Acromegaly, Metabolic Diseases
Conditions
Keywords
Acromegaly, Somatostatin treatment, metabolic effect
Brief summary
The treatment with SA still leaves some questions unanswered. Firstly, SA treatment often results in a concomitant suppression of the insulin secretion, which might lead to clinically significant glucose intolerance. Secondly, the traditional evaluation of disease activity by measuring circulating levels of GH and total IGF-I is not reliable enough Hypotheses: Treatment of acromegaly with SA versus surgery alone is associated with: * Glucose intolerance despite normalized insulin sensitivity * Modified peripheral GH activity in peripheral target organs assessed on molecular endpoints
Detailed description
Acromegaly is a rare disease usually caused by a benign growth hormone (GH) producing pituitary adenoma. In case of inadequate disease control, the condition is associated with significant morbidity and approximately a doubling of mortality compared to the background population. Medical treatment with somatostatin analogues (SA) has been employed for about 20 years and is a well-established treatment in cases where surgery is impossible or inadequate. The treatment with SA still leaves some questions unanswered. Firstly, SA treatment often results in a concomitant suppression of the insulin secretion, which might lead to clinically significant glucose intolerance. Secondly, the traditional evaluation of disease activity by measuring circulating levels of GH and total IGF-I is not reliable enough
Interventions
DRUGgenotropin
iii) intravenous exogenous bolus of GH (0.5 mg) followed by muscle and fat biopsies.
Sponsors
University of Aarhus
Study design
Allocation
NON_RANDOMIZED
Intervention model
PARALLEL
Primary purpose
BASIC_SCIENCE
Masking
NONE
Eligibility
Sex/Gender
ALL
Age
18 Years to No maximum
Healthy volunteers
Yes
Inclusion criteria
* \> 18 years * treated acromegaly * considered suitable
Exclusion criteria
* pregnancy
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| Metabolism - including GH, IGF-I, FFA, glc and insulin. Concentration and AUC (area under the curve) | 3 years | GH (ug/l), IGF-I (ug/l), FFA (mmol/l) , glc (mmol/l) and insulin (pmol/l) |
Secondary
| Measure | Time frame | Description |
|---|---|---|
| concentration of serum and interstitial GH, bioactive IGF-I as well as total IGF-I | 3 years | GH (ug/l), IGF-l (ug/l), bioactive IGF-l (ug/l) |
Other
| Measure | Time frame | Description |
|---|---|---|
| GH, and insulin signal transduction in muscle and fat biopsies and regulation of lipolysis. | 3 years | By western blot technique protien levels of (arbitrary densitomety units) AKT, pAKT threonin, pAKT serine, STAT5, pSTAT5, PTEN, p85alpha, mTOR, pmTOR. By PCR technique (relative nRNA expression) mRNA levels of IGF-1, SOCS1, SOCS2, SOCS3, CISH, PTEN, Pik3r |
| patient characterization | 3 years | sex (M/F), age (year), disease duration (years), BMI (kg/m2) |
Countries
Denmark
Outcome results
None listed