View clinical trials related to Growth Hormone Deficiency.
Filter by:Primary objective: to evaluate the practicability and acceptability of STYLOMAX®, a new injection device for MAXOMAT®, in children, for 1 year.
Adult patients with hypopituitarism under adequate conventional hormone replacement therapy have reduced life expectancy due to excess vascular events (1-4). Deficiency in GH secretion (GHD) is likely to play a major role in determining the excess mortality, since it is associated with lipid abnormalities, visceral adiposity, glucose intolerance, insulin resistance, hypertension, cardiac abnormalities and increased intima-media thickness (IMT) at major arteries (5). Beneficial effects of growth hormone (GH) replacement on cardiovascular risk factors have been demonstrated in several studies of hypopituitary GHD patients (5). GH replacement improves body composition and lipid profile (5): it is accepted that management of dyslipidaemia is crucial in primary and secondary prevention of cardiovascular disease and part of the excess vascular risk associated with hypopituitarism is likely to be due to dyslipidaemia (6). A meta-analysis of blinded, randomized, placebo-controlled trials with low doses and long-duration GH treatment showed that GH replacement has beneficial effects on cardiovascular risk by improving lean and fat body mass, total and LDL cholesterol levels, and diastolic blood pressure (7). Besides, GH replacement also induces improvement in cardiovascular markers (8), and cardiac performance (9). In small cohorts of GHD adults, beneficial effects of GH replacement for 6-24 mos have also been reported on surrogate parameters of atherosclerosis, such as intima-media thickness (IMT) at major arteries (10-13), while 6 months of GH deprivation is associated with an impairment of the cardiovascular risk profile (12). In a consistent series of men and women with hypopituitarism we reported, however, that two years of GH replacement is not adequate to normalize IMT levels at common carotid arteries (13). To give further insights on the likelihood of reversal of early atherosclerosis in severe GHD patients after prolonged GH replacement, we designed this 5-yr prospective, controlled study. Only men aged ≤50 yrs and with severe GHD were enrolled to avoid gender and aging interference (13). Main outcome measure was IMT at common carotid arteries; secondary measure was prevalence of insulin-resistance syndrome according with the American College of Endocrinology (14).
Growth hormone (GH) is important for growth in childhood, but also has important effects on a number of tissues throughout life. GH deficiency and GH excess (acromegaly, caused by a pituitary tumour) are both cause serious abnormalities of metabolism and long−standing abnormal GH status causes abnormal heart function. In both cases cardiovascular disease is a leading cause of early (premature) death. In the current study we wish to investigate the energy status of the heart in patients with GH excess and deficiency and compare that with age−matched controls. We will perform a blood test to study metabolic parameters. We will perform measurements before treatment, after normalisation of improvement of GH levels and 2 years after start of treatment. Objectives 1. Determine cardiac and skeletal muscle energy metabolism in patients with GH excess (=acromegaly) or GH deficiency and detect changes after normalisation of GH and IGF−1 levels. (IGF−I is a hormone directly influenced by GH) 2. To correlate muscle energy metabolism parameters to GH and IGF−1 status in the control subjects and in both patient groups 3. Determine the prevalence of coronary artery calcifications in patients with GH excess and GH deficiency and correlate this with their metabolic status 4. To correlate coronary artery calcifications to abdominal obesity. Patients will be identified by Endocrinology physicians involved in the study in outpatients clinics or Endocrine wards and they will receive standard care for their disease. Tests related to endocrine hormone abnormalities will be performed as usual clinical practice. The study will involve three 3−hour visits to the Oxford Research Centre and two 1−hour visits to London Scanning Centre. The visits at the Oxford research centre will include Cardiac and skeletal investigations - Standard cardiac MRI will be used to measure right and left ventricular morphology and global function. - 31P Magnetic Resonance Spectroscopy (MRS) to monitor heart muscle energy levels (by measuring intracellular PCr and ATP in heart muscle). - Heart failure severity (so called 'NYHA status') will be determined from the 6 min walk test. - Peak oxygen uptake will be estimated from a metabolic gas exchange analysis performed during maximal treadmill exercise testing. - Skeletal muscle MR imaging and spectroscopy will be performed at rest and during exercise. - Fasting blood test will be performed, see details in protocol. - Electrocardiogram (ECG) - Epworth Sleepiness Scale questionnaire and 5 point test for sleep apnoea The visits at the London Scanning Centre will include - Electron beam coronary CT (EBCT) to assess coronary disease. The number of coronary disease lesions will be measured in several coronary arteries and values will add up to an overall score. In addition a single picture will be taken at the level of the umbilicus (belly button) to measure fat tissue within the abdomen. Patient selection: Patients will be recruited at St. Bartholomew's Hospital (Dr P. Jenkins and Prof. A. Grossman), King's Hospital (Dr S. Aylwin) and St Thomas's Hospital (Dr P. Carroll) in London, Royal Free Hospital (Prof P. Boloux), the John Radcliffe Hospital Oxford (Prof J. Wass), Addenbrooks Hospital Cambridge (Dr H. Simpson), Sheffield (Dr J. Newell−Price), and Stroke−on−Trent (Prof R. Clayton) from the Endocrine Wards and outpatient clinics. This constitutes a large recruitment base. We estimate that 45 new acromegaly patients and 60−80 new GHD patients per year will be screened. Patients will be selected on the basis of clinical diagnosis of acromegaly or GH deficiency (see details of these in the formal protocol). Patients will be managed according to the clinical protocols of the referring centre. The patients will have a report of their investigation results with their treating physicians. Control subjects will be selected from the general population via advertisements. They will undergo all tests in the Oxford centre once. Expected value of results: These studies will increase our knowledge of the metabolic changes associated with GH excess and GH deficiency, which can lead to increased cardiac morbidity and mortality in both cases. Our studies will help to clarify the mechanism of abnormal cardiac function. The study has been powered to have appropriate number of subjects within a two year period, therefore we anticipate that it will last from start to finish 4 years.
In the present double blind, placebo-controlled, parallel study we evaluated the impact of 12 weeks thiazolidinedione (TZD) administration on basal and insulin-stimulated substrate metabolism in growth hormone-replaced adults with growth hormone deficiency.
This study aims to examine the safety, tolerability and pharmacokinetics of transdermal delivery of human Growth Hormone (hGH or somatropin) using the ViaDerm device in adult patients with Growth Hormone Deficiency Syndrome.
To examine the clinical genetic and biochemical characteristics of children with growth hormone deficiency.
Objective: This study is designed to determine whether growth hormone treatment in children 8 to 18 years of age alters function of the lining of the arteries. This may play a role in increasing or decreasing the risk of heart disease. Methods. Twenty children, for whom growth hormone therapy will be otherwise provided, will be studied before and 3 months after starting growth hormone. Subjects can be on other hormonal replacements but no other medications. Each study will be done in the fasting state. The blood vessel function will be determined by measuring the change in forearm blood flow before and after blocking flow to the arm for 5 minutes. Blood will be drawn after the test to measure glucose, insulin and fats.
Specific Aim 1 Healthy male and female subjects and growth hormone (GH) deficient subjects display sexually dimorphic GH responses to GHRH administration Specific Aim 2 GH responses to GHRH in both healthy controls and in GH deficient patients correlate with expression and activity of the stimulatory G proteins, G alpha q and G alpha S. G protein levels correlate with gonadal steroid levels. Specific Aim 3 Sexually dimorphic GH responses to GHRH are enhanced in Tanner Stage V compared to Tanner Stage 1 individuals
The study aims at identifying the predictive markers after one month of Saizen therapy in Growth Hormone Deficiency (GHD) and Turner Syndrome children.
This project is designed to answer the question: Is there an acute IGFBP-3 response in normal children? Our specific hypothesis states that under the influence of growth hormone secretagogues, intact IGFBP-3 molecule will undergo proteolysis and liberate IGFBP-3 fragments, along with other components of the ternary complex. This proteolysis will result in measurable rise in IGFBP-3, which will indicate the subject’s growth hormone status. Short children with growth hormone deficiency will not show an IGFBP-3 response.