|- candidate number||6676|
|- NTR Number||NTR2085|
|- ISRCTN||ISRCTN wordt niet meer aangevraagd.|
|- Date ISRCTN created|
|- date ISRCTN requested|
|- Date Registered NTR||29-okt-2009|
|- Secondary IDs||MEC-2008-288 METC|
|- Public Title||Hypopituitarism in patients after
Screening and treatment.
|- Scientific Title||Hypopituitarism in patients after
Screening and treatment.
|- hypothesis||The aim of the present study is: |
1. To determine the incidence of hypopituitarism in subjects after SAH, using a routine hormonal screening protocol;
2. To identify prognostic neurological determinants for the development of hypopituitarism following SAH;
3. To evaluate the value of the GRPH-6 test in the acute phase of SAH in determinating the presence of growth hormone deficiency.
|- Healt Condition(s) or Problem(s) studied||Subarachnoid hemorrhage (SAH), Hypopituarism|
|- Inclusion criteria||1. Subarachnoid hemorrhage;|
2. Signed and dated informed consent document.
|- Exclusion criteria||Subjects with any of the following items will be excluded from the study:|
1. Any hypothalamic/pituitary disease diagnosed prior to SAH;
2. History of cranial irradiation;
3. Prior significant trauma capitis;
4. Another significant intracranial lesion (apart from SAH or its sequellae);
5. Any other medical or psychiatric condition or laboratory abnormality that may impose a risk for participation in the study or interfere with the interpretation of the study (according to the judgment of the investigators).
|- mec approval received||yes|
|- multicenter trial||no|
|- Type||2 or more arms, non-randomized|
|- planned startdate ||5-jan-2009|
|- planned closingdate||5-jan-2011|
|- Target number of participants||120|
|- Interventions||Replacement of hormone defeciencies as required.|
|- Primary outcome||1. To determine the prevalence of hypopituitarism in patients after SAH;|
2. To identify neurological parameters that predict hypopituitarism after SAH;
3. To determine the value of a Ghrelin test shortly after SAH, to identify subjects with GHD.
|- Secondary outcome||1. To determine the impact of hypopituitarism on physical functioning, activity pattern and participation;|
2. To evaluate the effect of GH replacement on residual functional physical fitness, fatigue and quality of life.
|- Timepoints||1. Visit 1: During admission for SAH;|
2. Visit 2: Week 12 (3 months after SAH);
3. Visit 3: Week 18 (6 weeks after start hormone suppletion)
(Only for patients with established hormone deficiency);
4. Visit 4: Week 24 (6 months after SAH);
5. Visit 5: Week 28 (4 weeks after start GH-suppletion);
6. Visit 6: Week 44 (20 weeks after start GH-suppletion);
7. Visit 7: Week 60 (36 weeks after start GH-suppletion).
|- Trial web site||N/A|
|- status||open: patient inclusion|
|- CONTACT FOR PUBLIC QUERIES|| F. Kooten, van|
|- CONTACT for SCIENTIFIC QUERIES|| F. Kooten, van|
|- Sponsor/Initiator ||Erasmus Medical Center, Rotterdam|
(Source(s) of Monetary or Material Support)
|- Brief summary||Spontaneous subarachnoidal hemorrhage (SAH) occurs with an incidence of six cases per 100.000 patient years, with a case mortality amounting to 50% (1). In patients who survived SAH, high rates of functional limitations are found along with quality-of-life impairment, such as fatigue, decreased mobility, loss of motivation, reduced independence in activities of daily living and decreased social functioning (1,2). |
The residual functional problems in patients after SAH are often unexplained, but may largely resemble those occurring in patients with untreated hypopituitarism. Corticotrophin and TSH deficiency may present with symptoms such as fatigue, weakness, headache, altered mental activity or impaired memory. Symptoms attributable to Growth Hormone deficiency include lack of vigor, decreased exercise tolerance and decreased social functioning with loss of quality of life (2).
Recent studies in long-term survivors of SAH have shown varying incidences (from 20 up to 50%) of hypopituitarism, with growth hormone deficiency (GHD) occurring in 15 - 25% of patients (3,2,4,5). This neuroendocrine dysfunction could be the result of damage to the hypothalamic/pituitary system caused by post hemorrhagic local tissue pressure, toxic effects of the extravasated blood, ischemia caused by vasospasm, high intracranial pressure, hydrocephalus or local destruction during cerebral surgery. At present, it is not possible to identify which SAH patients are at risk of developing hypopituitarism. The clinical effects of optimal hormone replacement therapy on residual symptoms in SAH patients is unknown
|- Main changes (audit trail)|
|- RECORD||29-okt-2009 - 11-nov-2009|