Stretching exercises for costochondritis pain.

The term costochondritis (ChC) indicates a painful and persistent inflammation at the costochondral or costosternal junction. The usual conservative treatment (NSAIDs), local splinting, local heat) and sometimes disappointing. The aim of this study is to evaluate the effect of stretching exercises in a group of patients affected with ChC. This retrospective open study involved 51 outpatients with diagnosis of ChC: thirty four consecutive patients were treated with stretching exercises, 34 patients matched for age, pain and disease duration constituted the control group. All the patients had spontaneous pain at least in the one of the costochondral junctions at the third to seventh rib. The intensity of spontaneous pain was measured by means of the visual analogic scale of Scott-Huskisson. The homogeneity of the two groups at the beginning of the study was checked for VAS, for disease duration and age by means of Mann-Whitney test for non-parametric measures. The statistical analysis of pain was done by Friedman analysis of variance and Student-Newman-Keuls multiple comparisons tests. The results showed a progressive significant amelioration in patients treated with stretching exercises as respect as the control group (p<0.001). The goal of therapy of costochondritis is to reduce inflammation and the pain. The NSAIDs, local injection of anaesthetic or steroid has insufficient effectiveness. The possibility to improve the pain by means of simple stretching exercises can supply a useful instrument in order to treat the condition of these patients.

Sonographic assessment of soft tissue alterations in osteoarthritis of the knee.

Osteoarthritis (OA) is the most common joint disorder to affect the knee, and the single most important cause of disability in aged elderly people. Radiological criteria for knee OA (focal loss of cartilage, osteophytosis, subchondral cysts and subchondral sclerosis) reflect late manifestations and significant joint damage only. Ultrasound examination is useful in revealing disruption of the periarticular tissue that contributes to symptoms and disability in advanced disease. Nevertheless, ultrasound examination is very important in early OA of the knee when it can give information about soft tissues and cartilage involvement also in absence of clinical symptoms.

Falls in a rehabilitation setting: functional independence and fall risk.

AIM: With this study we wanted to determine the incidence, characteristics and consequences of falls in our rehabilitation setting. METHODS: An observational study was carried out in a rehabilitation setting for postacute orthopedic and neurological inpatients. Three-hundred and twenty patients were enrolled. Falls risk factors (Downton index [DI] and other known parameters), disability (functional independence measure [FIM]) and balance (Berg balance scale [BBS]) were assessed at admission. Falls that occurred during the rehabilitation stay were prospectively classified (St. Louis Older Adult Service and Information System [OASIS] system) and analyzed. RESULTS: Forty patients experienced a fall (12.5%). The faller group was characterized by a major clinical complexity; 70% of fallers were neurological patients and 30% presented cognitive impairment (mini mental state examination [MMSE] <24). They presented a statistically significant worse score on FIM (motor and cognitive), BBS and DI at admission, with 74% predictability of falls as measured by total FIM score and age. Falls recorded with the OASIS classification showed a prevalence (52.5%) for not bipedal (wheelchair transfer) and self-generated falls; 35% were intrinsic falls (caused by subject-specific factors) and 12.5% extrinsic falls (caused by environmental factors). Falls resulted in only minor clinical consequences, except for one rib fracture, but led to a significant increase in length of stay. CONCLUSIONS: In a rehabilitation centre, for good management of resources and safe prescriptions of a patient's independence in activities of daily living, fall risk is better evaluated with appropriate scales.

Dopaminergic modulation of hexarelin-induced GH and PRL secretion in hyperprolactinemia.

Hexarelin (Hex), a synthetic GH-releasing peptide, has recently been found to possess a weak PRL-releasing effect in normals. The aims of this study were to investigate the effect of Hex on GH and PRL secretion in 10 hyperprolactinemic women (HPRL) and 7 controls (C). All subjects underwent stimulus testing with placebo, bromocriptine (Br) (2.5 mg po at time -60), Hex (2 micrograms/kg/bw i.v.), and Br plus Hex. During placebo, HPRL showed a higher (p < 0.01) PRL area under curve (AUC) than C. Br significantly (p < 0.01) reduced PRL AUC both in HPRL and in C. Hex was able to induce a slight but significant (p < 0.05) PRL release in both groups. PRL response to Hex was abolished (p < 0.01 vs Hex) by Br priming in HPRL, while it was only blunted (p < 0.05 vs Hex) in C. Br induced a significant (p < 0.01) GH increase in both groups. However, GH AUC after Br was significantly higher (p < 0.01) in C than HPRL. Hex induced a significant (p < 0.01) GH release both in HPRL and in C. Br priming did not modify GH response to Hex in HPRL while it slightly (p < 0.05) increased GH response to Hex in C, suggesting that neuroendocrine modifications present in HPRL might, per se, be able to impair GH response to Br plus Hex, thus giving rise to receptor competition. Hex had a weak PRL-releasing effect in both groups studied, this was only blunted by Br priming in C but was abolished in HPRL, suggesting that oversensitivity to DA-ergic agents present in HPRL could be able to antagonize completely Hex action.

Desmopressin and low-dose ACTH test in rheumatoid arthritis.

OBJECTIVE: To ascertain whether a different regulation and sensitivity of the hypothalamic-pituitary-adrenal axis exists and whether a type of cortisol resistance is present in rheumatoid arthritis (RA) patients, a chronic disease in whose pathogenesis modifications of the steroid milieu are involved. DESIGN: We studied the basal and dynamic response of ACTH and adrenal steroids to various stimuli acting on the hypophysis or directly on the adrenal gland. METHODS: We studied ten RA patients (39.8 +/- 7.4 (S.D.) years), defined according to the American Rheumatism Association, and seven healthy control patients (34.1 +/- 9.6 (S.D.) years). All subjects underwent testing, in random order, with placebo, desmopressin (DDAVP) (10 microg i.v.), ovine corticotropin-releasing hormone (oCRH) (1 microg/kg body weight) and low-dose ACTH (5 microg i.v.), during the follicular phase of two different menstrual cycles. Blood samples were collected at different times for ACTH and adrenal steroids assay. Baseline estradiol (E2), testosterone and IGF-I levels were also evaluated. All subjects collected urine specimens for 24 h urine free cortisol (UFC). RESULTS: No difference in E2, testosterone or UFC was found between RA patients and controls. IGF-I levels were significantly (P < 0.01) lower in RA patients (110.6 +/- 6.4 microg/l) than in controls (207.0 +/- 37.9 microg/l). Mean baseline dehydroepiandrosterone (DHEA) and delta4-androstenedione levels of the four tests were significantly (P < 0.05) lower in RA patients than in controls. In RA, a negative correlation was found between mean DHEA levels, class of disease (r = -0.67, P < 0.05) and erythrocyte sedimentation rate (r = -0.63, P < 0.05). After placebo no difference in ACTH and cortisol area under curves (AUCs) was found between RA patients and controls. After DDAVP no cortisol or ACTH response was found in RA patients, while a significant (P < 0.05) ACTH release was found in controls. Only in RA patients was DDAVP able to induce a significant (P < 0.01) DHEA increase. After oCRH a similar significant response in ACTH (P < 0.05), cortisol (P < 0.01), and DHEA (P < 0.01) was found in both groups. After low-dose ACTH, a similar significant (P < 0.01) cortisol response was found in both RA patients and controls; indeed in RA patients DHEA AUC (2196.0 +/- 321.8 nmol/l per 90 min) was significantly lower (P < 0.01) than DHEA AUC (4280.8 +/- 749.0 nmol/l per 90 min) in controls. A similar significant (P < 0.01), though not abnormal, 17-hydroxyprogesterone response to ACTH was found in both groups. CONCLUSIONS: Our study underlines reduced adrenal steroid and IGF-I levels, but not the previously described cortisol resistance in RA patients; it shows that baseline and dynamic cortisol levels are 'normal' but inadequate in the setting of a sustained inflammatory disease like RA. The reduced basal and low-dose ACTH-induced DHEA levels could reflect both a reduced sensitivity of the adrenal gland to exogenous corticotropin and a decreased steroid synthesis due to a partial adrenal enzymatic defect (P450 17,20 lyase).

Effects of sumatriptan on growth hormone releasing hormone-stimulated growth hormone secretion in acromegaly.

Sumatriptan (SU), a specific 5-HT1D receptor agonist, was recently shown to be able to increase growth hormone (GH) levels in normals, but not in acromegalics, while no effect was seen on prolactine (PRL). SU is also able to produce an increase in GH response to growth hormone releasing hormone (GHRH) in prepubertal children. In this study we investigated whether SU administration influences GHRH-induced GH secretion in 8 acromegalics, and 6 age-matched normal volunteers, as a control group. We evaluated the effects of SU (6 mg s.c.) or placebo (PL) administration on GHRH (1 microgram/kg bw i.v.)-induced GH and PRL secretion. After SU priming the GH response to GHRH did not changed in acromegalics, but significantly decreased in controls, in comparison with that observed after PL plus GHRH. In acromegalics, no difference in GH peak was seen after SU plus GHRH and PL plus GHRH, nor was any difference seen in AUC between tests. In controls, no difference was seen in GH peaks, while SU priming significantly (P < 0.03) decreased the AUC 90-120 min of GH after GHRH administration. In acromegalics, SU did not change the slight GHRH-induced increase in PRL levels. Our study documents that 5-HT1 D receptors do not interfere with GHRH-stimulated GH secretion in acromegalic subjects. In normals, SU is able to decrease GH response to GHRH, thus confirming that 5-HT1D receptors are able to modulate GH secretion in normals.

Nitric oxide modulates in vivo and in vitro growth hormone release in acromegaly.

Nitric oxide (NO) has recently been shown to modulate pituitary secretion both in vivo and in vitro. The aim of this study was to investigate the effects of this chemical transmitter on spontaneous and growth-hormone-releasing hormone (GHRH)-induced growth hormone (GH) secretion in acromegalic patients, as well as from GH-secreting tumors maintained in vitro. The study was carried out in 7 acromegalic patients (46.2 +/- 2 years) and in 5 normal subjects (40.1 +/- 1.5 years). GH and prolactin (PRL) secretion were assayed during the administration of isosorbide dinitrate (ID, 5 mg, orally), an NO donor, GHRH, and ID plus GHRH. During ID, a significant (p < 0.05) increase (37%) over basal GH levels was only observed in acromegalics. There was no change in GH levels in response to GHRH or ID plus GHRH in either group. No significant change in PRL levels was observed in either group during ID, while GHRH, with or without ID, induced a slight increase in PRL levels in acromegalics only. Tumor specimens were obtained by selective transsphenoidal adenomectomy, and the cells were plated and incubated for 1, 2 and 24 h in the presence of sodium nitroprusside, a releaser of NO (SNP, 0.3 or 0.6 mM), of GHRH (10-8 M) or of both. SNP significantly (p < 0.001) increased GH levels in a dose-dependent manner (R = 0.99, p = 0.02), but was unable to modify the GH response to GHRH. In acromegalics, a significant correlation (R = 0.822, p < 0.045) and a correlation near the limit of significance (R = 0.73, NS) were observed respectively between the in vivo GH response to ID and the in vitro response to SNP at 24 h. No significant effect was observed on PRL secretion during SNP incubations, while GHRH produced a significant increase in PRL after 2 and 24 h incubation in acromegalics. These observations indicate that NO plays a stimulatory role in vivo and in vitro on GH secretion in acromegalic patients.

Lack of effect of desmopressin on ACTH and cortisol responses to ovine corticotropin-releasing hormone in anorexia nervosa.

Both arginine vasopressin (AVP) and corticotropin-releasing hormone (CRH) are involved in the release of ACTH in man. Desmopressin (DDAVP), a synthetic analogue of AVP, has been shown to have a CRH-like action (able to promote ACTH and cortisol release) in animals but not in normal man. Nevertheless, DDAVP is able to release ACTH and cortisol in ACTH-dependent Cushing's disease. We studied eight anorexia nervosa (AN) patients [as AN is a condition in which chronic activation of the hypothalamic-pituitary-adrenal (HPA) axis is commonly reported] in a refeeding phase of the disease, to evaluate whether, after weight gain, ACTH and cortisol response to ovine corticotropin-releasing hormone (oCRH) [1 microgram i.v. DDAVP alone and as pretreatment to oCRH (1 microgram kg-1 BW i.v.)-induced secretion of ACTH and cortisol. We studied six normal women as control subjects. No significant differences in ACTH and cortisol responses to oCRH were found between AN patients and control subjects. DDAVP was not able to stimulate ACTH or cortisol release in AN patients or in control subjects, but in the latter it was able to significantly enhance (P < 0.05) ACTH [area under curve (AUC): 590.0 +/- 104.4 pmol L-1 120 min-1] and cortisol (AUC: 28899.0 +/- 6935.2 nmol L-1 120 min-1) responses to oCRH (ACTH AUC: 325.7 +/- 101.7 pmol L-1 120 min-1, cortisol AUC: 14197.4 +/- 2930.0 nmol L-1 120 min-1). The present data show that DDAVP does not stimulate ACTH and cortisol in AN patients or, as previously reported, in normal subjects. However, DDAVP is able to enhance ACTH and cortisol release after oCRH administration in normal subjects but not in AN patients. This finding could be due to a down-regulation of hypophyseal DDAVP V3 receptors in AN as a direct consequence of the hypercortisolaemic status usually present.

Cholinergic modulation of growth hormone, prolactin and thyroid stimulating hormone responses to thyrotropin-releasing hormone in normal aging.

Endocrine changes occur during the normal aging process. These include alterations in GH, TSH and, to a lesser extent, PRL secretion. Pyrodistigmine (PD) increases basal GH secretion in a widely variable manner and partially reverses the blunted GH response to GHRH found in elderly subjects. The aims of this study were to verify the finding of a paradoxical GH response to TRH (200 micrograms iv) and to evaluate the effect of priming with PD (120 mg orally) on basal and TRH-stimulated GH, TSH and PRL secretion in 7 euthyroid subjects (aged 75-96 years). Hormonal responses after control saline and PD were also evaluated. PD did not modify TSH or PRL responses to TRH. A slight increase in GH secretion was observed after PD. A clear-cut increase in GH levels after TRH was found in 4 out of 7 subjects. TRH-induced GH secretion was significantly increased by pretreatment with PD. Functional abnormalities in the neuroendocrine control of GH secretion in aging could explain, at least in part, the appearance of GH release after TRH. Cholinergic neurotransmission, which is thought to be stimulated by PD administration, seems to be involved in the non-specific GH release after TRH administration in elderly subjects.

Sumatriptan does not stimulate PRL and GH secretion in acromegaly.

OBJECTIVE: Serotoninergic receptors are involved in the regulation of PRL and GH secretion. We studied the effects of sumatriptan, a new 5-HT1D receptor agonist, on PRL and GH secretion in active acromegaly. EXPERIMENTAL DESIGN: After their informed consent, all subjects were submitted to sumatriptan or placebo administration in single blind and in a random order. The time interval between the tests was of 7 days. ENVIRONMENT: We examined all patients in the morning, after 12 hours of fasting. All subjects were in recumbent position during the tests. Pulse rate and blood pressure were monitored during the test. SUBJECTS: Eight acromegalics (42-65 years) and 10 age-matched (33-63 years) normal subjects. PROTOCOL: Blood samples were taken after needle insertion kept patent by slow saline solution infusion. PRL and GH secretion were evaluated after sumatriptan (6 mg sc) and placebo. Blood samples were taken before (45, 15 and 0 minutes) and every 15 minutes for 2 hours after sumatriptan or placebo administration. RESULTS: No significant changes in PRL secretion were observed after sumatriptan in both groups of subjects. A significant increase in GH levels after sumatriptan was observed in controls but not in acromegalics. An age-related negative trend in GH response to sumatriptan was observed in controls. CONCLUSIONS: Our study indicated that 5-HT1D receptors are not involved in PRL and GH secretion in middle-aged acromegalics.

Treatment of acromegaly with octreotide: effectiveness and tolerability of its pulsatile administration by portable pump.

This study was undertaken to evaluate effectiveness and tolerability of octreotide administered in active acromegaly by pulsatile means and compare these data with intermittent three-times-a-day therapy. We studied 13 acromegalics with active disease. All patients received octreotide subcutaneously administered in a pulsatile way using a portable pump delivering 25 micrograms every 120 minutes and in an intermittent way (100 micrograms three times daily) (TID). From pretreatment values (56.5 +/- 13.4 micrograms/L) the 24-h integrated mean GH levels (IC-GH) were significantly reduced both during pulsatile and TID octreotide administration (P < 0.01). IC-GH was significantly lower during pulsatile therapy (17.0 +/- 5.2 micrograms/L) than during TID (22.0 +/- 11.5 micrograms/L; P < 0.05). Before octreotide, IGF-I levels were 669.8 +/- 85.7 micrograms/L; during octreotide therapy they were reduced in 12/13 patients (TID 340.2 +/- 41.5 micrograms/L, pulsatile 338.1 +/- 55.3 micrograms/L; P < 0.01). A correlation between IC-GH and IGF-I levels was observed only during TID administration of octreotide (R = 0.652; P < 0.05). The 24-hour GH pattern fluctuated widely before the start of octreotide therapy. During TID administration, GH levels tended to rise again before the following octreotide injection; this did not occur during pulsatile therapy. Side effects were fewer during pulsatile (15%) than TID (31%) octreotide administration (NS). Asymptomatic gallstones appeared in 1 patient. In conclusion subcutaneous pulsatile octreotide administration in acromegalic patients by means of a small portable pump seems able to produce, a steadier control of GH-IGF-I hypersecretion and fewer side effects than TID administration at same dosage.

Differing responses of cortisol to oCRF during endonasal and oral treatment with DDAVP.

Arginine vasopressin (AVP) exerts a potentiating effect on the responses of cortisol and ACTH to ovine CRF (oCRF). A stimulation test using AVP plus oCRF to assess ACTH reserve has been proposed. In central diabetes insipidus, long-term substitution therapy is commonly undertaken with desmopressin (DDAVP), an analogue of the natural hormone which has a greater antidiuretic action but whose effects on the ACTH-cortisol axis are still controversial. The aim of our study was to evaluate the variations in the responses of ACTH and cortisol to oCRF in various phases of the treatment of central diabetes insipidus: no treatment, endonasal treatment with DDAVP solution and oral treatment with DDAVP in tablet form. Seven patients suffering from central diabetes insipidus underwent testing with oCRF during the various phases of treatment. In the absence of DDAVP treatment, normal responses were registered for cortisol (basal 164.1 +/- 29.4 ng ml-1, peak 396.1 +/- 37.9 ng ml-1; P < 0.05) and ACTH (basal 20.4 +/- 3.9 pg ml-1, peak 86.3 +/- 20.9 pg ml-1; P < 0.05) in all patients. During oral treatment with DDAVP, no variation in cortisol response to oCRF was seen. By contrast, when DDAVP was administered endonasally, a significant reduction in cortisol responsiveness to oCRF (secretory area: 2429 +/- 548 ng ml-1 120 min) was noted in comparison with that found during the other two tests (no treatment: 3070 +/- 704 ng ml-1 120 min; oral DDAVP: 3419 +/- 650 ng ml-1 120 min; P < 0.05) performed.(ABSTRACT TRUNCATED AT 250 WORDS)

[An ergonomic analysis of 5 technics for moving patients]]. / Analisi ergonomica di cinque tecniche di spostamento del paziente.

Nursing personnel and physical therapists refer to the lifting and moving of patients as the most important determinant of occupationally related low-back pain. This study was conducted in 12 nurses and 12 patients, to compare three methods of transferring patients from bed to wheelchair; (I) manual lifting, (II) an assistive device-a walking belt (with both one- and two-person transfers) and (III) a mechanical hoist. After completion of a given transfer, nurses were asked to rate the physical stress and how secure they felt the method was. Patients were asked to rate how secure and comfortable they felt. We also recorded the time required to make each transfer. The walking belt two persons had the most favourable ratings (the least stressful and most secure and comfortable), however transfers with this method took longer than those with the manual methods (although less than transfers with the hoist). Both nurses and patients rated one-person manual lifting as most stressful and least secure. Two-person transfer methods were preferred to the corresponding one-person methods. The hoist was the least suitable transfer method in view of the corresponding one-person methods. The hoist was the least suitable transfer method in view of the considerable physical stresses to the nurses, perceived lack of safety, discomfort for the patients and time involved.

Delta sleep-inducing peptide administration does not influence growth hormone and prolactin secretion in normal women.

The aim of this study was to analyze the effects of delta sleep-inducing peptide (DSIP) on growth hormone (GH) and prolactin (PRL) secretion in eight healthy women with normal cycles (aged 17-36 years). GH and PRL secretion was studied in five women after DSIP (25 micrograms/kg bw IV over 30 min), arginine chlorhydrate (0.5 g/kg bw IV over 30 min) and simultaneous DSIP plus arginine chlorhydrate administration. In three other women the circadian rhythm of GH and PRL was studied during DSIP (25 micrograms/kg bw from 2130h to 2230h) and placebo IV infusion. Serum GH and PRL levels were normal under basal conditions and no effects were noted after the infusion of DSIP. The GH and PRL circadian rhythm was not modified by DSIP administration. DSIP did not influence GH and PRL responsiveness to arginine chlorhydrate. We found that at dosages which are known to modify ECG patterns, DSIP is unable to modify spontaneous or arginine chlorhydrate-induced GH and PRL secretion.

Effect of cholinergic tone on growth hormone-releasing hormone-induced secretion of growth hormone in normal aging.

Aging is associated with an impairment in the GH response to GHRH and to several other stimuli of GH secretion. We evaluated the effect of pyridostigmine (PD) or placebo pretreatment (Protocol A: placebo or 120 mg PD orally at 8 a.m.; Protocol B: placebo or 60 mg PD twice orally at 9 p.m. and 7 a.m.) on GH responsiveness to GHRH (1 micrograms/kg BW bolus i.v. at 9 a.m.) in 15 normal elderly males (65-92 years) and in 14 normal young adults (20-37 years). GH response to GHRH was significantly reduced in elderly subjects compared to young adults (p < 0.05). PD (Protocol A) increased GH release in both elderly and young subjects. In elderly men, PD enhanced GH response to GHRH. The phenomenon was more evident when PD was administered according to Protocol B (p < 0.01). The area under the curve of GH was significantly greater after PD plus GHRH than it was after placebo plus GHRH (p < 0.01). In young adults, PD induced an increase in GH responsiveness to GHRH when administered according to Protocol A (p < 0.05) but not Protocol B. Both GH peak and AUC of GH after PD plus GHRH (Protocols A and B) in elderly subjects were not significantly different from the same parameters found in young subjects after placebo plus GHRH. Our data confirm that pituitary somatotrophin responsiveness to GHRH in man changes with aging. PD restores GH responsiveness to GHRH in elderly subjects. The effect of PD on GH secretion suggests that cholinergic mechanisms may be involved in GH control in normal aging.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of a met-enkephalin analogue on growth hormone, prolactin, gonadotropins, cortisol and thyroid stimulating hormone in healthy elderly men.

The aim of the study was to evaluate the effect of the guanyl derivative of the opioid analogue D-ala2,MePhe4-Met-enkephalin-(o)-ol (G-DAMME) on pituitary secretion in healthy elderly men. Nine healthy elderly men (65-88 years) and 10 young adults (20-30 years) were studied. GH, PRL, gonadotropins, cortisol (to evaluate the effect on ACTH) and TSH were measured after G-DAMME (0.25 mg iv) or placebo administration. In elderly men, the GH response to G-DAMME was reduced or absent, while prompt GH release was found in all young men. G-DAMME lowered LH levels in young men but not in elderly men. No significant variations in FSH levels after G-DAMME and placebo were noted in either group of subjects. A similar and significant rise in PRL and TSH, and a fall in cortisol, after G-DAMME was observed in both elderly and young adults. We have demonstrated that the sensitivity to opioid modulation by G-DAMME on PRL, TSH and cortisol secretion is unchanged with aging. On the other hand, the data indicate that LH and GH responsiveness to G-DAMME change with age.

Growth hormone secretion in aging. Effect of pyridostigmine on growth hormone responsiveness to growth hormone-releasing hormone.

Recent studies in adults have shown that cholinergic enhancement by pyridostigmine (PD) has a stimulatory effect on growth hormone (GH) response to GH-releasing hormone (GHRH). PD probably reduces somatostatin release from the hypothalamus by increasing the central cholinergic tone. The aim of this study was to evaluate the effect of PD (120 mg orally) or placebo pretreatment on GH responsiveness to GHRH (1 micrograms/kg b.w. i.v.) or placebo in 10 normal elderly males (68-92 years). PD induced a significant increase in GH secretion (GH peak 7.3 +/- 1.8 micrograms/L, mean +/- SEM) over the basal value (0.9 +/- 0.2 micrograms/L; P less than 0.01) and enhanced GH response to GHRH (peak after GHRH: 17.0 +/- 3.8 micrograms/L; after PD plus GHRH: 42.6 +/- 12.2 micrograms/L; P less than 0.05). There was a significant difference in the secretory areas of GH among tests (P less than 0.05). The secretory area was greater after PD plus GHRH (2722 +/- 801 micrograms/L/120 min) than after GHRH (1185 +/- 206 micrograms/L 120 min; P less than 0.01). The effect of PD on GH secretion suggests that cholinergic mechanisms may be involved in GH control in normal aging. During the life-span cholinergic neurons and/or the somatostatin pathways could exert a differential effect on GH control.

Growth hormone and prolactin response to growth hormone-releasing in anorexia nervosa.

Anorexia nervosa (AN) is associated with several endocrine disorders. In order to investigate the role of these alterations, growth hormone-releasing hormone (GHRH) was administered in a group of 9 AN patients and in 9 healthy normal-weight women as control. Growth hormone (GH) and prolactin (PRL) levels were evaluated in both groups after GHRH and saline solution administration. In the AN group, luteinizing hormone (LH), follicle-stimulating hormone (FSH), thyrotropin (TSH) and cortisol serum levels were evaluated during GHRH administration; somatomedin-C (Sm-C) basal levels were also determined. In both groups, GHRH induced a prompt GH increase, which was significantly higher in AN patients (55.3 +/- 2.9 ng/ml, mean +/- SE) than in normal subjects (9.8 +/- 2.6 ng/ml: p less than 0.01). A significant positive correlation between mean GH basal values and GH peak after GHRH was observed only in the control group (R = 0.82, p less than 0.01). No significant relationship between GH mean peak and body mass index (BMI) or Sm-C, estradiol (E2) and glucose serum levels was found in AN patients. However, a positive significant correlation with triiodothyronine (T3) basal values was observed in this group (R = 0.80, p less than 0.01). Both groups showed no variation in PRL serum levels after GHRH infusion. Our data suggest the presence of a central derangement in hypothalamic control of pituitary function in patients with AN, which is not necessarily due to weight loss alone.