scholarly journals Adjuvant Growth Hormone for Ovulation Induction with Gonadotropins in the Treatment of a Woman with Hypopituitarism

2012 ◽  
Vol 2012 ◽  
pp. 1-3 ◽  
Author(s):  
Ariadne Daniel ◽  
Shereen Ezzat ◽  
Ellen Greenblatt
Keyword(s):  
Growth Hormone ◽  
Ovulation Induction ◽  
Gh Deficiency ◽  
Pregnancy Rates ◽  
Small Subset ◽  
High Dose ◽  
Human Menopausal Gonadotropin ◽  
Deficient Patient ◽  
Igf I ◽  
Higher Doses

Objective. To report the prestimulation use of adjuvant GH for gonadotropin ovulation induction in a woman with hypopituitarism and GH deficiency who previously failed to respond.Design, Patients, and Measurements. A 31-year-old nulliparous woman presented with hypopituitarism and GH deficiency after failing ovulation induction with high dose gonadotropins. A trial of GH was undertaken for 5 months prior to ovulation induction resulting in normalization of IGF-I levels.Results. Women with hypopituitarism are known to have lower pregnancy rates after ovulation induction with need for higher doses of gonadotropins. A small subset of these patients do not ovulate. This patient had successful ovulation induction and pregnancy with prestimulation GH.Conclusions. This case suggests that the use of adjuvant GH in a GH-deficient patient several months before the use of human menopausal gonadotropin results in ovulation and pregnancy.

scholarly journals Utility of P300 auditory event related potential latency in detecting cognitive dysfunction in growth hormone (GH) deficient patients with Sheehan's syndrome and effects of GH replacement therapy

2004 ◽  
pp. 153-159 ◽  
Author(s):  
A Golgeli ◽  
F Tanriverdi ◽  
C Suer ◽  
C Gokce ◽  
C Ozesmi ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Cognitive Function ◽  
Replacement Therapy ◽  
Patient Group ◽  
Gh Deficiency ◽  
Event Related Potential ◽  
Sheehan’S Syndrome ◽  
Gh Replacement ◽  
Igf I ◽  
Sheehan's Syndrome

OBJECTIVE: Impaired cognitive function has been demonstrated in adults with growth hormone (GH) deficiency (GHD) by using different neuropsychological tests. Despite several studies, present knowledge about the impact of GHD and GH replacement therapy (GHRT) on cognitive function is limited. P300 event-related potential (ERP) application is a well-established neurophysiological approach in the assessment of cognitive functions including the updating of working memory content and the speed of stimulus evaluation. GHD is a well-known feature of Sheehan's syndrome and cognitive changes due to GHD and the effects of GHRT remain to be clarified. The present study was designed to investigate the effects of GHD and 6 months of GHRT on cognitive function in patients with Sheehan's syndrome by using P300 latency. DESIGN AND METHODS: The study comprised 14 patients with Sheehan's syndrome (mean age, 49.5+/-7.8 years) and 10 age-, education- and sex-matched healthy controls. With hormone replacement therapy, basal hormone levels other than GH were stable before enrollment and throughout the GHRT. The diagnosis of GH deficiency was established by insulin-tolerance test (ITT), and mean peak level of GH in response to insulin hypoglycemia was 0.77+/-0.35 mIU/l. Treatment with GH was started at a dose of 0.45 IU (0.15 mg)/day in month 1, was increased to 0.9 IU (0.30 mg)/day in month 2 and was maintained at 2 IU (0.66 mg)/day. Initially baseline auditory ERPs in patients and controls were recorded at frontal (Fz), central (Cz), and parietal (P3 and P4) electrode sites. In the patient group, ERPs were re-evaluated after 6 months of GH replacement therapy. During each session P300 amplitude and latency were measured. RESULTS: Mean serum insulin-like growth factor-I (IGF-I) concentration in the patient group before GHRT was 23+/-13 ng/ml. After 6 months of GH therapy mean IGF-I significantly increased to an acceptable level, 234+/-71 ng/ml (P<0.05). The mean latencies (at all electrode sites) of the patients before GHRT were found to be significantly prolonged when compared with those of normal controls (P<0.05). After 6 months of GHRT mean P300 latencies (at all electrode sites) were decreased significantly when compared with latencies before treatment (P<0.05). CONCLUSIONS: The present study, using P300 ERP latencies, therefore suggests an impairment of cognitive abilities due to severe GHD in patients with Sheehan's syndrome and an improvement of cognitive function after 6 months of physiological GHRT. Moreover, this was a novel application of P300 ERP latencies in cognitive function detection in patients with GHD. Further studies with different patient groups need to be done to assess the clinical use of this electrophysiological method in the diagnosis of cognitive dysfunction due to GHD.

scholarly journals The Use of High Dose Letrozole in Ovulation Induction and Controlled Ovarian Hyperstimulation

2011 ◽  
Vol 2011 ◽  
pp. 1-4 ◽  
Author(s):  
Elizabeth A. Pritts ◽  
Alexander K. Yuen ◽  
Shefaali Sharma ◽  
Robert Genisot ◽  
David L. Olive
Keyword(s):  
Ovulation Induction ◽  
Detrimental Effect ◽  
Endometrial Thickness ◽  
Controlled Ovarian Hyperstimulation ◽  
High Dose ◽  
Ovarian Hyperstimulation ◽  
Dose Administration ◽  
Treatment Groups ◽  
Starting Dose ◽  
Higher Doses

Letrozole, an aromatase inhibitor, has been demonstrated to be effective as an ovulation induction and controlled ovarian hyperstimulation agent. However, dose administration has generally been limited to 5 days at 2.5 to 7.5 mg daily. We undertook a retrospective review of over 900 treatment cycles using letrozole in doses as high as 12.5 mg per day. Results indicate that such doses do indeed offer benefit to patients; in that there is increased follicular growth and a higher number of predicted ovulations with higher doses of the drug. However, increasing doses does not produce a detrimental effect upon endometrial thickness. High-dose letrozole may be of value in women who fail to respond adequately to lower doses. Furthermore, randomized trials are needed to determine whether high-dose letrozole might actually be optimal as a starting dose for certain treatment groups.

Growth Hormone Therapy in Children with Kabuki Syndrome: 1-year Treatment Results

2017 ◽  
Vol 88 (3-4) ◽  
pp. 258-264 ◽  
Author(s):  
Dina A. Schott ◽  
Willem J.M. Gerver ◽  
Constance T.R.M. Stumpel
Keyword(s):  
Growth Hormone ◽  
Gh Deficiency ◽  
Standard Deviation Score ◽  
Height Velocity ◽  
Kabuki Syndrome ◽  
Body Proportions ◽  
Leg Length ◽  
Gh Treatment ◽  
Igf I ◽  
Rhgh Treatment

Background/Aims: Kabuki syndrome (KS) is a rare genetic malformation syndrome, resulting in characteristic features such as short stature. We investigate whether growth hormone (GH) treatment increases linear height and influences body proportions in KS children. Methods: In this prospective study, 18 genetically confirmed prepubertal KS children (9 females and 9 males) aged from 3.8 to 10.1 years (mean 6.8 ± 2.1 years) were treated with recombinant human GH (rhGH) for 1 year. Calculations for height, height velocity, BMI, sitting height, and subischial leg length were made. Bone age, insulin-like growth factor (IGF-I), and IGF binding protein 3 (IGFBP-3) were also measured. Results: This study showed an increase in height standard deviation score (SDS) for the whole group from –2.40 to –1.69 (p < 0.05) after 1 year of rhGH treatment. The change in height SDS within 1 year was >0.7 SDS for 10 subjects and >0.5 SDS for 3 subjects. The mean IGF-I SDS at the start of the study was –0.70 (±1.07), which increased after 12 months to 1.41 (±0.91) (p < 0.05). KS children who received rhGH at a younger age displayed significantly greater increases in height than those who started when they were older. The same was true for both gene mutation KMT2D versus KDM6A and for GH deficiency versus non-GH deficiency KS children (p < 0.05). Throughout the course of rhGH treatment, the subjects’ body proportions remained normal. Conclusions: All participants experienced catch-up growth during the year of rhGH treatment, but without an influence on body proportions.

scholarly journals Does adiposity status influence femoral cortical strength in rodent models of growth hormone deficiency?

2009 ◽  
Vol 296 (1) ◽  
pp. E147-E156 ◽  
Author(s):  
A. E. Stevenson ◽  
B. A. J. Evans ◽  
E. F. Gevers ◽  
C. Elford ◽  
R. W. J. McLeod ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Cortical Bone ◽  
Gh Deficiency ◽  
Monosodium Glutamate ◽  
Residual Activity ◽  
Hormone Deficiency ◽  
Rodent Models ◽  
Femoral Strength ◽  
Igf I ◽  
Geometric Variables

Growth hormone (GH)-deficiency is usually associated with elevated adiposity, hyperleptinemia, and increased fracture risk. Since leptin is thought to enhance cortical bone formation, we have investigated the contribution of elevated adiposity and hyperleptinemia on femoral strength in rodent models of GH deficiency. Quantification of the transpubertal development of femoral strength in the moderately GH-deficient/hyperleptinemic Tgr rat and the profoundly GH-deficient/hypoleptinemic dw/dw rat revealed that the mechanical properties of cortical bone in these two models were similarly compromised, a 25–30% reduction in failure load being entirely due to impairment of geometric variables. In contrast, murine models of partial (GH antagonist transgenic) and complete (GH receptor-null) loss of GH signaling and elevated adiposity showed an impairment of femoral cortical strength proportionate to the reduction of GH signaling. To determine whether impaired femoral strength is exacerbated by obesity/hyperleptinemia, femoral strength was assessed in dw/dw rats following two developmental manipulations that elevate abdominal adiposity and circulating leptin, neonatal monosodium glutamate (MSG) treatment, and maintenance on an elevated fat diet. The additional impairment of femoral strength following MSG treatment is likely to have resulted from a reduction in residual activity of the hypothalamo-pituitary-GH-IGF-I axis, but consumption of elevated dietary fat, which did not reduce circulating IGF-I, failed to exacerbate the compromised femoral strength in dw/dw rats. Taken together, our data indicate that the obesity and hyperleptinemia usually associated with GH deficiency do not exert a significant influence over the strength of cortical bone.

scholarly journals Final height in isolated GH deficiency type 1A: effects of 5-year treatment with IGF-I

2001 ◽  
pp. 379-383 ◽  
Author(s):  
MF Messina ◽  
F De Luca ◽  
M Wasniewska ◽  
M Valenzise ◽  
F Lombardo ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Gh Deficiency ◽  
Final Height ◽  
Phenotypic Expression ◽  
Hormone Deficiency ◽  
Target Height ◽  
Igf I ◽  
Puberty Onset ◽  
The One ◽  
Deficiency Type

Data concerning final height (FH) in isolated growth hormone deficiency type 1A (IGHD1A) are scanty and controversial. In this paper we report the FH outcome of two girls with IGHD1A who were treated either with GH only (first patient) or with GH during the first 8 years and successively with IGF-I (second patient). In the first patient, FH was only slightly subnormal and slightly taller with respect to target height (TH). Surprisingly, FH was severely subnormal and very far from TH in the patient who underwent IGF-I therapy for >5 years: an auxological outcome similar to the one recently reported in the only two cases in the literature of patients with IGHD1A who have been treated with IGF-I until near FH achievement. We conclude that IGHD1A could have a very heterogeneous phenotypic expression in terms of FH and that IGF-I therapy, even though initiated some years before puberty onset and prolonged for more than 5 years, may not be able to ensure the normalization of height prognosis and the achievement of an FH close to TH.

The hormonal regulation of the oestrogen receptor in rat liver: an interplay involving growth hormone, thyroid hormones and glucocorticoids

1994 ◽  
Vol 142 (2) ◽  
pp. 285-298 ◽  
Author(s):  
B Freyschuss ◽  
L Sahlin ◽  
B Masironi ◽  
H Eriksson
Keyword(s):  
Growth Hormone ◽  
Continuous Infusion ◽  
Hormonal Regulation ◽  
Messenger Rna ◽  
Oestrogen Receptor ◽  
Female Rats ◽  
High Dose ◽  
Mrna Levels ◽  
Gapdh Mrna ◽  
Igf I

Abstract The regulation of the formation of the hepatic oestrogen receptor (ER) in adult female rats was studied by assaying steady state levels of ER and ER messenger RNA under different endocrine conditions. Hypophysectomy (HX) drastically reduced ER levels from 67·5 ± 7·9 to 8·4 ± 0·5 (means ± s.e.m.) fmol/mg cytosolic protein. Continuous infusion of growth hormone (GH) to HX animals tripled ER and doubled ER mRNA levels. Treatment with triiodothyronine T3) in a high dose (10 μg/day) doubled ER mRNA levels. The effects of T3 were dose-dependent, since a lower dose (1 μg/day) increased neither ER nor ER mRNA levels. ER mRNA concentrations were increased by GH to 481 ± 44% and by T3 to 372 ± 35% of HX control levels 4 h after single injections of the hormones in HX animals. The glucocorticoid dexamethasone (DEX) alone increased neither ER nor ER mRNA levels in HX animals. DEX and GH in combination increased ER 5-fold and ER mRNA 2-fold compared with control levels in HX animals, whereas DEX and T3 in combination increased neither ER nor ER mRNA levels. Treatment with prolactin affected neither ER nor ER mRNA levels in HX rats. Insulin-like growth factor I (IGF-I) mRNA and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mRNA levels were measured. GAPDH mRNA levels were increased 2·5-fold in HX rats by DEX and T3 in combination and almost 2-fold by DEX and GH in combination. IGF-I mRNA levels in HX rats were increased 4·5-fold by continuous infusion of GH alone, 6-fold by GH and T3 in combination, and 2·5-fold by GH and DEX in combination. These data indicate that both GH and T3 act directly on the liver to increase ER mRNA levels. GH, the most important of these hormones, also acts at the translational and/or post-translational level to increase ER protein levels. DEX treatment suppresses the stimulatory effects of T3, but not of GH. Journal of Endocrinology (1994) 142, 285–298

Comparison between weight-based and IGF-I-based growth hormone (GH) dosing in the treatment of children with GH deficiency and influence of exon 3 deleted GH receptor variant

2009 ◽  
Vol 19 (2) ◽  
pp. 179-186 ◽  
Author(s):  
Frederico Guimarães Marchisotti ◽  
Alexander Augusto Lima Jorge ◽  
Luciana Ribeiro Montenegro ◽  
Karina Berger ◽  
Luciani Renata Silveira de Carvalho ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Gh Deficiency ◽  
Gh Receptor ◽  
Igf I

New approach to the diagnosis of growth hormone deficiency in adults

1996 ◽  
Vol 134 (3) ◽  
pp. 352-356 ◽  
Author(s):  
Ezio Ghigo ◽  
Gianluca Aimaretti ◽  
Laura Gianotti ◽  
Jaele Bellone ◽  
Emanuela Arvat ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Hormone Deficiency ◽  
Gh Deficiency ◽  
Serum Insulin ◽  
Normal Subjects ◽  
Hormone Deficiency ◽  
New Approach ◽  
Igf I ◽  
Ghrh Test ◽  
Gh Deficiency In Adults

Ghigo E, Aimaretti G, Gianotti L, Bellone J, Arvat E, Camanni F. New approach to the diagnosis of growth hormone deficiency in adults. Eur J Endocrinol 1996;134:352–6. ISSN 0804–4643 Pyridostigmine (PD), a muscarinic cholinergic agonist, and arginine (ARG) clearly increase the growth hormone (GH) response to growth hormone-releasing hormone (GHRH) in man. The current study was undertaken to investigate the value and safety of PD + GHRH and ARG + GHRH tests as well as the measurement of serum insulin-like growth factor I (IGF-I) in diagnosing GH deficiency in adults. Fifty-four patients considered GH deficient from extensive organic or idiopathic pituitary disease and 326 healthy adults were studied. The IGF-I concentrations were lower than the 3rd percentile of normal values in only 31 of the 54 (57.4%) patients with hypopituitarism. However, the IGF-I levels in hypopituitary patients and in normal subjects overlapped more frequently between 41 and 60 years (50%) and between 61 and 80 years (92.3%) as opposed to between 20 and 40 years (8.6%). In contrast to the IGF-I measurement, the ranges of peak GH responses to PD + GHRH and ARG + GHRH tests were clearly differentiated between the hypopituitary (0.2–6.8 and 0.1–9.5 μg/l, respectively) and normal subjects 17.7–114 and 16.1–119 μg/l, respectively). However, the PD + GHRH test was reliable only in subjects of 20–40 years of age. In conclusion, IGF-I measurement had no value in the diagnosis of GH deficiency in adults aged over 40 years, but is reliable enough when young adults of 20–40 years of age are considered. Both PD + GHRH and ARG + GHRH testing should be considered more reliable biochemical measurements of GH deficiency. In contrast to the PD + GHRH test, the ARG + GHRH test is reliable throughout the adult lifespan and appears to be the most appropriate for patient compliance and safety. F Camanni, Divisione di Endocrinologia, Ospedale Molinette, C.so Dogliotti 14, 10126 Torino, Italy

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