| 41. |
- Norrman, Lise-Lott, et al.
(author)
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Baseline characteristics and the effects of two years of growth hormone (GH) replacement therapy in adults with GH deficiency previously treated for acromegaly.
- 2008
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In: The Journal of clinical endocrinology and metabolism. - : The Endocrine Society. - 0021-972X .- 1945-7197. ; 93:7, s. 2531-8
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Journal article (peer-reviewed)abstract
- CONTEXT: The effects of GH replacement in GH-deficient (GHD) adults previously treated for acromegaly are not well known. OBJECTIVE, DESIGN, AND PATIENTS: In this single-center, open-labeled, prospective study, 10 consecutive GHD adults with cured acromegaly (A group) and 10 matched GHD adults with previous nonfunctioning hypopituitary disease (NF group) were included. Comparisons were made at baseline and in the responses in body composition, muscle strength, bone mass, and metabolic indices during 2 yr of GH replacement. RESULTS: At baseline, upper leg local muscle endurance and serum low-density lipoprotein-cholesterol concentration were more impaired in the A group. The A group contained three patients with hypertension, one with diabetes mellitus type 2, and one with hyperlipidemia. The NF group had only one patient with hypertension. There were no significant between-group differences in the responses to the GH therapy. Body composition and serum lipid pattern improved in both groups without any deterioration of glucose homeostasis. At study end, no difference remained between the two groups in any variable. During the 2-yr treatment, one patient had a myocardial infarction and two had cerebral infarctions in the A group, whereas no vascular event occurred in the NF group. CONCLUSIONS: GHD patients with previous acromegaly have an impaired cardiovascular risk profile and decreased local muscle endurance as compared with other GHD patients. Two-year GH replacement eliminated these differences, but vascular events occurred more frequently in the A group. Therefore, GHD patients with cured acromegaly will benefit from GH replacement, but careful monitoring of cardiovascular status is needed.
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| 42. |
- Olsson, Daniel S, 1983, et al.
(author)
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Comparing progression of non-functioning pituitary adenomas in hypopituitarism patients with and without long-term GH replacement therapy.
- 2009
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In: European journal of endocrinology / European Federation of Endocrine Societies. - 1479-683X. ; 161:5, s. 663-9
-
Journal article (peer-reviewed)abstract
- OBJECTIVE: An important safety issue with GH replacement therapy (GHRT) in hypopituitary patients with a history of a pituitary adenoma is the risk for tumour recurrence or enlargement. Design Case-control study. SUBJECTS AND METHODS: We studied tumour progression rate in 121 patients with hypopituitarism on the basis of non-functioning pituitary adenomas (NFPA) receiving long-term GHRT. A group of 114 NFPA patients not receiving GHRT who were matched in terms of duration of follow-up, gender, age, age at diagnosis and radiotherapy status were used as a control population. The average duration of GHRT was 10+/-4 years (range 2-17). RESULTS: In patients with a known residual adenoma, 63% had no detectable enlargement of tumour during the study. In patients who had no visible residual tumour prior to GHRT, 90% did not suffer from recurrence. In total, the 10-year tumour progression-free survival rate in patients with NFPA receiving GHRT was 74%. In the control population not receiving GHRT, the 10-year progression-free survival rate was 70%. Radiotherapy as part of the initial tumour treatment reduced the rate of tumour progression in both GHRT and non-GHRT patients to a similar extent. CONCLUSIONS: The rate of tumour progression was similar in this large group of GHRT patients and the control population not receiving GHRT. Our results provide further support that long-term use of GH replacement in hypopituitarism may be considered safe in patients with residual pituitary adenomas.
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| 43. |
- Peker, Yüksel, 1961, et al.
(author)
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Sleep apnoea and quality of life in growth hormone (GH)-deficient adults before and after 6 months of GH replacement therapy
- 2006
-
In: Clin Endocrinol (Oxf).. - : Wiley. ; 65:1, s. 98-105.
-
Journal article (peer-reviewed)abstract
- OBJECTIVE: To investigate the sleep architecture and breathing as well as quality of life (QoL) in adults with GH deficiency (GHD) before and 6 months after GH replacement therapy. DESIGN: A prospective observational study. PATIENTS: Nineteen consecutive adults with GHD (11 men, eight women; mean age 53, range 21-73 years) were studied. MEASUREMENTS: An overnight sleep study was performed and the Minor Symptom Evaluation Profile (MSEP), Functional Outcome of Sleep Questionnaire (FOSQ), Short Form 36 (SF-36) and Epworth Sleepiness Scale (ESS) questionnaires were applied at baseline and after the treatment period. RESULTS: For the whole group, there were no significant changes in mean total sleep time (TST; 370 min vs. 374 min), proportion of slow-wave sleep (SWS; 17.8%vs. 18.4%) and rapid eye movement (REM) sleep (12.1%vs. 13.9%) on GH replacement. Mean apnoea-hypopnoea index (AHI) was high and remained unchanged (28.2/h before vs. 28.0/h following GH replacement). Twelve patients (63%) were found to have obstructive sleep apnoea (OSA; AHI >or= 10/h) at baseline. Compared with GH-deficient patients without OSA (AHI 3.9/h), the OSA patients (AHI 42.4/h) had less SWS (11.4%vs. 28.6%, P = 0.010) and REM sleep (10.1%vs. 15.5%, P = 0.036). A marginal increase was observed in REM sleep time (10.1% before vs. 12.7% after GH; P = 0.048) while SWS was unchanged in this group. Moreover, MSEP for General Well-being and Responsiveness, FOSQ scores for General Productivity, Activity Level and Vigilance as well as SF-36 domains for Vitality and Mental Health were improved. CONCLUSIONS: Contrary to some previous observations in a smaller group of patients, our data suggest that GH therapy does not induce or aggravate OSA in GH-deficient adults. Moreover, GH therapy may improve some of the QoL dimensions in these patients.
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| 44. |
- Sigurjónsdóttir, Helga A, 1964, et al.
(author)
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GH effect on enzyme activity of 11betaHSD in abdominal obesity is dependent on treatment duration.
- 2006
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In: European journal of endocrinology / European Federation of Endocrine Societies. - : Oxford University Press (OUP). - 0804-4643 .- 1479-683X. ; 154:1, s. 69-74
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Journal article (peer-reviewed)abstract
- OBJECTIVE: In the past years the interaction of GH and 11beta hydroxysteroid dehydrogenase (11betaHSD) in the pathogenesis of central obesity has been suggested. DESIGN: We studied the effects of 9 months of GH treatment on 11betaHSD activity and its relationship with body composition and insulin sensitivity in 30 men with abdominal obesity, aged 48-66 years, in a randomised, double-blind, placebo-controlled trial. METHODS: Urinary steroid profile was used to estimate 11betaHSD type 1 and 2 (11betaHSD1 and 11betaHSD2) activities. Abdominal s.c. and visceral adipose tissues were measured using computed tomography. Glucose disposal rate (GDR) obtained during a euglycaemic-hyperinsulinaemic glucose clamp was used to assess insulin sensitivity. RESULTS: In the GH-treated group the 11betaHSD1 activity decreased transiently after 6 weeks (P < 0.01) whereas 11betaHSD2 increased after 9 months of treatment (P < 0.05). Between 6 weeks and 9 months, GDR increased and visceral fat mass decreased. Changes in 11betaHSD1 correlated with changes in visceral fat mass between baseline and 6 weeks. There were no significant correlations between 11betaHSD1 and 11betaHSD 2 and changes in GDR. DISCUSSION: The study demonstrates that short- and long-term GH treatment has different effects on 11betaHSD1 and 11betaHSD2 activity. Moreover, the data do not support that long-term metabolic effects of GH are mediated through its action on 11betaHSD.
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| 45. |
- Sigurjónsdóttir, Helga A, 1964, et al.
(author)
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Lack of regulation of 11beta-hydroxysteroid dehydrogenase type 1 during short-term manipulation of GH in patients with hypopituitarism.
- 2009
-
In: European journal of endocrinology / European Federation of Endocrine Societies. - 1479-683X. ; 161:3, s. 375-80
-
Journal article (peer-reviewed)abstract
- OBJECTIVE: Evidence from long-term clinical studies measuring urinary steroid ratios, and from in vitro studies, suggests that GH administered for longer than 2 months down-regulates 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1), thereby reducing cortisol regeneration in liver and adipose tissue. We aimed to measure acute effects of GH on 11beta-HSD1 in liver and adipose tissue in vivo, including using a stable isotope tracer. DESIGN: Observational studies of GH withdrawal and reintroduction in patients with hypopituitarism. METHODS: Twelve men with benign pituitary disease causing GH and ACTH deficiency on stable replacement therapy for >6 months were studied after GH withdrawal for 3 weeks, and after either placebo or GH injections were reintroduced for another 3 weeks. We measured cortisol kinetics during 9,11,12,12-(2)H(4)-cortisol (d4-cortisol) infusion, urinary cortisol/cortisone metabolite ratios, liver 11beta-HSD1 by appearance of plasma cortisol after oral cortisone, and 11beta-HSD1 mRNA levels in subcutaneous adipose biopsies. RESULTS: GH withdrawal and reintroduction had no effect on 9,12,12-[(2)H](3)-cortisol (d3-cortisol) appearance, urinary cortisol/cortisone metabolite ratios, initial appearance of cortisol after oral cortisone, or adipose 11beta-HSD1 mRNA. GH withdrawal increased plasma cortisol 30-180 min after oral cortisone, increased d4-cortisol clearance, and decreased relative excretion of 5alpha-reduced cortisol metabolites. CONCLUSIONS: In this setting, GH did not regulate 11beta-HSD1 rapidly in vivo in humans. Altered cortisol metabolism with longer term changes in GH may reflect indirect effects on 11beta-HSD1. These data do not suggest that glucocorticoid replacement doses need to be increased immediately after introducing GH therapy to compensate for reduced 11beta-HSD1 activity, although dose adjustment may be required in the longer term.
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| 46. |
- Sigurjónsdóttir, Helga A, 1964, et al.
(author)
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Liquorice in moderate doses does not affect sex steroid hormones of biological importance although the effect differs between the genders.
- 2006
-
In: Hormone research. - : S. Karger AG. - 0301-0163. ; 65:2, s. 106-10
-
Journal article (peer-reviewed)abstract
- BACKGROUND/AIM: Liquorice is commonly consumed, at least in the western world, and we have earlier shown that even moderate doses of liquorice have significant effects on the cortisol metabolism by inhibiting 11beta-hydroxysteroid dehydrogenase type 2. The suggestion that liquorice decreases the testosterone levels in men makes it vital to study the effect of moderate doses of liquorice on sex steroid hormones. METHODS: Fifteen women and 21 men (healthy volunteers and subjects with essential hypertension) consumed 100 g of liquorice (150 mg glycyrrhetinic acid) daily in a 9-week, open-treatment trial. Blood and 24-hour urine samples were collected for hormone analysis before and after 4 weeks of liquorice consumption and 4 weeks after cessation of liquorice intake. RESULTS: The liquorice induced a moderate decrease in the serum concentrations of dehydroepiandrostenedione sulphate in men (p = 0.002). The relative change in serum levels of dehydroepiandrosterone sulphate differed between the genders (p = 0.03). No significant changes were observed in the serum testosterone levels after 4 weeks of liquorice consumption, and the urine excretion of androgens (etiocholanolone and androstenedione) did not change. CONCLUSIONS: Liquorice in moderate doses primarily affects the cortisol metabolism and only marginally the androgen hormones. Gender may influence the action of liquorice.
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| 47. |
- Sigurjónsdóttir, Helga A, 1964, et al.
(author)
-
The liquorice effect on the RAAS differs between the genders.
- 2006
-
In: Blood pressure. - : Informa UK Limited. - 0803-7051 .- 1651-1999. ; 15:3, s. 169-72
-
Journal article (peer-reviewed)abstract
- OBJECTIVE: Liquorice-induced increase in blood pressure (BP) is more profound in subjects with essential hypertension (HT) than in healthy individuals. Liquorice induces pseudohyperaldosteronism by inhibiting the 11beta-hydroxysteroid dehydrogenase type 2 and is also known to inhibit the renin-angiotensin-aldosterone system (RAAS). We explored the difference in response in BP, considering the RAAS and the genders. DESIGN: Patients with HT (eight men and three women, mean age 40.7 years) and healthy controls (13 men and 12 women, mean age 31.2 years) consumed 100 g of liquorice (150 mg glycyrrhetinic acid) daily for 4 weeks. METHODS: Blood, urine samples and BP were evaluated before and after 4 weeks of liquorice consumption and 4 weeks after cessation of liquorice consumption. RESULTS: The relative change in serum aldosterone levels differed between the genders (p < 0.02), men being more responsive than women, but not between patients with HT and healthy subjects. CONCLUSION: The liquorice-induced inhibition of aldosterone secretion differs between the genders and is not influenced by the BP levels. This difference between the genders has not been exposed before.
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| 48. |
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| 49. |
- Svensson, Johan, 1964, et al.
(author)
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Adiponectin, leptin, and erythrocyte sodium/lithium countertransport activity, but not resistin, are related to glucose metabolism in growth hormone-deficient adults.
- 2005
-
In: The Journal of clinical endocrinology and metabolism. - : The Endocrine Society. - 0021-972X .- 1945-7197. ; 90:4, s. 2290-6
-
Journal article (peer-reviewed)abstract
- In a randomized, placebo-controlled, crossover study under metabolic ward conditions, 10 GH-deficient adults received 1-wk GH replacement therapy (9.5 microg/kg.d). The effect of this treatment on the erythrocyte sodium/lithium countertransport (SLC) activity and on serum levels of adiponectin, resistin, leptin, IGF binding protein-1 (IGFBP-1) and IL-6 was determined. The 1-wk GH replacement impaired glucose homeostasis determined from an oral glucose tolerance test. The other measured variables in serum were unchanged by GH replacement. At baseline, serum adiponectin level was inversely correlated and serum leptin level was positively correlated with measures of glucose tolerance and insulin sensitivity. The changes in serum leptin level and erythrocyte SLC activity were positively correlated, and the change in serum IGFBP-1 level was negatively correlated, correlated with changes in measures of glucose metabolism. In conclusion, short-term GH treatment induced glucose intolerance but did not significantly change the erythrocyte SLC activity and the serum levels of adipokines, arguing against direct effects of GH on these measures. However, baseline values or changes in erythrocyte SLC activity, adiponectin, leptin, and IGFBP-1 correlated with glucose metabolism. This suggests that these factors are of importance for glucose homeostasis in GH-deficient adults, most likely through GH-independent mechanisms.
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| 50. |
- Svensson, Johan, 1964, et al.
(author)
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GH secretory pattern in young adults who discontinued GH treatment for GH deficiency and decreased longitudinal growth in childhood.
- 2006
-
In: European journal of endocrinology / European Federation of Endocrine Societies. - : Oxford University Press (OUP). - 0804-4643. ; 155:1, s. 91-9
-
Journal article (peer-reviewed)abstract
- OBJECTIVE: Some adolescents who discontinue GH treatment due to GH deficiency (GHD) and short stature in childhood do not have classical GHD at retesting in adult life. It is unknown whether there is a neuroendocrine disturbance in the spontaneous pattern of GH release in these patients. DESIGN/PATIENTS/METHODS: Thirty-seven adolescents, who had received treatment with GH due to impaired longitudinal growth, were included. The adolescents were divided into two groups; one (GHD; n = 19) with classical GHD in adult life and another (GH sufficient (GHS); n = 18) without classical adult GHD. One year after GH discontinuation, 24-h GH profiles were performed with blood sampling every 30 min. Sixteen matched healthy controls were also studied. All blood samples were analysed using an ultrasensitive GH assay and then, approximate entropy (ApEn) and deconvolution analysis were performed. RESULTS: The GHD group had higher mean ApEn level than the healthy controls (P < 0.05). As measured by deconvolution analysis, they had lower basal GH secretion (P < 0.01), increased number of GH peaks (P < 0.001), but lower burst mass (P < 0.001), lower percentage pulsatile GH secretion (P < 0.001) and lower total GH secretion (P < 0.001), compared with control subjects. Adolescents in the GHS group had a pattern of 24-h GH release similar to that in healthy controls. CONCLUSION: Young adults with childhood-onset severe GHD have a high-frequency, low-amplitude GH secretion with decreased orderliness. The adolescents without classical GHD in adult life maintain a pattern of spontaneous GH release that is not statistically different from that in the healthy controls.
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