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J Schopohl

Publications and source records attributed to J Schopohl.

54 records · Page 3Linked to original sources
PubMed1989

Evaluation of selective transsphenoidal adenomectomy by endocrinological testing and somatomedin-C measurement in acromegaly.

A series of 29 previously untreated patients with acromegaly underwent transsphenoidal adenomectomy. Pre- and postoperative evaluation consisted of measuring growth hormone (GH) secretory dynamics during an oral glucose tolerance test (OGTT), the insulin hypoglycemia test, and the thyrotropin- and gonadotropin-releasing hormone (TRH/GnRH) test, and by obtaining the basal somatomedin-C level. After surgery, clinical and biochemical amelioration was achieved in all but two patients. In the whole group, basal GH and somatomedin-C levels decreased from a mean (+/- standard error of the mean) of 52.3 +/- 12.7 to 11.1 +/- 6.3 ng/ml and from 7.6 +/- 0.7 to 2.5 +/- 0.5 U/ml, respectively. Application of different criteria of cure revealed that 19 patients (66%) had basal GH levels below 5 ng/ml, 17 patients (59%) had normal somatomedin-C values, 16 patients (55%) had complete GH suppression (less than 1 ng/ml) during OGTT, and 13 patients (45%) met the above-mentioned criteria with disappearance of the paradoxical GH response to TRH/GnRH test. Evaluation of GH secretion by insulin hypoglycemia testing was useless in assessing the outcome after neurosurgery. When only patients with a normal somatomedin-C level and complete GH suppressibility during OGTT were considered "cured," the main favorable prognostic factor was intrasellar tumor localization, since 15 (75%) of 20 patients were "cured," as opposed to only one (11%) of nine with extrasellar extension of the adenoma. During the follow-up period, no tumor recurrence was detected in any of the "cured" patients. In these subjects somatomedin-C levels remained stable in all except two patients, who showed a slow increase within the normal range of somatomedin-C concentration. These data confirm that transsphenoidal surgery is the most effective form of treatment in previously untreated acromegalic patients and that normalization of somatomedin-C levels reflects normal GH secretion. Measurement of somatomedin-C could replace more extensive endocrinological testing during monitoring of treated acromegalic patients.

Acromegaly↗
PubMed1988

Effects of theophylline infusion on the growth hormone (GH) and prolactin response to GH-releasing hormone administration in acromegaly.

Since theophylline has been shown to blunt the GH response to growth hormone-releasing hormone (GHRH) in normal subjects, we investigated whether the same effect of theophylline administration could be reproduced in patients with active acromegaly. Ten acromegalic patients received on two different days 100 micrograms GHRH iv alone and the same GHRH dose during a constant infusion of theophylline (3.56 mg/min), beginning 2 h before GHRH administration. In the whole group theophylline did not affect basal GH secretion significantly (from a mean of 44.6 +/- 14.4 at 0 min to 41.8 +/- 13.5 ng/ml at 120 min). However, the amount of GH released after GHRH stimulation was lower when theophylline was concomitantly infused (7525 +/- 3709 ng min/ml vs. 12038 +/- 6337 ng min/ml; p less than 0.05). The inhibitory effect of theophylline was not homogeneous, since either marked or minimal reductions of the GHRH-stimulated GH secretion occurred. Serum PRL levels increased after GHRH administration in 6 patients and theophylline infusion had no influence upon this response. Peak GHRH levels were not different in both studies (14.9 +/- 1.7 and 17.1 +/- 4.0 ng/ml, respectively). Free fatty acid levels rose progressively during theophylline administration (from 0.66 +/- 0.10 at 0 min to 1.04 +/- 0.10 mEq/l at 240 min) and were significantly higher than after GHRH stimulation alone from 180 min up to the end of the test. Our results demonstrate that in active acromegaly theophylline blunts the GH response to GHRH, though this effect is not uniformly seen in all patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗
PubMed1988

Arginine stimulates growth hormone secretion by suppressing endogenous somatostatin secretion.

To determine how arginine (Arg) stimulates GH secretion, we investigated its interaction with GHRH in vivo and in vitro. Six normal men were studied on four occasions: 1) Arg-TRH, 30 g arginine were administered in 500 mL saline in 30 min, followed by an injection of 200 micrograms TRH; 2) GHRH-Arg-TRH, 100 micrograms GHRH-(1-44) were given iv as a bolus immediately before the Arg infusion, followed by 200 micrograms TRH, iv; 3) GHRH test, 100 micrograms GHRH were given as an iv bolus; and 4) TRH test, 200 micrograms TRH were given iv as a bolus dose. Blood samples were collected at 15-min intervals for 30 min before and 120 min after the start of each infusion. Anterior pituitary cells from rats were coincubated with Arg (3, 6, 15, 30, and 60 mg/mL) and GHRH (0.05, 1, 5, and 10 nmol/L) for a period of 3 h. Rat GH was measured in the medium. After Arg-TRH the mean serum GH concentration increased significantly from 0.6 to 23.3 +/- 7.3 (+/- SE) micrograms/L at 60 min. TRH increased serum TSH and PRL significantly (maximum TSH, 11.1 +/- 1.8 mU/L; maximum PRL, 74.6 +/- 8.4 micrograms/L). After GHRH-Arg-TRH, the maximal serum GH level was significantly higher (72.7 +/- 13.4 micrograms/L) than that after Arg-TRH alone, whereas serum TSH and PRL increased to comparable levels (TSH, 10.2 +/- 3.0 mU/L; PRL, 64.4 +/- 13.6 micrograms/L). GHRH alone increased serum GH to 44.9 +/- 9.8 micrograms/L, significantly less than when GHRH, Arg, and TRH were given. TRH alone increased serum TSH to 6.6 +/- 0.6 mU/L, significantly less than the TSH response to Arg-TRH. The PRL increase after TRH only also was lower (47.2 +/- 6.8 micrograms/L) than the PRL response after Arg-TRH. In vitro Arg had no effect on basal and GHRH-stimulated GH secretion. Our results indicate that Arg administered with GHRH led to higher serum GH levels than did a maximally stimulatory dose of GHRH or Arg alone. The serum TSH response to Arg-TRH also was greater than that to TRH alone. We conclude that the stimulatory effects of Arg are mediated by suppression of endogenous somatostatin secretion.

Adult↗
PubMed1988

Evidence for a nonspecific factor interfering in the radioimmunoassay of somatoliberin-like immunoreactivity in human seminal plasma.

In the present study we investigated the nature of somatoliberin-like immunoreactivity in human seminal plasma. In unextracted seminal plasma, somatoliberin-like immunoreactivity represented 3.8 micrograms/l somatoliberin, with a dilution curve that ran almost completely parallel to that of synthetic somatoliberin standard. After extraction by adsorption on hydrophobic C 18 Sep-pak cartridges or immunoaffinity chromatography, no somatoliberin-like immunoreactivity in seminal plasma could be detected. After gel permeation chromatography on a Sephadex G-50 fine column, all somatoliberin-like immunoreactivity of unextracted seminal plasma was recovered at the void volume of the column. When equal volumes of unextracted seminal plasma and radioiodinated somatoliberin were coincubated for two days at 4 degrees C, gel chromatography revealed the disappearance of the normal [125I]somatoliberin peak, replaced by a new peak eluting shortly after the total volume of the column. When unextracted seminal plasma was heated at 90 degrees C for 10 min or submitted to ultrafiltration, the interfering factor was no longer detectable. Our data show that enzymic degradation of radioiodinated somatoliberin led to misleadingly high concentrations of somatoliberin-like immunoreactivity in seminal plasma. These phenomena should therefore be considered when performing radioimmunoassays of short chain peptides in biological fluids.

Chromatography, Affinity↗
PubMed1986

Combined pituitary function-test with four hypothalamic releasing hormones.

Anterior pituitary function was investigated in ten healthy subjects by administering a combination of 200 micrograms thyrotropin releasing hormone (TRH), 100 micrograms gonadotropin releasing hormone (GnRH), 100 micrograms growth hormone releasing factor (GRF1-44), and 100 micrograms human corticotropin releasing factor (CRF). The same test protocol was performed in all subjects after pretreatment with 0.25 mg terguride. Five subjects were tested only with TRH and GnRH, five only with CRF, and six only with GRF. There was a prompt increase in all hormones after the administration of the four releasing hormones (RH). Pretreatment with terguride lowered the prolactin (PRL) increase (p less than 0.01) as well as the thyrotropin (TSH) peak (p less than 0.05) compared with the test without dopamine agonist pretreatment. The PRL levels after combined RH administration were significantly higher than after TRH and GnRH alone. Although four of the five subjects had higher TSH levels after combined RH administration than after TRH and GnRH alone, the difference was not significant. Other hormones were not significantly influenced by the combined RH administration or dopamine agonist pretreatment. Despite the fact that the interaction of the different releasing hormones and dopamine agonists influences the pituitary hormone response, combined RH administration seems to be a useful test for evaluating pituitary function also in patients receiving dopamine agonist therapy.

Adrenocorticotropic Hormone↗
PubMed1986

Corticotropin-releasing factor (CRF): stimulation in normal controls and in patients with Cushing's syndrome.

Synthetic ovine and human CRF were given as an i.v. bolus to six healthy volunteers in four and two different dosages, respectively (oCRF: 25, 50, 100 and 200 micrograms; hCRF: 50 and 100 micrograms). There was a significant increase of ACTH and cortisol after the injection of all dosages though the dose-response relationship was only significant between the 50 and 100 micrograms dose of oCRF. No significant differences between ACTH and cortisol secretion after oCRF and hCRF were observed. Repetitive stimulation by hCRF led to repetitive release of identical amounts of ACTH. The CRF test with the 100 micrograms dosage was used in patients with proven Cushing's syndrome (n = 30). Results showed that the CRF test is useful in making the differential diagnosis of established Cushing's syndrome. In patients with ACTH-dependent Cushing's disease (n = 21), normal or elevated basal ACTH levels were significantly higher after stimulation by CRF compared to normal controls, with one exception. The pattern of cortisol secretion after CRF administration corresponded to the pattern of ACTH secretion in these patients. In two patients with ectopic ACTH syndrome, extremely elevated ACTH and cortisol levels did not change or showed only a small increase after CRF administration. In patients with unilateral adrenal adenoma or carcinoma (n = 7), suppressed ACTH levels did not rise after CRF administration. In addition, no significant change in cortisol secretion could be observed. After surgical removal of cortisol-producing adrenal tumors, the ACTH response to CRF can be demonstrated when cortisol levels are still undetectable. Pulsatile administration of CRF in one patient after unilateral adrenalectomy revealed that ACTH responses to CRF normalize rapidly but cannot be sustained if CRF administration is withdrawn, suggesting that the cause of adrenal failure after unilateral adrenalectomy for Cushing's syndrome or with long-term corticoid therapy is due to hypothalamic CRF deficiency. The suppression of ACTH responses to CRF in glucocorticoid-treated patients correlated with the daily corticoid dosage. Since the ACTH hyper-response to CRF in six patients with Cushing's disease was suppressed by short-term dexamethasone treatment, the pituitary as a target site for feedback inhibition also was demonstrated.

ACTH Syndrome, Ectopic↗
PubMed1986

Intravenous application of ovine and human corticotropin releasing factor (CRF): ACTH, cortisol and CRF levels.

Synthetic ovine corticotropin releasing factor (oCRF) and human CRF were given as an intravenous bolus to 6 healthy volunteers in 4 different dosages (oCRF: 25, 50, 100 and 200 micrograms) respectively, 2 different dosages (hCRF: 50 and 100 micrograms). ACTH and cortisol were measured over a 2-hour period after CRF injection. CRF immunoreactivity was measured with a newly developed homologous radioimmunoassay for both oCRF and hCRF. All CRF dosages tested led to a definite ACTH response compared to placebo control. No dose dependency of side effects was observed. Furthermore, there was no clear-cut dose response relationship between the injected CRF dosages and the maximal ACTH- and cortisol levels. However, when the area under the ACTH and cortisol-response curves after oCRF were compared a dose-response relationship emerged, which could not be demonstrated in the same way for the two hCRF dosages. Serum CRF immunoreactivity correlated to the injected dosage. The halftime of serum disappearance for oCRF was 18 min, and hCRF, 9 min. The maximal ACTH responses after injection of oCRF and hCRF were not significantly different.

Adrenocorticotropic Hormone↗
PubMed1986

Corticotropin-releasing factor in humans. I. CRF stimulation in normals and CRF radioimmunoassay.

The biological activity of ovine (o) and human (h) corticotropin-releasing factor (CRF) in normal volunteers was investigated, using bolus injections with different CRF dosages. There was a significant increase of ACTH, beta-endorphin and cortisol after the injection of all dosages. Repetitive stimulation and continuous infusion of hCRF lead to repetitive release of identical amounts of ACTH or constant elevation of ACTH levels. oCRF and hCRF serum immunoreactivity was measured with specific radioimmunoassays after bolus injection, pulsatile administration and infusion of CRF. The half-time of serum disappearance after acute injection studies was calculated as 9 min for hCRF dand 18 min for oCRF. The 'metabolic clearance' of hCRF calculated using the infusion study was 2.72 ml/min X kg. Endogenous CRF immunoreactivity was detectable in 14 patients during insulin hypoglycemia and in 86 out of 97 pregnant females. Furthermore, CRF could be extracted from human placenta. The chromatographic pattern of extracted placenta CRF, pregnancy serum CRF and CRF standard preparation was identical. Furthermore, CRF immunoreactivity was detectable in some patients with different causes of ACTH hypersecretion.

Adrenocorticotropic Hormone↗
PubMed1986

Growth hormone-releasing hormone infusion in patients with active acromegaly.

To determine GH-releasing hormone (GHRH)-stimulated GH secretion in patients with active acromegaly, nine patients received a 50-microgram GHRH-(1-44) bolus dose followed by a 2-h infusion with 100 micrograms GHRH/h, after which a second 50-microgram GHRH bolus dose was given. Serum GH, PRL, and immunoreactive GHRH levels were measured from 2 h before to 1 h after the end of the infusion and compared with hormone levels in six normal subjects subjected to the same protocol. In addition, seven of the nine acromegalic patients received 100 micrograms GHRH as an iv bolus dose, followed by a 2-h saline infusion on a different day. After the 100-micrograms GHRH bolus dose, the mean GH level increased from 55.9 +/- 18.0 (+/- SE) to 148.5 +/- 40.0 ng/ml within 15 min. Thereafter, GH levels decreased and were significantly lower at 90 and 120 min compared to the peak level 15 min after GHRH injection. After the 50-micrograms GHRH bolus dose, all acromegalic patients except two also had a clear-cut rise of GH levels, with the mean GH level increasing from 37.5 +/- 13.2 to 108.4 +/- 55.0 ng/ml at 60 min. Thereafter, elevated GH levels were sustained in the acromegalic patients throughout the GHRH infusion. In contrast, normal subjects had a significant decrease in the initially elevated GH levels, despite continuous GHRH infusion. There were no significant differences between PRL secretion and immunoreactive GHRH levels in either group. These findings suggest that patients with active acromegaly not only have elevated basal GH levels, but also have a greater ready releasable GH pool and/or accelerated GH turnover compared to those of normal subjects, which cannot be exhausted by a 2-h GHRH infusion.

Acromegaly↗
PubMed1986

Growth hormone (GH) and prolactin responses to repetitive administration of GH-releasing hormone in acromegaly.

We investigated the pattern of GH secretion in response to repetitive GH-releasing hormone (GHRH) administration in patients with active acromegaly and in normal subjects. Twelve acromegalic patients (nine women and 3 men; aged 21-76 yr) were studied. Eight had never been treated, whereas four had undergone neurosurgery but still had active disease. All patients and eight normal subjects received three doses of 50 micrograms GHRH, iv, at 2-h intervals. Seven patients were retested 6-8 weeks after transsphenoidal removal of a pituitary adenoma. There was a marked serum GH rise in acromegalic patients and normal subjects after the first GHRH dose [area under the curve, 2070 +/- 532 (+/- SE) vs. 1558 +/- 612 ng/min X ml, respectively; P = NS]. Successive GHRH doses stimulated GH release only in acromegalic patients (second dose, 1123 +/- 421 ng/min X ml; third dose, 2293 +/- 1049 ng/min X ml). In normal subjects, the GH response to the second and third GHRH doses was blunted (second dose, 86 +/- 32 ng/min X ml; third dose, 210 +/- 63 ng/min X ml; P less than 0.01). PRL secretion did not change in normal subjects, whereas 6 of 12 acromegalic patients had PRL release after each GHRH dose (PRL responders to GHRH). Transsphenoidal surgery led to normalization (less than 5 ng/ml) of the preoperatively elevated GH levels in all but 2 patients, who, however, had reduction of somatomedin-C levels. The amount of GH released in the postoperative test was significantly lower than that released preoperatively (first dose, 722 +/- 209 vs. 2945 +/- 743 ng/min X ml; second dose, 358 +/- 117 vs. 1737 +/- 633 ng/min X ml; third dose, 320 +/- 144 vs. 1776 +/- 676 ng/min X ml, respectively; P less than 0.05 in all instances). Thus, patients with active acromegaly, but not normal subjects, respond to repetitive GHRH administration at 2-h intervals with an increase in GH levels. This increase may be due to a larger releasable GH pool and/or faster GH turnover in the adenomatous cell.

Acromegaly↗
PubMed1986

Repetitive and continuous administration of human corticotropin releasing factor to human subjects.

ACTH secretion was studied in response to repetitive and continuous administration of human corticotropin releasing factor (CRF) in 14 healthy volunteers and 2 patients with secondary adrenal insufficiency. ACTH increases during repetitive CRF administration were within the same range in normal subjects independent of the intervals (60-180 min) between the CRF pulses (100 micrograms iv). When CRF was infused continuously (100 micrograms/h for 3 h) after an initial CRF bolus injection (100 micrograms iv), ACTH and cortisol remained elevated during the infusion at a nearly constant level (ACTH: 60 +/- 5 pg/ml; cortisol: 21.2 +/- 1 micrograms/dl; means +/- SE). A second CRF bolus injection at the end of the infusion did not lead to a significant further increase of ACTH and cortisol levels. This shows that there is no desensitisation or depletion of a ready releasable pool, as it is observed with other pituitary hormones after releasing hormone stimulation. Pulsatile administration of CRF in 2 patients with secondary adrenal insufficiency due to previous cortisol or glucocorticoid excess, respectively, revealed a blunted response to the first pulse which became normal after the following pulses. The latter could not be sustained until the next morning without CRF given overnight. These findings point to a hypothalamic defect being the cause of hypocortisolism after long-term cortisol suppression.

Adrenal Insufficiency↗
PubMed1985

Corticotropin releasing factor (CRF): diagnostic implications.

Nine normal volunteers received an intravenous bolus injection of 50, 100, and 200 micrograms ovine Corticotropin releasing factor. There was no dose response relationship between the injected oCRF dosage and stimulated ACTH, beta-endorphin, and cortisol secretion. When human synthetic CRF was injected (50 and 100 micrograms i.v.) no significant difference compared to the oCRF induced ACTH stimulation was observed. In contrast to the lacking relationship between the CRF dosage and the biological response there was a clearcut dose response relationship between the amount of oCRF injected and the CRF immunoreactivity measured 15 minutes after injection with a specific oCRF radioimmunoassay. No serious side effects were observed when the 100 micrograms CRF dosage was used as standard dose in the CRF test in patients with diseases of the hypothalamo-pituitary-adrenal axis. In patients with Cushing's syndrome the CRF test is helpful for the differential diagnosis (ACTH dependent Cushing's disease, autonomous cortisol secretion due to an adrenal adenoma or carcinoma, ectopic ACTH syndrome). In addition the CRF test is of prognostic value after surgical or neurosurgical therapy of Cushing's syndrome. Furthermore secondary adrenal failure after operative therapy can be documented by the CRF test. In patients on corticoid therapy the degree of suppression of CRF induced ACTH secretion correlated to the dosage and the duration of corticoid therapy. The main suppressive effect of corticoids on the hypothalamo-pituitary-adrenal axis seems to take place at the pituitary level. In patients with secondary adrenal failure the analysis of ACTH secretion after CRF administration allows the differential diagnosis between hypothalamic and pituitary ACTH hyposecretion. In conclusion the administration of oCRF has been shown to be a well tolerated and useful tool in the differential diagnosis of the causes of hyper- and hypofunction of the hypothalamo-pituitary-adrenal axis. Though there was only 10% cross reactivity with synthetic human CRF, CRF immunoreactivity could be detected in 53 out of 55 pregnant females. The results of measuring endogenous CRF levels in patients with diseases of the hypothalamo-pituitary-adrenal axis are preliminary but endogenous CRF levels measured by the heterologous oCRF radioimmunoassay, correlated well to the clinical situation and the ACTH-levels. These results have to be verified with a homologous hCRF radioimmunoassay.

Adrenal Gland Diseases↗
PubMed1985

Growth hormone releasing factor-test in acromegaly: comparison with other dynamic tests.

Human pancreatic growth hormone releasing factor (hpGRF1-44) was given intravenously as a 100 micrograms bolus to 20 patients with active acromegaly. The GH-responses were variable, ranging from an increase of 8 to 2813% from the basal level (mean +/- SE, 428 +/- 136%). Sixteen GRF-responders (delta% greater than or equal to 100%) were arbitrarily distinguished from four GRF non-responders, whose GH-levels increased less than 100% from basal level after GRF-administration. The outcome of the GRF-test did not correlate with the results of other dynamic tests of GH-secretion in acromegaly (oral glucose tolerance test, insulin hypoglycaemia, TRH-, LHRH-, CRF-stimulation). In 10 patients who had not been treated before, the GH-increments after GRF were higher than those in seven patients who had previously been subjected to transsphenoidal surgery, though they still had clinically and biochemically active acromegaly. Ten acromegalics, who were tested with GRF, were later treated surgically by the transsphenoidal route and were reevaluated with GRF-stimulation 2 months after surgery. Eight patients appeared clinically cured of whom four had complete normalization and four had significantly lower basal and conventionally stimulated GH-levels postoperatively. These patients also had normal postoperative GH-responses to GRF, which had been significantly higher before surgery compared with normal controls. It is concluded that the GRF-test in acromegaly does not help in establishing the diagnosis. The normalization of the GH-response to GRF after transsphenoidal surgery seems to represent additional evidence for normalization of GH-secretion, though the latter is not proven by the normal outcome of this test.

Acromegaly↗
PubMed1985

Growth hormone releasing factor induces prolactin secretion in acromegalic patients but not in normal subjects.

The effect of an iv injection of growth hormone releasing factor (GRF) on Prl secretion in healthy volunteers and patients with active acromegaly was investigated. Thirteen normal subjects received 100 micrograms GRF 1-44, and 19 acromegalics received 100 micrograms GRF 1-44. Nine normals and 9 patients were given the diluent only and served as placebo control. In healthy volunteers GRF did not affect Prl secretion significantly when compared to placebo, whereas in acromegalics Prl levels after GRF were higher than after placebo. We have divided acromegalics in Prl-responders to GRF (n = 11) and Prl-non-responders (n = 8) using the criterion of strict parallelism between GH and Prl secretion after GRF. In cases with no GH response to GRF a clear increase of Prl levels with the maximum 15-30 min after GRF was also regarded as a Prl response. Acromegalic Prl-responders and Prl-non-responders did not significantly differ in age, sex, previous therapy, and basal GH and Prl levels. However, Prl-non-responders had a significantly reduced response of both GH and Prl to TRH (GH: 147.3 +/- 16.0 vs 590.1 +/- 127.8%; mean +/- SE; Prl: 159.4 +/- 32.6 vs 504.9 +/- 109.3%). It is concluded that 50 or 100 micrograms GRF does not affect Prl secretion in normal subjects. In contrast, in acromegaly GRF leads to Prl secretion in more than half of all patients.

Acromegaly↗
PubMed1984

Stimulation of growth hormone secretion with human growth hormone releasing factors (GRF1-44, GRF1-40, GRF1-29) in normal subjects.

Peptides of different chain lengths (GRF1-44, GRF1-40, GRF1-29) were given as a 50 micrograms i.v. bolus to five normal volunteers. Blood was collected before and until 120 min after GRF injection. No serious side effects were recorded. All GRF peptides led to a clearcut and significant increase of GH levels compared to placebo controls with the maximum occurring 15-30 min after GRF injection. There was no significant difference in the maximal GH increase after the different GRF peptides. When GRF1-44 was administered to five normal subjects over 2 days in 6- and 18-h intervals, respectively, significant increase of GH levels were recorded after each injection compared to placebo controls. Again, there was no significant difference between the maximal GH rises during the different tests. These findings show that the short GRF1-29 peptide may be used for diagnosis and therapy. In addition, in contrast to continuous infusion and administration of GRF in short intervals, GRF application in 6-h intervals leads to adequate GH responses.

Adult↗
PubMed1984

Growth hormone releasing factor infusion does not sustain elevated GH-levels in normal subjects.

To evaluate the dynamics of GH-secretion after infusion of growth hormone releasing factor, human pancreatic growth hormone releasing factor (hpGRF1-44) was infused over 2 and 5 h at a dosage of 100 micrograms hpGRF1-44/h into 11 healthy subjects. The infusion was started and terminated with a 50 micrograms hpGRF1-44 bolus injection. In 5 subjects 200 micrograms TRH was given 4 h after starting the infusion. In addition, 4 healthy subjects received 50 micrograms hpGRF1-44 bolus injection every 2 h. GRF, somatostatin, GH, Prl, and TSH were measured by radioimmunoassay. The initial 50 micrograms GRF bolus increased GH-levels in all 11 subjects with a maximum at 30 min (24.1 +/- 5.1 ng/ml +/- SE). However, though hpGRF1-44 was continuously infused and GFR-levels remained elevated, GH decreased to a minimum 270 min after start of infusion (2.6 +/- 0.6 ng/ml). The GH-response to the second bolus at the end of the infusion was lower compared to the first response (14.6 +/- 3.4 ng/ml after 2 h and 7.6 +/- 2.5 ng/ml after 5 h). TRH did not lead to a GH-increase during hpGRF1-44 infusion though Prl and TSH rose normally. The intermittent bolus injection of 50 micrograms hpGRF1-44 led to continuously decreasing GH-responses to the same GRF-dosage (I. bolus: 16.5 +/- 1.6 ng/ml; II. bolus: 4.2 +/- 0.8 ng/ml; III. bolus: 3.4 +/- 0.5 ng/ml). No change in somatostatin levels was observed. These findings show that GRF infusion or bolus injection in short intervals does not sustain elevated GH-levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗