels (P<0.001 and <0.01) and were within the range for normal children.Synthetic TRH stimulates the simultaneous release of TSH and HPr in normal children and most hypopituitary patients. When the concentrations of thyroxine (T4) and triiodothyronine (T3) are low, the levels of HPr before and after TRH are elevated. After thyroid replacement therapy, HPr levels decrease to normal.T4 and/or T3 may condition the production or effects of prolactin-inhibiting factor (PIF) activity. The TSH and HPr responses after TRH in hypopituitary patients will determine whether the primary defect resides in the pituitary or hypothalamus, but cannot delineate the hypothalamic defect as a deficiency of hypothalamic hormone production or neurohumoral transmission.

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“…TRH deficiency appears, therefore, to have been confirmed by producing chemical euthyroidism by replacement of the presumedly missing hormone. Several other patients, however, have been described who, like L. C., and K. C., had low serum thyroid hormone and low-normal basal TSH levels and normal TSH responses to a single dose of TRH (18)(19)(20)(21)(22). The marked fall in the initially subnormal TSH response to TRH in M. J., the patient with presumed pituitary insensitivity to TRH, was accompanied by rises in serum T3 and T4, but rises so small that the final levels were still subnormal.…”

Section: Discussionmentioning

confidence: 99%

Repetitive Administration of Thyrotropin-Releasing Hormone Results in Small Elevations of Serum Thyroid Hormones and in Marked Inhibition of Thyrotropin Response

Snyder¹,

Utiger²

1973

J. Clin. Invest.

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A B S T R A C T Repetitive administration of thyrotropinreleasing hormone (TRH) to human subjects was used to produce small elevations of endogenous serum triiodothyronine (T3) and thyroxine (T4) levels and thereby to determine the effect of these small elevations on the serum thyrotropin (TSH) response to subsequent doses of TRH. Each subject received 13 consecutive doses of 25 ,Ag TRH at 4-h intervals. Serum Ta, T4, and TSH levels were measured before the 1st, 7th, and 13th doses ("basal levels") and for the 4 h after each of these doses.In 10 normal subjects, the mean TSH response fell from 14.6 AU/ml after the 1st TRH dose to 6.9 and 3.0 AU/ml after the 7th, and 13th doses. These falls in TSH response were accompanied by rises in the mean basal serum Ts levels from 81 to 115 to 114 ng/100 ml (normal range, 70-150 ng/100 ml) and rises in the mean basal serum T4 from 6.7 to 8.6 to 9.5 ,Ag/lOO ml (normal range, 5-11 Ag/lOO ml).

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Serum Thyrotropin Responses to Synthetic Thyrotropin-Releasing Hormone in Normal Children and Hypopituitary Patients. A NEW TEST TO DISTINGUISH PRIMARY RELEASING HORMONE DEFICIENCY FROM PRIMARY PITUITARY HORMONE DEFICIENCY

Cited by 95 publications

References 15 publications

Ontogenetic patterns of thyrotropin-releasing hormone-like material in rat hypothalamus, pancreas, and retina: selective effect of light deprivation.

Ontogenetic patterns of thyrotropin-releasing hormone-like material in rat hypothalamus, pancreas, and retina: selective effect of light deprivation.

Human prolactin and thyrotropin concentrations in the serums of normal and hypopituitary children before and after the administration of synthetic thyrotropin-releasing hormone

Repetitive Administration of Thyrotropin-Releasing Hormone Results in Small Elevations of Serum Thyroid Hormones and in Marked Inhibition of Thyrotropin Response

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