View clinical trials related to Acromegaly.
Filter by:The purpose of this study is to investigate whether 6 months preoperative treatment with the somatostatin analogue octreotide improves the surgical outcome in patients with acromegaly.
The purpose of the protocol is to evaluate the correlation between plasma lanreotide levels and Growth Hormone (GH)/Insulin Like Growth Factor 1 (IGF-1) dynamics and clinical improvement in patients with acromegaly treated with lanreotide Autogel (Somatuline ATG)
The objective of this study is to evaluate, in acromegalic patients with disease persistence after surgery who are treated with somatostatin analogues, the histopathological, clinical, morphological and biochemical factors which are predictive of hormonal control.
The purpose of the protocol, is to evaluate if lanreotide Autogel 120 mg is effective in the control of Growth Hormone (GH) secretion in patients with active acromegaly.
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.
The research is aimed at identifying new predisposition genes for endocrine tumours. Our focus initially is on pituitary adenomas including growth hormone-secreting tumors (somatotrophinomas) and prolactin secreting tumours (prolactinomas), but we wish to extend work to other pituitary tumour cases/families. The recruitment process will be as follows. 1. We will recruit patients from our own Endocrine outpatient clinics and inpatient wards. In addition we will ask colleagues in other Endocrinology Departments (or other specialties such as Clinical Genetics,Pathology, General Medicine ) to identify potentially suitable patients with endocrine & pituitary tumours from their records. We shall focus on patients with good evidence of inheritance of their condition: relatively early onset; or multiple lesions; or other affected family members. Conditions where the predisposing genes have been identified (principally MEN) will be excluded from study. Patients directly contacting us can also enter the study. 2. The Consultant looking after the patient will contact the patient to initially inform him/her of the study. 3. We will then contact the patient (generally by telephone) to discuss the study and what it would entail in terms of information and samples. 4. Subject to agreement in (3), patient will receive 'Information Sheet for patients with pituitary tumour' and 'Consent Form' and will have blood sampling in Consultant's clinic. 5. We will contact additional family members (if appropriate) after an initial approach by the family member already recruited to the study. The additional family members may have developed tumours similar to those of the proband, or may be unaffected individuals who provide useful information for gene identification purposes (for example, spouses may greatly aid the power of gene mapping by linkage. They will receive the "Information Sheet for family members". analysis). 8. Archival tissue will be obtained from HTA licensed tissue banks. This is an established bank whose licence is primarily for diagnosis but can be used for research. 9. We will undertake laboratory work, such as genetic linkage analysis, candidate gene mutation screening and studies of loss of heterozygosity in tumours, to identify the genes predisposing to the condition, such as the AIP gene. In addition we would like to screen other genes related to the chaperon AIP molecule, such as AhR, and other genes currently identified (PDE4A5, survivin and Tom20 protein) or may not been identified. Blood samples for DNA and RNA will coded with unique ID numbers. Pituitary and other endocrine tumour samples will be collected at surgery and kept in liquid nitrogen or -80 C. They will be coded with unique ID numbers. Candidate gene sequencing will be performed in the Barts and the London Medical School Genome Centre. RNA expression studies from blood or adenoma tissue samples will be performed by RT-PCR. Protein expression studies will be performed by Western blotting or immunohistochemistry. The first gene we wish to study causes familial acromegaly, a disease resulting from a pituitary adenoma secreting growth hormone. To establish if the candidate gene is also causing possibly sporadic (not familial) cases of the disease, samples (blood and tissue) will be collected from patients with sporadic disease and will be analysed as above.
Epidemiological data indicate that patients with active acromegaly have reduced life expectancy because of cardiovascular (60%) and respiratory diseases (25%) mainly (1-10). A post-treatment GH value <5 mU/liter (equal to <2.5 μg/liter) and IGF-I in the normal range for age are recognized as the most predictive survival indices. Since their introduction into clinical use approximately two decades ago, somatostatin analogs have been considered a cornerstone of medical therapy for acromegaly. After 12 months of treatment with octreotide-LAR, control of GH and IGF-I excess, is achieved in 54% and 63% of unselected patients (11). The proportion of subjects achieving IGF-I normalization increases significantly with time (12). Significant tumor shrinkage has also been reported in a number of studies (13,14): an average 50% tumor decrease is achieved when the drug is used exclusively, or before surgery or radiotherapy (14). In 99 unselected newly diagnosed patients after 12 months of treatment with somatostatin analogues we reported control of GH levels in 57.6% and IGF-I levels in 45.5% and a greater than 50% tumor shrinkage in 44.4% (15). The dose of LAR in different studies ranged from 10-40 mg every 28 days (q28d): high doses are generally administered in patients who do not control GH and IGF-I excess with lower doses. As reported in the meta-analysis (11) the rate of IGF-I normalization tended to be lower as octreotide-LAR dose was raised: 90% in patients treated with 10 mg, 61% with 20 mg and 53% with 30 mg. However, some further benefit by increasing the dose of octreotide-LAR was reported in some studies (16-18). Data on dose escalation of octreotide-LAR given as first-line therapy in newly diagnosed patients with acromegaly are lacking.
The purpose of this study is to determine whether subjects with acromegaly (or their partners) are able to self administer Somatuline Autogel at home.
This study will assess the pharmacokinetic profile and the safety/tolerability profile of single and monthly doses of pasireotide LAR intramuscular (i.m.) injection in patients with acromegaly and patients with carcinoid disease
A multicentre, prospective, open label study of acromegalic patients evaluating the efficacy and safety of different dose-intervals of Lanreotide Autogel 120mg according to international standards and compared to previous treatment with Octreotide LAR 10, 20 or 30 mg.