Effects of up to 15 years of recombinant human GH replacement therapy on the skeleton in adult GH deficiency: the Leiden Cohort Study

2014 ◽  
Author(s):  
Natasha Appelman-Dijkstra ◽  
Kim Claessen ◽  
Neveen Hamdy ◽  
Alberto Pereira ◽  
Nienke Biermasz
Keyword(s):  
Cohort Study ◽  
Replacement Therapy ◽  
Gh Deficiency ◽  
Gh Replacement ◽  
Adult Gh Deficiency

scholarly journals Successful pregnancy and delivery in a patient with adult GH deficiency: role of GH replacement therapy

2011 ◽  
Vol 58 (1) ◽  
pp. 65-68 ◽  
Author(s):  
Satoko Sakai ◽  
Takanobu Wakasugi ◽  
Kunimasa Yagi ◽  
Akitsu Ohnishi ◽  
Naoko Ito ◽  
...  
Keyword(s):  
Replacement Therapy ◽  
Gh Deficiency ◽  
Successful Pregnancy ◽  
Gh Replacement ◽  
Adult Gh Deficiency ◽  
Pregnancy And Delivery

scholarly journals Discontinuing Long-Term GH Replacement Therapy—A Randomized, Placebo-Controlled Crossover Trial in Adult GH Deficiency

2012 ◽  
Vol 97 (9) ◽  
pp. 3185-3195 ◽  
Author(s):  
Helena Filipsson Nyström ◽  
Edna J. L. Barbosa ◽  
Anna G. Nilsson ◽  
Lise-Lott Norrman ◽  
Oskar Ragnarsson ◽  
...  
Keyword(s):  
Replacement Therapy ◽  
Crossover Trial ◽  
Gh Deficiency ◽  
Gh Replacement ◽  
Adult Gh Deficiency

scholarly journals A Case With Adult GH Deficiency Complicated With Osteogenesis Imperfecta: Effect of GH Replacement on Bone Mineral Density

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A564-A564
Author(s):  
Tomomi Taguchi ◽  
Takuya Toki ◽  
Akinori Hayashi ◽  
Koji Takano
Keyword(s):  
Bone Mineral Density ◽  
Osteogenesis Imperfecta ◽  
Replacement Therapy ◽  
Bone Mineral ◽  
Gh Deficiency ◽  
Stimulation Test ◽  
Z Score ◽  
Mineral Density ◽  
Gh Replacement ◽  
Adult Gh Deficiency

Abstract Background: Osteogenesis imperfecta (OI) is an inherited connective tissue disorder with many phenotypic presentations. Bisphosphonates are the mainstay of pharmacologic fracture prevention therapy, although they aren’t officially approved for the treatment of OI. Clinical Case: The patient was born by breech delivery. After he had multiple fractures at the age of two years, he was diagnosed with osteogenesis imperfecta (OI) type I by genetic analysis (c.1299 + 1G> A mutation in the COL1A1 gene). On the growth curve, his height fell below -2SD at the age of six years. When he was 12 years old, he visited another hospital because of short stature (Hight 119 cm: -2.7SD). Pituitary MRI revealed pituitary stalk disruption and pituitary atrophy. Endocrinological examinations (ITT, TRH, LHRH, arginine stimulation tests) showed severe GH deficiency. Growth hormone replacement therapy was started. At the age of 16 years, he was diagnosed to have central hypothyroidism and central diabetes insipidus, and levothyroxine and DDAVP were started. His bone mineral density of the lumbar spine was 0.546 g/cm2, and alendronate was started. At the age of 17, central hypogonadism was diagnosed by LHRH stimulation test, and HCG injections were initiated. His bone mineral density continued to increase by GH replacement, HCG injections and bisphosphonate and reached 0.820 g/cm2 (Z-score: -0.27) by the age of 18 years. GH replacement was discontinued (final height 180 cm). At that age, his bone mineral density declined to 0.717 g/cm2 at the age of 25 years, although he stayed on an alendronate and HCG injections. At that time, total testosterone 890 ng/dL (142<n<923 ng/dL) was within normal range, but IGF-1 level was below the lower limit (44 ng/mL; -4.6SD, 225<n<337 ng/mL). He was referred to our hospital for transition to adult endocrine care. Endocrinologic evaluation revealed low serum cortisol level in the early morning (2.26 µg/dL, 7.07<n<19.6 μg/dL). GH-releasing peptide-2 stimulation test revealed severe GH deficiency (peak GH 0.18 ng/mL, n> 15 ng/mL (1)) and replacements with GH and hydrocortisone were initiated. After the GH replacement, the bone mineral density started to increase to 0.954 g/cm2 (Z-score: -0.5). Conclusion: So far as we know, this is the first case report of OI with panhypopituitarism treated with GH and bisphosphonate. This case suggests that bisphosphonate alone is not sufficient to maintain bone mineral density complicated with both OI and severe GHD. GH replacement therapy was inevitable to increase bone mineral density in this patient. Reference: (1) Kazuo Chihara et al. A simple diagnostic test using GH-releasing peptide-2 in adult GH deficiency. Eur J Endocrinol.2007;157;19-27.

scholarly journals Metabolic Co-Morbidities Revealed in Patients with Childhood-Onset Adult GH Deficiency after Cessation of GH Replacement Therapy for Short Stature

2008 ◽  
Vol 55 (6) ◽  
pp. 977-984 ◽  
Author(s):  
Izumi FUKUDA ◽  
Naomi HIZUKA ◽  
Kumiko YASUMOTO ◽  
Junko MORITA ◽  
Makiko KURIMOTO ◽  
...  
Keyword(s):  
Replacement Therapy ◽  
Short Stature ◽  
Gh Deficiency ◽  
Childhood Onset ◽  
Gh Replacement ◽  
Adult Gh Deficiency

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.

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