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P J Trainer

Publications and source records attributed to P J Trainer.

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The place of pegvisomant in the management of acromegaly.

Conventional treatments for acromegaly include surgery, radiotherapy, dopamine agonists and somatostatin (SMS) analogues, which effect disease control by lowering circulating growth hormone (GH). Due to variability in tumour characteristics, combinations of these treatment modalities leave a significant number of patients with sub-optimal serum GH and insulin-like growth factor-I (IGF-I) levels, which have been linked to increased morbidity and mortality. The GH receptor antagonist pegvisomant is a genetically engineered analogue of GH that prevents functional dimerisation of the growth hormone receptor (GHR); a process that is critical to GH action at the cellular level. A crucial amino acid substitution at Gly(120) to Arg(120) within the third alpha helix of the antagonist prevents functional GHR dimerisation. Pegvisomant represents a novel treatment for acromegaly as, unlike existing treatment modalities, the effectiveness of pegvisomant is independent of pituitary tumour characteristics. Initial clinical studies in patients with active acromegaly have demonstrated serum IGF-I normalisation in over 90% of patients receiving 20 mg per day, such that, in terms of serum IGF-I normalisation, pegvisomant now represents the most effective medical treatment for acromegaly. Although there are limited long-term data on the use of pegvisomant and questions regarding pituitary tumour growth and altered liver function remain, this therapy offers the prospect of serum IGF-I normalisation in the vast majority of patients with active acromegaly.

Acromegaly↗

Successful treatment of resistant acromegaly with a growth hormone receptor antagonist.

BACKGROUND/OBJECTIVE: Pegvisomant is a pegylated analogue of human GH and functions as a potent GH receptor antagonist. This novel mode of action gives it the potential to achieve biochemical control in patients with acromegaly whose disease activity cannot be satisfactorily controlled by conventional therapy. We have documented the clinical details of seven patients with residual active acromegaly after surgery and/or radiation therapy successfully treated with pegvisomant. PATIENTS/METHODS: Seven patients (four male, mean age 47 years, range 34-67 years) who participated in two separate clinical trials of pegvisomant have completed 2 years (four patients) or 1 year (three patients) of treatment. All had active acromegaly (mean serum GH level >5 mU/l; serum IGF-I elevated for age) that could not be controlled with standard medical therapy (dopamine agonist and/or a somatostatin analogue) following appropriate primary treatment with surgery and/or radiotherapy. RESULTS: On a median dose of 20 mg/day (range 15-40) pegvisomant, serum IGF-I fell from a mean of 920+/-351 ng/ml (s.d.) to 258+/-91 ng/ml and was normalised in all seven patients. These changes were associated with improvements in soft tissue enlargement and general well being. Treatment was well tolerated and no change in pituitary tumour size was evident on MRI scans performed every 6 months. CONCLUSIONS: Treatment with pegvisomant is safe and efficacy is maintained after 2 years. Serum IGF-I may be normalised in patients who are refractory to conventional therapy.

Acromegaly↗

Treatment of acromegaly with the growth hormone-receptor antagonist pegvisomant.

BACKGROUND: Patients with acromegaly are currently treated with surgery, radiation therapy, and drugs to reduce hypersecretion of growth hormone, but the treatments may be ineffective and have adverse effects. Pegvisomant is a genetically engineered growth hormone-receptor antagonist that blocks the action of growth hormone. METHODS: We conducted a 12-week, randomized, double-blind study of three daily doses of pegvisomant (10 mg, 15 mg, and 20 mg) and placebo, given subcutaneously, in 112 patients with acromegaly. RESULTS: The mean (+/-SD) serum concentration of insulin-like growth factor I (IGF-I) decreased from base line by 4.0+/-16.8 percent in the placebo group, 26.7+/-27.9 percent in the group that received 10 mg of pegvisomant per day, 50.1+/-26.7 percent in the group that received 15 mg of pegvisomant per day, and 62.5+/-21.3 percent in the group that received 20 mg of pegvisomant per day (P<0.001 for the comparison of each pegvisomant group with placebo), and the concentrations became normal in 10 percent, 54 percent, 81 percent, and 89 percent of patients, respectively (P<0.001 for each comparison with placebo). Among patients treated with 15 mg or 20 mg of pegvisomant per day, there were significant decreases in ring size, soft-tissue swelling, the degree of excessive perspiration, and fatigue. The score fortotal symptoms and signs of acromegaly decreased significantly in all groups receiving pegvisomant (P< or =0.05). The incidence of adverse effects was similar in all groups. CONCLUSIONS: On the basis of these preliminary results, treatment of patients who have acromegaly with a growth hormone-receptor antagonist results in a reduction in serum IGF-I concentrations and in clinical improvement.

Acromegaly↗

Cushing's disease.

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Antineoplastic Agents, Hormonal↗

Pegvisomant: a growth hormone receptor antagonist for the treatment of acromegaly.

Growth hormone receptor (GHR) dimerization is a prerequisite to the generation of growth hormone (GH) action. Pegvisomant is a GHR antagonist that has been designed to bind to the GHR at the cell surface and hence block this process. Initial studies suggest that pegvisomant is a highly effective antagonist of GH action in patients with acromegaly. The blockade of GH action, rather than the inhibition of pituitary GH secretion, represents a novel concept in the medical management of acromegaly. In this review, the design, efficacy, challenges and future role of pegvisomant are discussed.

Acromegaly↗

How common are polycystic ovaries and the polycystic ovarian syndrome in women with Cushing's syndrome?

OBJECTIVE: Women with Cushing's syndrome (CS) may present with menstrual irregularity and symptoms/signs of hyperandrogenism, a phenotype similar to that of the polycystic ovarian syndrome (PCOS); however, currently there are no data on the prevalence of either polycystic ovaries (PCO) and/or PCOS in patients with CS. The aim of this study was to investigate their presence among women of reproductive age presenting with CS by analysing clinical, endocrinological and ultrasonographic features. DESIGN: Prospective study of all women within the reproductive age (range 18-40 years) who presented with CS between August 1994 and January 2000. SUBJECTS AND METHODS: Thirteen women (median age 32 years, range 18-39 years) with CS were evaluated. The diagnosis of CS was based on the presence of appropriate clinical features and an elevated serum midnight cortisol with failure to suppress 0900 hours serum cortisol to less than 50 nmol/l following a formal low-dose dexamethasone suppression test (LDDST). All women had their clinical features relevant to possible hyperandrogenism, menstrual disorder and infertility recorded, and circulating gonadotrophins, oestradiol, androgens and SHBG levels measured; ovarian ultrasonography was performed during their initial assessment. Relevant MR/CT imaging of the pituitary and/or adrenal glands was performed. RESULTS: Eleven women had ACTH-dependent CS [nine Cushing's disease (CD), one ectopic ACTH syndrome due to a bronchial carcinoid, one periodic CS of unknown origin); two patients had ACTH-independent CS (adrenal adenomas). All women with CS had at least one symptom/sign of hyperandrogenism (13 hirsutism, seven acne, five male-pattern alopecia). Nine women (70%) had menstrual disturbances (four oligomenorrhoea, four amenorrhoea, one polymenorrhoea) while four women (30%) had a normal menstrual pattern. Serum oestradiol levels for the group as a whole were similar to those observed in the early follicular phase of normally menstruating women; however, seven women had low oestradiol, LH and FSH levels suggestive of hypogonadotrophic hypogonadism. Serum androgen levels (testosterone, androstendione and DHEAS), even in the presence of symptoms/signs of hyperandrogenism, were within the normal reference range but SHBG levels were uniformly decreased even in women with normal menstrual cycles. There was a negative correlation between urinary free cortisol, but not mean serum cortisol, and serum oestradiol, testosterone and SHBG levels (r = - 0.8, r = - 0.86 and r = - 0.66, P<0.02, P<0.01 and P<0.05, respectively), but not LH or FSH levels. Despite the fact that seven of these 13 patients lacked normal gonadotrophin stimulation, ovarian volumes of both ovaries were relatively preserved: right 7.3 ml, range 2.8-12.8 ml, and left 5.3 ml, range 2.3-13 ml. Women who were defined as oestrogen sufficient (E2 > 140 pmol/l) had higher serum androstenedione, and lower urinary free cortisol levels, than women who were oestrogen deficient (E2 < 140 pmol/l). Six of the 13 women (46%) had ovarian morphology suggestive of PCO, four of six oestrogen sufficient women and two of seven oestrogen deficient women. The results did not differ according to the underlying cause of CS. CONCLUSIONS: PCO and PCOS are common in women with Cushing's syndrome; women with Cushing's syndrome and only moderately elevated cortisol secretion maintain gonadotrophin stimulation to the ovary with normal oestradiol levels, in contrast to women with Cushing's syndrome and higher cortisol secretion who develop hypogonadotrophic hypogonadism. However, even in the latter group, high ovarian volumes were maintained and some had ovarian morphology suggestive of PCO.

Adult↗

Adrenal enlargement and failure of suppression of circulating cortisol by dexamethasone in patients with malignancy.

The aim of this study was to further elucidate the activity of the hypothalamo-pituitary-adrenal (HPA) axis in patients with malignancy and to correlate this with the size of the adrenal glands. Fourteen patients with a variety of malignancies were studied prior to receiving cytotoxic chemotherapy. During routine staging computerized tomographic (CT) scans, the size of the body, medial and lateral limbs of the adrenal glands were measured and compared with those of a normal group of patients studied previously. Measurements of 09:00 h serum cortisol and plasma adrenocorticotropic hormone (ACTH) levels were made before and after the administration of dexamethasone (0.5 mg 6-hourly for 48 h) in addition to the peak cortisol response to i.v corticotropin releasing hormone (CRH). Overall, patients with malignancy had significantly larger adrenal glands than patients without malignancy; those with non-haematological malignancies had larger glands than patients with haematological malignancies. Following dexamethasone to suppress circulating cortisol levels, nine patients (64%) demonstrated abnormal resistance with cortisol levels > 50 nmol l(-1): mean value 294 nmol l(-1) (range 67-1147). Those patients who failed to suppress after dexamethasone had significantly larger adrenal glands than those that did suppress and tended to have non-haematological malignancies. ACTH levels were undetectable or low in three patients in whom it was measured and who did not suppress with dexamethasone. Following CRH, the cortisol levels were highest (823 and 853 nmol l(-1)) in two of these patients. Malignancy is associated with diffuse enlargement of the adrenal glands and resistance to dexamethasone-induced suppression of the HPA axis, which is not due to ectopic ACTH secretion. This disturbance of the normal control of the HPA axis is unexplained and its functional significance remains uncertain.

Adrenal Glands↗

Hexarelin as a test of pituitary reserve in patients with pituitary disease.

BACKGROUND: The insulin tolerance test (ITT) is the reference standard for the diagnosis of cortisol and growth hormone (GH) deficiency, but problems have occurred in small children in inexperienced hands and it is contraindicated in patients with cardiac disease and epilepsy. Hexarelin is a growth hormone-releasing peptide with GH-, ACTH/cortisol- and prolactin-releasing effects which involve both hypothalamic and direct pituitary mechanisms. We therefore investigated whether it could be used to test GH and ACTH/cortisol reserve in patients with pituitary disease. METHODS AND SUBJECTS: The changes in GH and cortisol in response to insulin-induced hypoglycaemia (intravenous human Actrapid 0.15 IU/kg) and hexarelin (2 microg/kg) in 19 patients with possible pituitary disease (5 males, mean age 39 years, range 21-70) were compared. The patients' responses during the hexarelin test were also compared to normal ranges of GH and cortisol responses established in healthy volunteers following hexarelin administration. RESULTS AND DISCUSSION: GH peak levels were significantly higher after hexarelin than after hypoglycaemia (mean +/- SEM; 67.1 +/- 16 vs. 26.9 +/- 6.8 mU/l respectively; P < 0. 001), while cortisol levels were significantly lower (420 +/- 34 vs. 605 +/- 50 nmol/l; P < 0.001). The peak responses of both hormones correlated significantly between the hexarelin and insulin-induced hypoglycaemia tests (r = 0.80, P < 0.001 for cortisol). Peak GH levels after hexarelin and ITT showed a significant positive correlation with IGF-I levels (r = 0.84 and r = 0.77, P < 0.001 for both). All patients with a subnormal GH response to hexarelin (<41.4 mU/l) had a peak GH response to ITT of <9 mU/l, and only one patient had a normal (although borderline) response to hexarelin with a subnormal GH response to the ITT. Although 17 of the 19 patients had corresponding cortisol responses to hexarelin and the ITT test (either failing or passing both), two patients had normal cortisol responses to hexarelin but subnormal responses to the ITT. A peak serum cortisol level following hypoglycaemia of >580 nmol/l is indicative of normal cortisol reserve, as established in patients undergoing surgery; only five of the normal volunteers and one of the thirteen patients with a normal ACTH/cortisol reserve on ITT had a peak cortisol >580 nmol/l in response to hexarelin. CONCLUSION: Adult patients who have a subnormal peak GH response to hexarelin are likely to be GH deficient on an insulin tolerance test. However, our data suggest that the hexarelin test is not a useful test of ACTH/cortisol reserve. The hexarelin test could be a useful first/screening test to diagnose adult GH deficiency, particularly in patients in whom an insulin tolerance test is contraindicated or who are already ACTH deficient and in whom the GH reserve alone is of interest.

Adrenocorticotropic Hormone↗

Quantitative growth hormone secretion and final adult height.

OBJECTIVE: The relationship of quantitative GH secretion to height, growth velocity and puberty is complex and has been the subject of extensive study in children. This study was designed to relate quantitative GH secretion to final height. SUBJECTS: Twenty tall (> 183 cm, 90th centile for adult height) and 20 short (< 166 cm, 10th centile) postpubertal men who had recently completed linear growth (age range 18-27 years). MEASUREMENTS: GH dynamics were studied on four occasions; insulin (0.15 units/kg, iv)-induced hypoglycaemia and GHRH (100 mg, iv) with and without the anticholinesterase, pyridostigmine (120 mg orally). Spontaneous nocturnal GH secretion was assessed by 20 minute sampling from 2100 h until 0600 h. GH was measured by IRMA. Analysis was by comparison of peak GH response and area under the curve (AUC). GH profiles were further analysed using the 'pulsar' programme. RESULTS: The mean height in the tall group was 187.7 cm (range 183-197) compared to 163.5 cm (range 160-166) for the short group. No difference existed between groups in the GH response to hypoglycaemia or GHRH with and without pyridostigmine. Area under the curve, pulse number, length and amplitude for spontaneous nocturnal GH secretion showed no significant difference between the tall and short subjects. Serum IGF-I (mean 230.5 +/- 15. 4 vs. 230.6 +/- 18.9 microg/l) did not differ between the groups. CONCLUSIONS: Quantitative GH secretion does not appear to be an important determinant of final height in healthy individuals.

Adult↗

The effect of growth hormone secretagogues and neuropeptide Y on hypothalamic hormone release from acute rat hypothalamic explants.

Growth hormone (GH) secretagogues (GH-releasing peptides and their non-peptide analogues) stimulate growth hormone release via specific G-protein coupled receptors both directly from the pituitary gland and through stimulation of the hypothalamus. The exact mechanism of action in the hypothalamus is not known. The presence of endogenous GH releasing hormone (GHRH) seems to be necessary for the in-vivo actions of growth hormone secretagogues (GHSs), but data suggest that further factors must be involved as well. The effect of GHSs is not entirely specific for the GH axis; they release prolactin and stimulate the hypothalamo-pituitary-adrenal axis causing elevations in circulating ACTH and cortisol levels in both animal and human studies. Recently, it has also been suggested that GHSs stimulate hypothalamic neuropeptide Y (NPY) neurones. In the present study, we have therefore investigated the direct effect of several GHSs (GHRP-6, hexarelin and the non-peptide analogues L-692, 429 and L-692, 585) on GHRH, somatostatin (SS), corticotrophin-releasing hormone (CRH) and arginine vasopressin (AVP) release in vitro in an acute rat hypothalamic incubation system. We also assessed the effect of NPY on GHRH, SS and AVP release. Freshly removed hypothalami were incubated in control media for 20 min and then in 1-4 consecutive 20-min periods in each of the test substances at different concentrations. There was no significant change in either the basal or potassium-stimulated release of GHRH or SS at low concentrations of any of the secretagogues; however, at millimolar doses a paradoxical inhibition of GHRH was observed with GHRP-6, hexarelin and L-692 585 (data are expressed as the ratio of treated to preceding basal release; at 20 min control group: 0.97+/-0.02, GHRP-6: 0.55+/-0.04, P<0.001 compared to control group; hexarelin: 0. 56+/-0.06, P<0.001, L-692,585: 0.70+/-0.03, P<0.001), while SS was stimulated after 60 or 80 min (at 80 min control: 0.80+/-0.03, hexarelin: 1.23+/-0.07, P<0.05 and L-692,585: 1.37+/-0.11, P<0.05). GHSs stimulated hypothalamic AVP release (at 20 min control: 0. 99+/-0.06 ratio to basal release, 10-4 M concentration of GHRP-6: 6. 31+/-1, P<0.001, hexarelin: 1.88+/-0.4, P<0.01, L-692,429: 1.90+/-0. 5, P<0.05 and L-692,585: 2.34+/-0.96, P<0.01), while no stimulatory effect was found on CRH release. NPY significantly stimulated SS and inhibited basal and potassium-stimulated GHRH release, while potentiating potassium-evoked AVP secretion. The Y1 receptor antagonist BIBP 3226 did not inhibit the effects of NPY on SS, GHRH or AVP release. We therefore conclude that, in this in-vitro rat hypothalamic incubation model, growth hormone secretagogues stimulate the release of AVP but have no effect on either GHRH, SS or CRH at low doses; at high doses paradoxically they inhibit the hypothalamic GH axis similar to in-vivo data in the rat. We speculate that these effects might be mediated by NPY.

Animals↗

Growth hormone receptor antagonists therapy for acromegaly.

Knowledge of the interaction between growth hormone (GH) and the growth hormone receptor (GHR) has led to the rational design of a GHR antagonist. An analogue of GH able to block the action of GH at the cellular level offers greater specificity of effect compared with current medical therapies and is not dependent on tumour characteristics. This chapter reviews the interaction between GH and the GHR, and discusses the outstanding issues regarding GHR antagonist therapy in acromegaly.

Acromegaly↗

A critical analysis of the value of simultaneous inferior petrosal sinus sampling in Cushing's disease and the occult ectopic adrenocorticotropin syndrome.

The clinical, biochemical, and radiological features of pituitary ACTH-dependent Cushing's syndrome (CS) [Cushing's disease (CD)] are often indistinguishable from those of occult ectopic ACTH-dependent CS (oEAS). We have evaluated, retrospectively, the results of simultaneous bilateral inferior petrosal sinus (IPS) ACTH sampling before and after CRH stimulation in 128 patients with ACTH-dependent CS: 107 patients with CD, 6 with oEAS, 1 with an adrenal adenoma, 1 with a pituitary gangliocytoma, and 1 with Nelson's syndrome; while, in the remaining 12, the source remains unclear. One hundred seven patients received human-sequence CRH (hCRH), and 11 received ovine CRH; another 6 patients underwent stimulation with desmopressin and hCRH, and 4 with desmopressin alone. A successful bilateral IPS catheterization and sampling (IPSCS) rate of 87.5% was obtained only after considerable experience had been gained. Sixty-nine patients with CD underwent successful bilateral IPSCS: the IPS-to-peripheral ratio of plasma ACTH value (IPS/P) rose from 9.5 +/- 1.4 to a maximum ratio of 55.8 +/- 7.5 in 67 patients, after CRH stimulation. The maximum ratio was obtained at 5 min in 60 of the 69 patients with CD; however, all 69 patients obtained a ratio of more than 2, at that time. In contrast, the 6 patients with occult ACTH-secreting neoplasms had a maximal IPS/P ratio of 1.3 +/- 0.16, and this did not change after CRH stimulation. A bilateral IPS/P ratio more than 2, obtained 5 min after CRH stimulation, had a sensitivity of 97% and a specificity of 100% in diagnosing CD. Two patients with proven active CD had an IPS/P ratio of less than 2. After successful bilateral IPSCS, the gradients between the IPS ACTH concentrations [IPS ACTH gradient (IPSG)] of more than 1.4, at 5 min after CRH stimulation, had a sensitivity of 83% in correctly lateralizing the pituitary microadenoma, compared with 72% sensitivity for magnetic resonance imaging (MRI) scanning. Furthermore, when IPSG and MRI findings were contradictory, IPSG was more often correct than MRI scanning. Although oEAS is a relatively uncommon cause of ACTH-dependent hypercortisolism (5.5% in our series), the accurate diagnosis of ACTH-dependent CS and localization of an intrapituitary microadenoma requires bilateral IPSCS with CRH stimulation, provided that the appropriate technical experience is available. hCRH is as effective a secretagogue as ovine CRH, and either may be used. The value of the combination of CRH and desmopressin stimulation requires more detailed investigation.

ACTH Syndrome, Ectopic↗

Computed tomography appearance of the thymus and anterior mediastinum in active Cushing's syndrome.

Computed tomography (CT) evaluation of the thymus and anterior mediastinum is an important aspect of the investigation of patients with ACTH-dependent Cushing's syndrome in order to exclude an ACTH-secreting carcinoid tumor. We have reviewed the CT imaging of the thymus and anterior mediastinum in a series of 85 patients (55 females; median age 41, range 7-77 yr) with active Cushing's syndrome as there are few data on the range of appearances in hypercortisolemic states. One patient had a thymic carcinoid tumor (24 x 18 mm). Of the others, 28/84 (33%) patients showed thymic remnant tissue, consisting of either nodule(s) at least 5 mm diameter (n = 21, mean diameters 12.5 +/- 5 x 9.6 +/- 4 mm), or triangular bilobed glands (n = 7, mean thickness of the body, right and left limbs 25 +/- 7, 14 +/- 3, and 12 +/- 5 mm). Thymic involution appeared in 56/84 (67%) patients, ranging from small nodule(s) of less than 5mm diameter to linear soft tissue strands and complete fatty replacement. Patients with thymic remnant tissue were younger than those with thymic involution (P < 0.05). The thymic carcinoid tumor could be distinguished from remnant tissue on the basis of age and size. The presence of anterior mediastinal nodule(s) in hypercortisolemia need not imply the presence of a thymic carcinoid tumor, although in older patients this should arouse suspicion.

ACTH Syndrome, Ectopic↗

The growth hormone secretagogue hexarelin stimulates the hypothalamo-pituitary-adrenal axis via arginine vasopressin.

GH secretagogues (GHSs) act via specific receptors in the hypothalamus and the pituitary gland to release GH. GHSs also stimulate the hypothalamo-pituitary-adrenal (HPA) axis via central mechanisms probably involving CRH or arginine vasopressin (AVP). We studied the effects of hexarelin, CRH, and desmopressin, an AVP analog, on the stimulation of the HPA axis in 15 healthy young male volunteers. Circulating ACTH, cortisol, GH and PRL concentrations were measured for 2 h after the injection of hexarelin, CRH, or desmopressin alone and the combination of hexarelin plus CRH or hexarelin plus desmopressin. Symptoms during the tests were assessed by visual analog scales. Hexarelin significantly increased ACTH and cortisol release (area under the curve, 3,444+/-696 ng/L x 125 min and 45,844+/-2,925 nmol/L x 125 min, respectively), and this effect was augmented by the addition of CRH in a dose that on its own produces maximal stimulation (6,580+/-1,572 ng/mL x 125 min and 63,170+/-2,616 nmol/L x 125 min; P = 0.01 and 0.001, respectively), but was not influenced by the addition of desmopressin (3,540+/-852 ng/mL x 125 min and 35,319+/-3,252 nmol/L x 125 min; not significant). CRH on its own caused similar or slightly higher ACTH and cortisol release than hexarelin alone. Desmopressin given alone elicited a rapid rise in circulating ACTH and cortisol, but its effects were less than those of any other treatment and were not augmented by hexarelin. Hexarelin also caused significant GH and PRL release, but these effects were not influenced by the coadministration of CRH or desmopressin. Visual analog scales showed an acute small increment in appetite with hexarelin. Our data suggest that the effect of GHSs on the HPA axis involve at least in part the stimulation of AVP release. In summary, we have shown that in healthy male volunteers, the effect of hexarelin on the HPA axis does not involve CRH, but may occur through the stimulation of AVP release.

Adrenal Glands↗

CT appearance of the adrenal glands in adrenocorticotrophic hormone-dependent Cushing's syndrome.

OBJECTIVE: The purpose of this study was to describe the size and appearance of the adrenal glands on CT in patients with adrenocorticotrophic hormone (ACTH)-dependent Cushing's syndrome and to correlate gland dimensions with circulating cortisol and ACTH levels. MATERIALS AND METHODS: We retrospectively analyzed clinical, biochemical, and imaging data for 53 patients referred for CT of the adrenals as part of an investigation for ACTH-dependent Cushing's syndrome at our institution between 1988 and 1997. Two observers, who were unaware of the endocrine data, measured the body and limb widths of the adrenal glands using an electronic cursor. RESULTS: Of the 53 patients, 37 (70%) were shown to have enlarged adrenal glands on CT. The mean width of the adrenal limbs positively correlated with the circulating cortisol and ACTH levels. The adrenals were larger in patients with ectopic ACTH syndrome than in patients with Cushing's disease (p < .02). Ten patients (19%) had nodules that were 10 mm or greater in diameter. CONCLUSION: The adrenal glands were often enlarged in patients with ACTH-dependent Cushing's syndrome, and the enlargement could be quantified on CT. However, having normalsized adrenals (observed in 30% the patients in our study) did not preclude such a diagnosis. We found that adrenal limb width positively correlates with ACTH and cortisol levels.

ACTH Syndrome, Ectopic↗

Serum collagen crosslinks as markers of bone turn-over during GH replacement therapy in growth hormone deficient adults.

OBJECTIVES: Bone metabolism is an important target for GH replacement therapy. However, in adults, treatment periods exceeding 12 months are required for a positive effect of GH on bone mineral density. Thus, to detect an early effect of GH on bone, markers of bone turn-over are important. Pyridinoline (PYR) and deoxypyridinoline (DPYR) are well-defined sensitive markers of bone resorption, but to date only urinary assays have been available. We report the use of a novel assay to measure changes in serum PYR and DPYR in GH deficient (GHD) adults during GH replacement therapy. STUDY DESIGN: The study consisted of a 6-month randomized, double-blind, placebo-controlled study of the administration of GH (Genotropin) (0.25 IU/Kg/week (0.125 IU/kg/week for the first four weeks)) followed by a 6-month open phase of GH therapy. PATIENTS: Thirty-five GHD adults (17 women; mean age 39.8 years; range 21.1-59.9) on conventional hormone replacement therapy as required, were studied. MEASUREMENTS: Bone formation was analysed using serum bone alkaline phosphatase (BAP) and serum osteocalcin (OC). Bone resorption was analysed using serum pyridinoline (PYR) and serum deoxypyridinoline (DPYR). Bone mineral density (BMD) was determined by dual energy X-ray absorptiometry (DEXA). RESULTS: After 6 months placebo treatment there were no significant changes in any of the bone markers analysed, nor in BMD. In the active arm of the study there was a significant increase in serum OC, BAP, PYR and DPYR (P = 0.03, P = 0.004, P = 0.003 and P = 0.01, respectively), remaining significantly elevated over their baseline levels for the subsequent 6 months of treatment (P = 0.04, P = 0.009, P = 0.003 and P = 0.04, respectively). No changes were observed in BMD in any of the groups after 6 months GH treatment. In the active arm of the study, after 12 months GH treatment there was a significant increase in BMD at both the lumbar spine and femoral neck (P = 0.01 for both sites). CONCLUSIONS: In summary, the present study confirms that administration of GH treatment to GHD adult patients significantly activates bone remodelling, with the effect of GH both in bone formation and bone resorption markers being maximal after 6 months of treatment. The serum assay for PYR and DPYR has a number of practical and theoretical advantages over the urine assay and gave similar results to those previously reported for the urine assay.

Adult↗