Diagnostic Value of Thyrotrophin-Releasing Hormone in Pituitary and Hypothalamic Diseases

Snyder, Peter J.; Jacobs, Laurence S.; Rabello, Maria M.; Sterling, Francis H.; Shore, Ronald N.; Utiger, Robert D.; Daughaday, William H.

doi:10.7326/0003-4819-81-6-751

Cited by 141 publications

(33 citation statements)

References 28 publications

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“…In vivo GHRF slightly but significantly stimulates plasma Prl in primates [4], In vitro, no Prl release from rat pituitary cells is observed [5], although at very high GHRF concentrations (1 nM) a GHRF-dose-dependent Prl release is observed with ovine pituitary cells [6]. Increase in basal plasma Prl concentrations is found in one-third of patients with pituitary or hypothalamic diseases, regardless of the cause [7,8]. Hypothalamic disorders may present with normal or elevated plasma Prl levels [7], Such an elevated plasma Prl level is almost always observed after an interrup tion of hypothalamo-pituitary communica tions [7], This study was undertaken to document plasma Prl variations after a single intrave nous bolus of GHRF in patients with growth failure due to GH deficiency, idiopathic or secondary to a brain tumor.…”

Section: Introductionmentioning

confidence: 99%

Effect of Acute Intravenous Growth Hormone-Releasing Factor on Plasma Prolactin in Short Children and Patients with Growth Hormone Deficiency

et al. 1985

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Four normal subjects and 54 growth hormone (GH)-deficient patients including 43 children with growth failure were given an intravenous bolus of growth hormone-releasing factor (GHRF). Plasma prolactin (Prl) and GH after GHRF were studied. Basal plasma Prl was either normal or elevated and could not predict the GH response to GHRF. A correlation was found, within the group with basal hyperprolactinemia, between basal Prl and the net Prl increase after GHRF. No correlation was found between the net GH and the net Prl increase after GHRF. Plasma Prl was significantly, although weakly, increased after GHRF in the normal subjects.

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Section: Introductionmentioning

confidence: 99%

Effect of Acute Intravenous Growth Hormone-Releasing Factor on Plasma Prolactin in Short Children and Patients with Growth Hormone Deficiency

et al. 1985

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“…It is reported that patients with hypothalamic lesions and IGHD often, but not invariably (Snyder et al 1974;Roitman et al 1980), show delayed and prolonged TSH responses to TRH (Hall et al 1972; Kaplan et al 1972;Faglia et al 1973;Illig et al 1975;Burger and Patel 1977;Okada et al 1978 ;Gamier et al 1983). In this study, all IGHD patients were of euthyroid state, but they showed delayed TSH responses to TRH as was seen also in 2ry GHD patients.…”

Section: Discussionmentioning

confidence: 52%

GHRH and TRH tests in patients with idiopathic and secondary GH deficiency. With special reference to GH response patterns to GHRH.

Hanew

Sugawara

Utsumi

et al. 1990

Tohoku J. Exp. Med.

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Tests in Patients with Idiopathic and Secondary GH Deficiency -With Special Reference to OH Response Patterns to GHRH . Tohoku J. Exp. Med., 1990, 160 (3), [189][190][191][192][193][194][195][196][197][198][199][200][201][202] To study whether patients with idiopathic GH deficiency (IGHD) show a delayed GH response pattern to GHRH, 42 patients with IGHD, 14 patients with hypothalamic tumor (try GHD), and 23 normal short children (NSC) were examined as to their GH response patterns to GHRH together with their TSH and PRL response patterns to TRH. After TRH injection, the mean time of the TSH peak in IGHD (67.5 + 6.5 min, n = 36) and try GHD patients (81.7± 14.8 min, n = 9) was clearly delayed comparing to that of NSC (29.1 + 2.9 min, n =16 ; both p <0.01). Similarly, the mean time of the PRL peak in IGHD (38.3 + 3.6 min, n = 36) and try GHD patients (39.5 + 5.8, n =11) was significantly delayed comparing to NSC (22.0+3.5 min, both p <0.01). In IGHD patients, the delayed response pattern of TSH and PRL was more remarkable in patients who had breech delivery than in those with normal delivery. In contrast, the mean time of the GH peak was similar in I GHD (62.1±4.0 min, n =41), try GHD (64.1± 8.1 min, n =11) and NSC (58.0± 6.1 min, n =23). However, the decline from peak GH (120 min GH/peak GH) was significantly smaller in IGHD (54.3+ 4.2%) and try GHD (60.7+7.3%) than in NSC (39.0+8.1%) (both p<0.05). Further, in IGHD patients plasma GH response was greater in patients with normal delivery than in those with breech and asphyxia delivery. These results seem to indicate : 1) the stimulus-secretion mechanism is different between somatotrophs and thyrotrophs or lactotrophs in man, 2) IGHD patients have hypothalamic lesions as well as pituitary lesions, 3) such hypothalamo-pituitary lesions in IGHD patients are greater in patients with abnormal delivery than in those with normal delivery, idiopathic GH deficiency ; GHRH ; TRH ; GII ; TSH It is known that patients with hypothalamic lesions and idiopathic growth hormone deficiency (IGHD) often show delayed TSH responses to TRH adminis-

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“…Exaggerated and/or delayed TSH responses have been interpreted as being suggestive of hypothalamic lesions in several previous studies in both adults and children [4,5,6,7,8]. However, other authors have questioned the specificity of exaggerated and/or delayed TSH responses for hypothalamic lesions and have pointed out the often artificial distinction between pituitary and hypothalamic disease [10, 13, 22,26,27,28]. In particular, a delayed TSH response has been described in a patient with a mutation of the pituitary-specific transcription factor PIT1 in whom there was no evidence of hypothalamic dysfunction [29].…”

Section: Discussionmentioning

confidence: 99%

An Evaluation of the Thyrotrophin-Releasing Hormone Stimulation Test in Paediatric Clinical Practice

Crofton

Tepper²,

Kelnar³

2007

Horm Res Paediatr

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Aim: The aim of this retrospective study was to evaluate the clinical usefulness of the thyrotropin-releasing hormone (TRH) test in children with suspected hypothalamic or pituitary dysfunction. Methods: We reviewed the case notes of all patients in whom a TRH test had been performed over a 6-year period. Group 1 (n = 85, 34 males, aged 0.9–18.8 years) was the reference group with no evidence of hypothalamic, pituitary or thyroid dysfunction. Group 2 (n = 42, 24 males, 0.1–18.0 years) were being investigated for possible pituitary or hypothalamic insufficiency. Results: In Group 1, thyrotropin (TSH) responses were higher in females than males (p < 0.01). In Group 2, TSH responses were normal for gender in 26 patients, subnormal in 5, and exaggerated/delayed in 11. Four patients with normal TSH responses and 4 with exaggerated/delayed responses had persistently low free thyroxine (FT₄) or later developed low FT₄ and were treated with thyroxine. All those with subnormal TSH responses had normal FT₄ and were not treated. The TRH test did not reliably discriminate between hypothalamic and pituitary disorders. Conclusions: The TRH test did not give useful clinical information. Clinical decisions regarding thyroxine treatment were based on FT₄, not the TRH test. The TRH test should be abandoned in paediatric practice.

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Diagnostic Value of Thyrotrophin-Releasing Hormone in Pituitary and Hypothalamic Diseases

Cited by 141 publications

References 28 publications

Effect of Acute Intravenous Growth Hormone-Releasing Factor on Plasma Prolactin in Short Children and Patients with Growth Hormone Deficiency

Effect of Acute Intravenous Growth Hormone-Releasing Factor on Plasma Prolactin in Short Children and Patients with Growth Hormone Deficiency

GHRH and TRH tests in patients with idiopathic and secondary GH deficiency. With special reference to GH response patterns to GHRH.

An Evaluation of the Thyrotrophin-Releasing Hormone Stimulation Test in Paediatric Clinical Practice

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