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Biomedical subjects

J Schopohl

Publications and source records attributed to J Schopohl.

At least 37 records · Page 2Linked to original sources
PubMed1994

Olfactory function in patients with hypogonadotropic hypogonadism: an all-or-none phenomenon?

Hypogonadotropic hypogonadism (HH) refers to an endocrine defect of hypothalamic origin resulting in gonadal hypoplasia and frequently associated with anosmia or severely impaired olfactory function (Kallmann's syndrome). This apparently results from a disruption in the migration of neurons from the olfactory placode to the bulb and hypothalamus early in development, and so provides a unique opportunity to investigate olfactory function in human subjects with congenitally incomplete peripheral systems. Olfactory performance in 37 HH patients and 37 age-matched controls was compared using a modified version of the Munich Olfaction Test. This test is based on the sniff-bottle method and includes tests of (i) odor quality discrimination, (ii) intensity discrimination, (iii) detection thresholds, and (iv) recognition, hedonic evaluation and identification ability. The patients could be divided into two distinct groups differing significantly on all four subtests and showing no overlap in performance: 20 anosmics, conforming to Kallmann's syndrome, and 17 apparent normosmics whose performance was slightly poorer, but not significantly different to that of the controls. The unexpected failure to find a continuum of olfactory dysfunction now raises the question whether HH with or without anosmia represents two syndromes with distinct etiologies, or rather reflects the ability of the olfactory system to function well despite morphological impairment.

Adult↗
PubMed1994

Kallman syndrome versus idiopathic hypogonadotropic hypogonadism at MR imaging.

PURPOSE: To identify morphologic differences between Kallman syndrome (KS) and idiopathic hypogonadotropic hypogonadism (IHH) and establish a role for magnetic resonance (MR) imaging in these disorders. MATERIALS AND METHODS: Twenty-eight patients were compared with 10 eugonal male volunteers. Eighteen patients had KS (hypogonadotropic hypogonadism with anosmia) and 10 had IHH. All participants underwent hormone analysis, a sniff-bottle smell test, and gadolinium-enhanced MR imaging. Changes in the hypothalamic-hypophyseal region and the rhinencephalon were evaluated. RESULTS: MR imaging revealed intracranial morphologic changes in all patients on plain T1-weighted sections. Seventeen patients with KS demonstrated aplasia of an olfactory bulb; one olfactory sulcus was absent in six, rudimentary in four, and normal in eight. Olfactory bulbs were present in all 10 IHH patients and three showed one slightly hypoplastic bulb. Ten patients with KS and three with IHH showed an enlarged paranasal sinus system. Further MR findings were similar. CONCLUSION: MR imaging demonstrates abnormalities of the rhinencephalon present in KS patients and occasionally absent in IHH patients.

Adult↗
PubMed1994

In man the mu-opiate agonist loperamide specifically inhibits ACTH secretion induced by the cholecystokinin-like peptide ceruletide.

Ceruletide, a cholecystokinin-8-like peptide, was recently reported to stimulate ACTH secretion in man. The aim of this study was to investigate the effect of the mu-opiate agonist, loperamide, and the opiate antagonist, naloxone, on ceruletide-induced ACTH secretion in man. In 6 normal subjects, basal ACTH and cortisol plasma levels were significantly suppressed 3 h after loperamide administration (16 mg, orally) from 5 +/- 0 to 2 +/- 0 pmol/l and from 356 +/- 44 to 154 +/- 16 nmol/l. After stimulation with 8 ng ceruletide/kg body weight/min over a period of 5 min, the maximum ACTH levels (at 7.5 min) were significantly reduced by loperamide from 26 +/- 7 to 6 +/- 1 pmol/l and the maximum cortisol levels (at 30 min) were significantly reduced from 676 +/- 47 to 392 +/- 58 nmol/l. Furthermore, the ACTH peak (delta = 7.5 min) was significantly blunted by loperamide from 21 +/- 7 to 5 +/- 1 pmol/l and the integrated area under the curve from 0 to 120 min (delta AUC) of ACTH was significantly reduced from 40 +/- 11 to 14 +/- 4 pmol x 120 min/l. The cortisol peak (delta = 30 min) and the AUC of cortisol were not significantly diminished. The suppressive effect of loperamide on basal and ceruletide-induced ACTH and cortisol secretion was completely reversed by the administration of 0.8 mg naloxone, 20 min before and during infusion of ceruletide. The administration of naloxone itself had no significant effect on ACTH or cortisol levels. In conclusion, ACTH is released by peripherally administered ceruletide within a short period.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1994

Growth hormone (GH)-releasing peptide stimulation of GH release from human somatotroph adenoma cells: interaction with GH-releasing hormone, thyrotropin-releasing hormone, and octreotide.

The synthetic hexapeptide GH-releasing peptide (GHRP; His-D-Trp-Ala-Trp-D-Phe-Lys-NH2) specifically stimulates GH secretion in humans in vivo and in animals in vitro and in vivo via a still unknown receptor and mechanism. To determine the effect of GHRP on human somatotroph cells in vitro, we stimulated cell cultures derived from 12 different human somatotroph adenomas with GHRP alone and in combination with GH-releasing hormone (GHRH), TRH, and the somatostatin analog octreotide. GH secretion of all 12 adenoma cultures could be stimulated with GHRP, whereas GHRH was active only in 6 adenoma cultures. In GHRH-responsive cell cultures, simultaneous application of GHRH and GHRP had an additive effect on GH secretion. TRH stimulated GH release in 4 of 7 adenoma cultures; in TRH-responsive cell cultures there was also an additive effect of GHRP and TRH on GH secretion. In 5 of 9 adenoma cultures investigated, octreotide inhibited basal GH secretion. In these cell cultures, GHRP-induced GH release was suppressed by octreotide. In 5 of 5 cases, the protein kinase-C inhibitor phloretin partly inhibited GHRP-stimulated GH release, but not basal GH secretion. In summary, GH secretion was stimulated by GHRP in all somatotroph adenomas investigated, indicating that its unknown receptor and signaling pathway are expressed more consistently in somatotroph adenoma cells than those for GHRH, TRH, and somatostatin. Our data give further evidence that GHRP-stimulated GH secretion is mediated by a receptor different from that for GHRH or TRH, respectively, and that protein kinase-C is involved in the signal transduction pathway. Because human somatotroph adenoma cell cultures respond differently to various neuropeptides (GHRH, TRH, somatostatin, and others), they provide a model for further investigation of the mechanism of action of GHRP-induced GH secretion.

Adenoma↗
PubMed1993

Pulsatile gonadotrophin releasing hormone versus gonadotrophin treatment of hypothalamic hypogonadism in males.

In this study, pulsatile gonadotrophin releasing hormone (GnRH) therapy and gonadotrophin therapy were compared for male patients with idiopathic hypothalamic hypogonadism. Thirty-six patients, 19 with this condition, and 17 with Kallmann's syndrome, were included in the study. Their mean age was 21.1 +/- 3.0 years (+/- SD). They were divided into two groups of similar age, number and testicular volume. Pulsatile GnRH therapy was started with 4 micrograms GnRH s.c. every 2 h using a portable pump and gonadotrophin therapy with weekly i.m. injections of 3 x 2500 IU human chorionic gonadotrophin (HCG). After 8-12 weeks of HCG treatment, 150 IU human menopausal gonadotrophin (HMG) 2-4 times weekly were added and the dose of HCG reduced if necessary. Testosterone concentrations increased significantly more (P < 0.03) in the gonadotrophin group than in the GnRH group (22.5 +/- 8.1 versus 16.8 +/- 5.5 nmol/l). The rise in oestradiol levels was also significantly higher (P < 0.001) in the gonadotrophin group than in the GnRH group (150 +/- 70 versus 88 +/- 59 pmol/l). Five patients developed gynaecomastia during gonadotrophin therapy. An increased testicular volume (TV) occurred more rapidly (P < 0.001) and was significantly more pronounced (P < 0.001) after GnRH therapy (delta TV = 8.1 +/- 2.0 ml) than with gonadotrophins (delta TV = 4.8 +/- 1.8 ml). Sperm counts were performed in 14 patients given GnRH and in 17 patients given gonadotrophins. Ten patients given GnRH had positive sperm counts, ranging from 1.5 to 14 x 10(6) spermatozoa/ml; eight of those given gonadotrophins also developed spermatogenesis (2-26 x 10(6)/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Chorionic Gonadotropin↗
PubMed1993

Immunoreactive inhibin in human follicular fluid in an ovarian hyperstimulation programme for in vitro fertilization: correlations and different forms.

UNLABELLED: The inhibin concentration in 131 samples of human follicular fluid obtained from 31 women undergoing ovarian hyperstimulation for in vitro fertilization was measured using specific double antibody radioimmunoassay. We used the synthetic 1-32-alpha-inhibin as standard and radioiodinated 1-32-Tyr-alpha-inhibin as tracer. Antibodies were raised in rabbits by immunization with the synthetic peptide. Estradiol and progesterone concentrations were measured using commercial radioimmunoassays. RESULTS: The inhibin concentration correlated with the estradiol (r = 0.57, N = 88, p < 0.0001) and progesterone (r = 0.82, N = 88, p < 0.0001) concentrations in human follicular fluid. The dosage of human menopausal gonadotropin given to individual patients correlated with the average inhibin concentration measured in their follicles (r = 0.72, N = 23, p < 0.0001). Similarly, the size of follicles correlated with their inhibin content (r = 0.75, N = 131, p < 0.0001). Nineteen samples of human follicular fluid originating from follicles of different size and volume were examined using gel-chromatography. In each human follicular fluid the main form of inhibin (32 kDa) was recovered. In small follicles (3 ml) we found 12.8 +/- 9.1% (mean +/- SD) of the whole immunoreactive inhibin eluting in the area of Vo (> or = 80 kDa). In the larger follicles (4-7 ml), however, only 4.4 +/- 4.2% of this large inhibin form could be found. CONCLUSIONS: Our data confirm that human menopausal gonadotropin stimulates ovarian inhibin production. In addition to the estradiol and progesterone concentrations, the inhibin concentration may be an index of granulosa cell function and follicular maturation. The occurrence of large molecular weight forms of inhibin in small follicles remains unclear. They may represent large precursor molecules which are proteolytically cleaved in more mature follicles.

Adult↗
PubMed1991

Growth-hormone releasing hormone in a bronchial carcinoid.

The case is reported of a 43-year-old patient with a peripherally located bronchial carcinoid tumor containing large amounts of immunoreactive and bioactive growth-hormone releasing hormone (GHRH). Because no GHRH was found in the peripheral circulation, there was no quantitative or qualitative derangement of growth-hormone secretion. The tumor was excised completely by thoracotomy.

Adult↗
PubMed1991

Long-term treatment with SMS 201-995 in resistant acromegaly: effectiveness of high doses and continuous subcutaneous infusion.

Seventeen patients (8 women and 9 men) resistant to all other forms of therapy were treated with the somatostatin analogue SMS 201-995 (octreotide, Sandostatin). The duration of treatment ranged from 1 to 5 years. Mean GH levels of only 4 patients were suppressed under 5 micrograms/L during an 8 h serum profile with the standard dose of 0.1 mg 2 or 3 times daily. This standard dose suppressed mean GH levels in 10 other patients more than 50% of baseline, but for optimal effect higher doses up to 1.5 mg, 4 daily injections or continuous subcutaneous infusion (CSI) were needed. Octreotide had no influence on GH secretion in 3 patients. Suppression of mean GH levels under 5 micrograms/L was achieved in 10 patients. Normalization of insulin-like growth factor I (IGF-I) occurred in only 5 patients. Altogether, therapy with SMS 201-995 reduced GH levels from 23.8 +/- 32.2 micrograms/L (mean +/- SD) to 6.7 +/- 5.0 micrograms/L by 71.8% and IGF-I levels from 7.9 +/- 3.1 U/ml to 3.2 +/- 1.6 U/ml by 59.5%. We conclude that 1) treatment with SMS 201-995 in patients resistant to other forms of therapy may be less successful than previously reported for heterogenous groups of patients; 2) the dose regimen must be adapted to the individual patient for optimal effect and most of our patients needed higher doses than 300 micrograms daily; 3) 4 or maybe more daily injections or CSI seem to be most effective; and 4) in a minority of patients SMS has no influence on GH-secretion.

Acromegaly↗
PubMed1991

Plasma growth hormone (GH)-releasing hormone levels in patients with lung carcinoma.

OBJECTIVE: The aim was to investigate the serum levels of growth hormone releasing hormone and GH in patients with lung carcinoma. DESIGN After an overnight fast a plasma sample was collected for determination of growth hormone releasing hormone and GH. PATIENTS: The investigation was performed in 28 patients with non small cell lung carcinoma, in 44 patients with small cell lung carcinoma, and 10 patients with non malignant lung disease. A group of 37 normal subjects served as control. MEASUREMENTS: Growth hormone releasing hormone and GH were determined by radioimmunoassay. RESULTS: Patients with small cell lung carcinoma showed higher plasma growth hormone releasing hormone levels (49 +/- 9.4 ng/l) than control subjects (16.3 +/- 2.1 ng/l; P less than 0.05), patients with non small cell lung carcinoma (23.9 +/- 8.8 ng/l; P less than 0.05), and patients with non malignant lung disease (12.7 +/- 5.5; P less than 0.05). Basal GH level was lower than 5 micrograms/l in all patients except five patients with small cell lung carcinoma and one patient with non small cell lung carcinoma. CONCLUSIONS: The higher plasma growth hormone releasing hormone levels in patients with small cell lung carcinoma compared to normal controls and patients with non small cell lung carcinoma and patients with non malignant lung disease, confirm the frequent neuroendocrine activity of this particular tumour.

Adult↗
PubMed1991

Nocturnal asthma. Beta 2-adrenoceptors on peripheral mononuclear leukocytes, cAMP- and cortisol-plasma concentrations.

To evaluate pathophysiologic mechanisms of the predominantly nocturnal complaints in atopic bronchial asthma, the expression and function of beta 2-adrenoceptors on peripheral mononuclear leukocytes (pMNL), the cAMP--as well as the cortisol--plasma concentrations were studied in eight healthy men and ten so far untreated male asthmatic patients at 4-h intervals for 24 h. No difference was seen in the beta 2-adrenoceptor density (Bmax) on pMNL between healthy and asthmatic men (24-h means +/- SE: 908 +/- 59 sites per cell and 821 +/- 54 sites per cell, respectively). The equilibrium dissociation constant (Kd), however, was significantly higher in the asthmatic patients (24-h mean +/- SE: 8.8 +/- 1.2 pmol/L vs 3.0 +/- 0.2 pmol/L in healthy men, p less than 0.0001), which is equivalent to a lower affinity of the beta 2-adrenoceptors for the radioligand 125iodocyanopindolol. Bmax showed a statistically significant circadian variation, but Kd did not. The circadian variation in Bmax was reflected in the basal intracellular cyclic adenosine-monophosphate (cAMP) content of the cells investigated. High Kd values (equivalent to low receptor affinities) tended to be associated with small increases of the intracellular cAMP content after in vitro stimulation by 10(-7) mol/L isoprenaline (isoproterenol) (24-h mean +/- SE: 1.4 +/- 0.2 pmol/10(6) cells; r = -0.529, p = 0.05 at r = -0.549, n = 10). Plasma cAMP concentrations were found to be significantly lower in the asthmatic patients (24-h means +/- SE: 22.9 +/- 1.3 nmol/L vs 29.1 +/- 1.1 nmol/L, p less than 0.0001). Plasma cortisol concentrations were significantly higher in the asthmatic patients (24-h means +/- SE: 0.500 +/- 0.084 mumol/L vs 0.319 +/- 0.063 mumol/L). The results support the hypothesis that a lesion of the beta-adrenergic system contributes to the pathophysiology of atopic bronchial asthma. In the patients investigated in this study, such a lesion could be demonstrated in the affinity rather than in the number of beta 2-adrenoceptors expressed on peripheral cells of the immune system (pMNL). According to present-day knowledge of adrenergic effects on pMNL, such an affinity decrease of beta 2-adrenoceptors could account for overshooting immune responses. In association with other factors influencing respiratory function, it could be responsible for the predominantly nocturnal complaints in atopic bronchial asthma. Plasma cortisol concentrations did not appear to be related to the principal cause of "nocturnal asthma;" they rather reflected an endogenous defense mechanism to the disease.

Adult↗
PubMed1991

Comparison of gonadotropin-releasing hormone and gonadotropin therapy in male patients with idiopathic hypothalamic hypogonadism.

OBJECTIVE: To compare pulsatile gonadotropin-releasing hormone (GnRH) therapy with gonadotropin therapy in male patients with idiopathic hypothalamic hypogonadism. DESIGN: Prospective study. Patients had free choice between the two forms of therapy. SETTING: Patients were treated on an outpatient basis in our department. PATIENTS: Eighteen patients of matched age (mean [+/- SD] age: 21.1 +/- 3.0 years and 23.6 +/- 7.3 years) and similar testicular volume were treated in each group. INTERVENTIONS: Pulsatile GnRH therapy was started with 4 micrograms GnRH subcutaneously every 2 hours using a portable pump and gonadotropin therapy with 3 x 2,500 IU human chorionic gonadotropin (hCG) weekly injected intramuscularly. After 8 to 12 weeks of hCG treatment, 150 IU human menopausal gonadotropin two to four times weekly were added. RESULTS: Testosterone (T) and estradiol (E2) levels increased significantly higher (T: P less than 0.03; E2; P less than 0.001) in the gonadotropin group than in the GnRH group (T: 22.5 +/- 8.1 versus 16.8 +/- 5.5 nmol/L; E2: 150 +/- 70 versus 88. +/- 59 pmol/L). Five patients developed gynecomastia during gonadotropin therapy. The rise of testicular volume was significantly more pronounced (P less than 0.001) in the GnRH group (delta testicular volume = 8.1 +/- 2.0 mL) than in the gonadotropin group (delta testicular volume = 4.8 +/- 1.8 mL). Ten patients of the GnRH and 8 of the gonadotropin group had positive sperm counts, ranging from 1.5 to 26 x 10(6) spermatozoa/mL. The latter was achieved more rapidly in the GnRH group (12 +/- 1.6 versus 20 +/- 2.3 months: P less than 0.02). CONCLUSIONS: Endocrine and exocrine testicular function can be normalized by both forms of therapy. Gonadotropin therapy has more side effects. Gonadotropin-releasing hormone leads to a higher testicular volume and a more rapid initiation of spermatogenesis compared with gonadotropin therapy.

Adult↗
PubMed1990

[Morphology and clinical picture of thymus carcinoid].

A large mediastinal tumour was discovered radiologically in a 50-year-old man, with at times blood-tinged sputum and dyspnoea. Parasternal needle biopsy revealed a thymic carcinoid. After surgical excision of the tumour, which had argyrophilic foci (total weight of tumour 1,605 g), histochemical analysis demonstrated neuron-specific enolase, synaptophysin and chromogranin, as well as calcitonin (as the only hormone). For the first time in a thymic carcinoid, radioimmunoassay demonstrated growth-hormone-releasing hormone (2 micrograms/g tumour tissue). Post-operative radiotherapy (total dosage 50.5 Gy) was instituted because histological examination had shown invasion of the capsule and blood vessels. There has been no local recurrence or metastases after three years.

Biopsy, Needle↗
PubMed1990

Presence of growth hormone-releasing hormone-like immunoreactivity in human tumors: characterization of immunological and biological properties.

The distribution and physical and biological properties of GH-releasing hormone-like immunoreactivity (GHRH-IR) in human tissues and tumors was investigated using a specific GHRH RIA, gel chromatography, immunoaffinity chromatography, and bioassay with cultured rat anterior pituitary cells. Variable concentrations of GHRH-IR, ranging from 1.4-39.0 ng/g wet wt, were found in normal liver, lung, placenta, and pancreas. In the latter tissue, however, a different chromatographic profile and a marked decrease in GHRH-IR after immunoaffinity occurred, suggesting that GHRH-IR in pancreatic extracts is not native GHRH. In all tumors examined (n = 35) GHRH-IR could be detected, and four tumors (three carcinoids and one jejunal carcinoma) contained a very high amount of GHRH-IR (greater than 1000 ng/g wet wt). Affinity chromatography of tumor extracts led to a significant loss (greater than 50%) of GHRH-IR in nine tumors. The four tumors containing large amounts of GHRH-IR were obtained from two patients with active acromegaly and two patients who had no clinical evidence of acromegaly. Using antibodies with different specificities for GHRH-(1-44) and GHRH shortened at the C-terminus, varying concentrations of GHRH-(1-44) in these tumors were found, ranging from 10-87% of the total GHRH-IR. The biological activity of GHRH in the four tumor extracts was similar to that of synthetic GHRH alone or GHRH added to control tissue subjected to extraction. These results demonstrate the presence of GHRH-IR in the majority of normal tissues and tumors, which, though they may produce large amounts of biologically active GHRH, do not always lead to acromegaly.

Adolescent↗
PubMed1989

Interaction of L-dopa and GHRH on GH secretion in normal men.

To determine how L-dopa stimulates GH secretion, we investigated its interaction with GHRH in vivo. Six normal men were studied on 4 occasions: 1) L-dopa-TRH: 500 mg L-dopa orally followed by 200 micrograms TRH 60 min later; 2) L-dopa-GHRH-TRH: 100 micrograms GHRH 1-44 iv 30 min after L-dopa followed by 200 micrograms TRH iv; 3) GHRH-TRH: 100 micrograms GHRH iv at 0 min, 30 min later 200 micrograms TRH iv; 4) TRH test: 200 micrograms TRH iv as a bolus. After L-dopa-TRH GH-levels increased significantly from 0.6 micrograms/l to 25.8 +/- 9.6 (SE) micrograms/l at 60 min. Only a slight TSH and no PRL increase was observed after L-dopa-TRH. After L-dopa-GHRH-TRH the GH-increase was significantly higher (45.7 +/- 11.1 micrograms/l) compared to L-dopa-TRH alone. GHRH-TRH increased GH-levels to 52.5 +/- 12.1 micrograms/l, which was not significantly different from the GH-levels obtained when L-dopa-GHRH-TRH were given. TRH increased serum TSH and PRL to 6.3 +/- 0.7 microU/ml and 715 +/- 136 microU/ml, respectively, which was significantly higher compared to the TSH responses after L-dopa-TRH. The PRL and TSH increase after TRH only was also higher (TSH-max: 5.7 +/- 0.5 microU/ml; PRL-max: 899 +/- 154 microU/ml) compared to the TSH and PRL responses after L-dopa-TRH. Our results show that the combination of L-dopa with GHRH leads to the same GH response as GHRH only. However, both responses are significantly higher than the one after L-dopa alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Interaction of clonidine and GHRH on GH secretion in vivo and in vitro.

UNLABELLED: To investigate the mechanism by which clonidine stimulates GH-secretion in vivo and in vitro, we studied its interaction with GHRH. In vivo: eight or six normal male subjects were submitted to five protocols: (1) 150 micrograms clonidine orally followed by 50 micrograms GHRH 1-44 i.v. 2 h later, (2) 50 micrograms GHRH 1-44 i.v. followed by 150 micrograms clonidine orally 2 h later, (3) 150 micrograms clonidine orally followed by GHRH i.v. 30 min later, (4) 300 micrograms clonidine orally followed by 50 micrograms GHRH i.v. 3 h later and (5) 50 micrograms GHRH i.v. followed by 300 micrograms clonidine orally 90 min later. In vitro: Rat anterior pituitary cells were coincubated with clonidine (10(-11), 10(-9), 10(-7) and 10(-5) M) and GHRH (0.005, 0.05, 10 nM) for 4 h. RESULTS: 150 micrograms clonidine alone does not stimulate GH-secretion. Furthermore, the GH-increase was not significantly different when GHRH bolus was given before, after or together with clonidine. When 300 micrograms clonidine was given before GHRH GH-levels were significantly higher (max 28.6 +/- 8.0 mU/l) at 90 min, compared to when clonidine was given after GHRH (max 7.8 +/- 3.6 mU/l). The GHRH bolus after clonidine led to a significantly lower GH-increase (max 31.6 +/- 17.0 mU/l) compared to the GHRH-induced GH-increase (max 47.2 +/- 13.0 mU/l) before clonidine. In vitro, clonidine had no stimulatory effect on GHRH-stimulated GH secretion. These findings are compatible with clonidine leading to stimulation of GH by inducing endogenous GHRH release.

Adult↗
PubMed1989

Effects of repetitive administration of thyrotropin-releasing hormone at short intervals in acromegaly.

We investigated the pattern of GH secretion in response to repetitive TRH administration in patients with active acromegaly and in normal subjects. Nine acromegalic patients and 10 normal subjects received three doses of 200 micrograms of TRH iv at 90-min intervals. There was a marked serum GH rise in acromegalic patients after each TRH dose (net incremental area under the curve [nAUC]: first dose = 4448 +/- 1635 micrograms.min.l-1; second dose = 3647 +/- 1645 micrograms.min.l-1; third dose = 4497 +/- 2416 micrograms.min.l-1; NS), though individual GH responses were very variable. In normal subjects TRH did not elicit GH secretion even after repeated stimulation. Each TRH administration stimulated PRL release in acromegalic patients, though the nAUC of PRL was significantly higher after the first (1260 +/- 249 micrograms.min.l-1) than after the second and the third TRH administration (478 +/- 195 and 615 +/- 117 micrograms.min.l-1, respectively; P less than 0.01). In normal subjects too, PRL secretion was lower after repeated stimulation (first dose = 1712 +/- 438 micrograms.min.l-1; second dose = 797 +/- 177 micrograms.min.l-1; third dose = 903 +/- 229 micrograms.min.l-1 P less than 0.01), though different kinetics of PRL secretion were evident, when compared with acromegalic patients. TSH secretion, assessed in only 4 patients, was stimulated after each TRH dose, though a minimal but significant reduction of nAUC of TSH after repeated TRH challenge occurred. Both T3 and T4 increased steadily in the 4 patients. The same pattern of TSH, T3, and T4 secretion occurred in normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗