scholarly journals Skin morphological changes in growth hormone deficiency and acromegaly

2001 ◽  
pp. 147-153 ◽  
Author(s):  
M Lange ◽  
J Thulesen ◽  
U Feldt-Rasmussen ◽  
NE Skakkebaek ◽  
N Vahl ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Hormone Deficiency ◽  
Morphological Changes ◽  
Hormone Deficiency ◽  
Sweat Glands ◽  
Gh Treatment ◽  
Sweat Secretion ◽  
Increased Risk ◽  
Significant Difference ◽  
Eccrine Sweat

OBJECTIVE: To evaluate the histomorphology of skin and its appendages, especially eccrine sweat glands, in patients with GH disorders, because reduced sweating ability in patients with growth hormone deficiency (GHD) is associated with increased risk of hyperthermia under stressed conditions. DESIGN AND METHODS: A skin biopsy was obtained from 17 patients with GHD treated with GH, five patients with untreated GHD, 10 patients with active acromegaly and 13 healthy controls. RESULTS: The sweat secretion rate (SSR) was significantly decreased in both the untreated (median 41 mg/30 min, range 9-79 mg/30 min) and the GH-treated (median 98 mg/30 min, range 28-147 mg/30 min) patients with GHD compared with that in controls (median 119 mg/30 min, range 90-189 mg/30 min; P=0.001 and 0.01 respectively). Epidermal thickness was significantly decreased in both untreated (median 39 microm, range 28-55 microm) and GH-treated patients with GHD (median 53 microm, range 37-100 microm), compared with that in controls (median 66 microm, range 40-111 microm; P<0.02). A statistically non-significant tendency towards thinner epidermis (median 59 microm, range 33-83 microm) was recorded in acromegalic patients (P=0.08) compared with controls. There was no significant difference in the area of the sebaceous glands in the biopsies between the three groups and the controls. The area of eccrine sweat gland glomeruli was significantly decreased in the untreated patients with GHD (median 16407 microm2, range 12758-43976 microm2) compared with that in controls (median 29446 microm2, range 13511-128661 microm2; P=0.03), but there was no significant difference between the GH-treated patients with GHD and controls. CONCLUSIONS: We conclude that GH, either directly or via IGF-I, may have both a structural and a functional effect on human skin and its appendages, and that patients with GHD have histomorphological changes in skin compared with controls. Importantly, these changes are not fully reversed despite long-term and adequate GH treatment in patients with childhood onset GHD.

Pituitary volume in children with growth hormone deficiency, idiopathic short stature and controls

2016 ◽  
Vol 29 (10) ◽  
Author(s):  
Marion Kessler ◽  
Michael Tenner ◽  
Michael Frey ◽  
Richard Noto
Keyword(s):  
Growth Hormone ◽  
Magnetic Resonance ◽  
Growth Hormone Deficiency ◽  
Short Stature ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Magnetic Resonance Images ◽  
Idiopathic Short Stature ◽  
Hormone Deficiency ◽  
Significant Difference

AbstractBackground:The objective of the study was to describe the pituitary volume (PV) in pediatric patients with isolated growth hormone deficiency (IGHD), idiopathic short stature (ISS) and normal controls.Methods:Sixty-nine patients (57 male, 12 female), with a mean age of 11.9 (±2.0), were determined to have IGHD. ISS was identified in 29 patients (20 male, 9 female), with a mean age of 12.7 (±3.7). Sixty-six controls (28 female, 38 male), mean age 9.8 (±4.7) were also included. Three-dimensional (3D) magnetic resonance images with contrast were obtained to accurately measure PV.Results:There was a significant difference in the mean PV among the three groups. The IGHD patients had a mean PV 230.8 (±89.6), for ISS patients it was 286.8 (±108.2) and for controls it was 343.7 (±145.9) (p<0.001). There was a normal increase in PV with age in the ISS patients and controls, but a minimal increase in the IGHD patients.Conclusions:Those patients with isolated GHD have the greatest reduction in PV compared to controls and the patients with ISS fall in between. We speculate that a possible cause for the slowed growth in some ISS patients might be related to diminished chronic secretion of growth hormone over time, albeit having adequate pituitary reserves to respond acutely to GH stimulation. Thus, what was called neurosecretory GHD in the past, might, in some patients, be relative pituitary hypoplasia and resultant diminished growth hormone secretion. Thus, PV determinations by magnetic resonance imaging (MRI) could assist in the diagnostic evaluation of the slowly growing child.

scholarly journals Can plasma antioxidants prevent DNA damage in oxidative stress condition induced by growth hormone deficiency? A pilot study

PLoS ONE ◽  
2021 ◽  
Vol 16 (4) ◽  
pp. e0248971
Author(s):  
Antonio Mancini ◽  
Francesco Guidi ◽  
Carmine Bruno ◽  
Flavia Angelini ◽  
Edoardo Vergani ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Growth Hormone ◽  
Pilot Study ◽  
Oxidative Damage ◽  
Growth Hormone Deficiency ◽  
Hormone Deficiency ◽  
Serum Samples ◽  
Adult Growth ◽  
Significant Difference ◽  
Thymidine Glycol

Adult growth hormone deficiency (GHD), a condition characterized by increased oxidative stress, is related to augmented cardiovascular, metabolic and oncological risk. A case-control observational study has been performed to evaluate DNA oxidative damage analysing the production of thymidine-glycol in lymphocytes and its correlation with plasma antioxidant levels, evaluated as Total Antioxidant Capacity (TAC). GHD was diagnosed using GHRH 50μg iv+arginine 0,5 g/Kg test, with peak GH response <9 μg/L when BMI was <30 kg/m2 or <4 μg/L when BMI was >30 kg/m2. Three groups were identified: total GHD (n = 16), partial GHD (n = 11), and controls (n = 12). Thymidine-glycol, TAC and IGF-1 have been determined respectively in lymphocytes, plasma and serum samples. When considering thymidine-glycol, we found a significant difference between total vs partial GHD and controls. Unexpectedly thymidine-glycol was lower in total GHD, also accompanied with a significant increase in plasmatic TAC. Our results showed that in adult GHD condition, the production of antioxidant species, in response to increased oxidative stress, could exert a protective effect on thymidine-glycol formation, and consequently on DNA intracellular damages. This pilot study could be inserted in the complex scenario of oxidative damage of GHD, a subtle, yet poorly defined condition, worthy of further insights.

scholarly journals Adult height prediction by bone age determination in children with isolated growth hormone deficiency

2020 ◽  
Vol 9 (5) ◽  
pp. 370-378
Author(s):  
Thomas Reinehr ◽  
Martin Carlsson ◽  
Dionisios Chrysis ◽  
Cecilia Camacho-Hübner
Keyword(s):  
Growth Hormone ◽  
Growth Hormone Deficiency ◽  
Adult Height ◽  
Age Determination ◽  
Bone Age ◽  
Hormone Deficiency ◽  
Gh Treatment ◽  
Height Prediction ◽  
The Mean ◽  
Tw2 Method

Background The precision of adult height prediction by bone age determination in children with idiopathic growth hormone deficiency (IGHD) is unknown. Methods The near adult height (NAH) of patients with IGHD in the KIGS database was compared retrospectively to adult height prediction calculated by the Bayley–Pinneau (BP) prediction based on bone age by Greulich–Pyle (GP) in 315 children and based on the Tanner-Whitehouse 2 (TW2) method in 121 children. Multiple linear regression analyses adjusted for age at GH start, age at puberty, mean dose and years of of GH treatment, and maximum GH peak in stimulation test were calculated. Results The mean underestimation of adult height based on the BP method was at baseline 4.1 ± 0.7 cm in girls and 6.1 ± 0.6 cm in boys, at 1 year of GH treatment 2.5 ± 0.5 cm in girls and 0.9 ± 0.4 cm in boys, while at last bone age determination adult height was overestimated in mean by 0.4 ± 0.6 cm in girls and 3.8 ± 0.5 cm in boys. The mean underestimation of adult height based on the TW2 method was at baseline 5.3 ± 2.0 cm in girls and 7.9 ± 0.8 cm in boys, at 1 year of GH treatment adult height was overestimated in girls 0.1 ± 0.6 cm in girls and underestimated 4.1 ± 0.4 cm in boys, while at last bone age determination adult height was overestimated in mean by 3.1 ± 1.5 cm in girls and 3.6 ± 0.8 cm in boys. Conclusions Height prediction by BP and TW2 at onset of GH treatment underestimates adult height in prepubertal IGHD children, while in mean 6 years after onset of GH treatment these prediction methods overestimated adult height.

Effects of growth hormone deficiency (ghd) and gh treatment on early markers of atherosclerosis in children

2019 ◽  
Author(s):  
Flavia Barbieri ◽  
Nicola Improda ◽  
Andrea Esposito ◽  
Cristina Moracas ◽  
Valeria Gaeta ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Hormone Deficiency ◽  
Hormone Deficiency ◽  
Gh Treatment ◽  
Early Markers

Advances in the Understanding of Adult Growth Hormone Deficiency Syndrome – Diagnosis, Epidemiology and Management

2010 ◽  
Vol 6 (2) ◽  
pp. 45
Author(s):  
Torben Laursen ◽  
Keyword(s):  
Growth Hormone ◽  
Cardiovascular Diseases ◽  
Dynamic Testing ◽  
Gh Deficiency ◽  
Tolerance Test ◽  
Deficiency Syndrome ◽  
Hormone Deficiency ◽  
Gh Treatment ◽  
Adult Growth ◽  
Increased Risk

In patients with hypopituitarism, growth hormone (GH) deficiency is almost always present. Lack of other pituitary hormones may require prompt replacement, but lack of GH is also associated with several abnormalities, which can be improved by GH treatment. The aberrations include low bone mass and increased risk of fractures, abnormal body composition, e.g. increased fat mass and reduced lean body mass resulting in reduced muscle mass and strength. Decreased exercise capacity may be influenced by impaired cardiac performance and heat intolerance. Increased abdominal fat results in metabolic disturbancies, such as reduced insulin sensitivity and hyperlipidaemia, increasing the risk of cardiovascular diseases. Patients with hypopituitarism replaced with relevant hormones except GH have increased mortality due to cardiovascular diseases and increased morbidity. Thus, it is important to diagnose GH deficiency, which requires precise diagnostic criteria and methods. Dynamic testing of GH secretion with an insulin tolerance test or arginine plus GH-releasing hormone can be used.

scholarly journals The prevalence and volumetry of pituitary cysts in children with growth hormone deficiency and idiopathic short stature

2018 ◽  
Vol 0 (0) ◽  
Author(s):  
Nicholas Krasnow ◽  
Bradley Pogostin ◽  
James Haigney ◽  
Brittany Groh ◽  
Winston Weiler ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Hormone Deficiency ◽  
Short Stature ◽  
Growth Failure ◽  
Brain Magnetic Resonance Imaging ◽  
Idiopathic Short Stature ◽  
Hormone Deficiency ◽  
Gh Treatment ◽  
Cyst Volume ◽  
Pituitary Cysts

AbstractBackgroundPituitary cysts have been speculated to cause endocrinopathies. We sought to describe the prevalence and volumetry of pituitary cysts in patients with growth hormone deficiency (GHD) and idiopathic short stature (ISS).MethodsSix hundred and eighteen children evaluated for growth failure at the Division of Pediatric Endocrinology at New York Medical College between the years 2002 and 2012, who underwent GH stimulation testing and had a brain magnetic resonance imaging (MRI) prior to initiating GH treatment were randomly selected to be a part of this study. High resolution MRI was used to evaluate the pituitary gland for size and the presence of a cyst. Cyst prevalence, cyst volume and percentage of the gland occupied by the cyst (POGO) were documented.ResultsFifty-six patients had a cyst, giving an overall prevalence of 9.1%. The prevalence of cysts in GHD patients compared to ISS patients was not significant (13.5% vs. 5.7%, p=0.46). Mean cyst volume was greater in GHD patients than ISS patients (62.0 mm3vs. 29.4 mm3, p=0.01). POGO for GHD patients was significantly greater (p=0.003) than for ISS patients (15.3%±12.8 vs. 7.1%±8.0). Observers were blinded to patient groups.ConclusionsGHD patients had a significantly greater volume and POGO compared to ISS patients. This raises the question of whether cysts are implicated in the pathology of growth failure.

Sign in / Sign up

Export Citation Format

Share Document