Growth Hormone DeficiencyNCT00136032
Growth Hormone Administration and Its Effects on Cardiovascular Risk Factors in Growth Hormone Deficient Women
A study testing Somatropin in people with Growth Hormone Deficiency, run by Massachusetts General Hospital at 1 site in United States.
Trial summary
The purpose of the study is to evaluate the effects of growth hormone replacement on women with growth hormone deficiency. Growth hormone deficiency means the body no longer produces growth hormone due to a tumor or some kind of disease of the brain in an area called the pituitary/hypothalamic region. Read more about this study
- Who is it for?
- Ages 18 to 65 years, women only
- Conditions the study is for
- Growth Hormone Deficiency
- What is being tested?
- Somatropin
- Could I receive a placebo?
- Yes, some participants may receive a placebo
- How many people
- 63 participants
- Where
- 1 siteUnited States
- Study dates
- Jan 2002to Nov 2006
- Phase
- Interventional
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 to 65 years
- Women only
- No healthy volunteers
- Adult, Older adult
Who may be able to join
- GH deficiency due to pituitary or hypothalamic tumors or disease affecting this area. Subjects will have been treated with medication, surgery, radiation, or a combination of these. GH deficiency will be defined as a peak plasma GH of less than 5 ng/ml in response to insulin tolerance testing or growth hormone releasing hormone (GHRH) plus arginine stimulation test. In subjects with suspected hypothalamic dysfunction the arginine plus L-dopa stimulation test may be used, with a cutoff of 1.7 ng/ml for diagnosis of GH deficiency. Partial GH deficiency will be defined as a GH peak of 5 to 9 ng/ml (inclusive) during insulin tolerance testing or GHRH plus arginine testing.
- GH deficiency will also be diagnosed if insulin-like growth factor-I (IGF-I) levels are below 2 standard deviations for the age-sex normal range in a patient with at least two documented hormone deficiencies.
- Subjects must have evidence of a stable pituitary mass (for at least 12 months) if there is a history of a tumor except in the case of ACTH-producing microadenomas, where no follow-up imaging is required after cure.
- Subjects age 40 and over must have a screening mammogram if they have not already had one within one year prior to their baseline visit
Who cannot join
- Active Cushing's disease within 1 year
- History of acromegaly
- Untreated thyroid or adrenal insufficiency. Subjects on replacement therapy must be stable for at least 3 months prior to entry into the study.
- History of malignancy except for skin cancer and except for childhood solid malignancy with documented cure for > 10 years prior to starting the study
- Hemoglobin <10.0 gm/dl
- Hepatic or renal disease (SGPT/SGOT > 3x upper limit of normal (ULN) or creatinine levels >2.5 mg/dl)
Show all 11Show fewer
- Congestive heart failure (CHF) (New York Heart Association's classification system Class II-IV CHF will be excluded)
- History of unstable cardiovascular disease (coronary artery or cerebrovascular disease) or symptoms within one year prior to entry into the study
- Diabetes mellitus
- Pregnancy or nursing
- Active carpal tunnel syndrome
Trial locations and contacts
1 site in 1 country.
United States1 site
Massachusetts General Hospital
Boston, Massachusetts, 02114
About this study
Official title: Gender-Specific Effects of Physiologic GH Administration on Cardiovascular Risk Factors in Women With Growth Hormone Deficiency
The purpose of the study is to evaluate the effects of growth hormone replacement on women with growth hormone deficiency. Growth hormone deficiency means the body no longer produces growth hormone due to a tumor or some kind of disease of the brain in an area called the pituitary/hypothalamic region. This is the area of the brain where growth hormone is normally produced. We, the researchers at Massachusetts General Hospital, will establish the effects of growth hormone replacement on cardiovascular parameters (laboratory tests, the flexibility of the arteries, changes in heart rate) in women with growth hormone deficiency. Our goal is to see if this therapy:
- has effects on women's cardiovascular risk markers (special blood tests which indicate how healthy the heart and arteries are)
- has effects on women's types and levels of various substances circulating in their blood
- in women affects the stiffness of their arteries and heart rate variability in parallel with changes in cardiovascular risk markers
- has different effects depending on whether women are pre or post menopausal.
Participation in this study is expected to last approximately 12 months.
Read the detailed description
The aim of the study is to evaluate the gender specific effects of physiologic Growth Hormone (GH) replacement in women with GH deficiency on the basis of pituitary/hypothalamic region tumors, radiation, or surgery on cardiovascular risk markers and arterial distensibility. Cardiovascular mortality in growth hormone (GH) deficient adults has been shown to be increased in a number of retrospective studies. Increased arterial intima-media thickness, increased prevalence of atherosclerotic plaques and endothelial dysfunction have been reported in growth hormone deficient adults both in childhood and adulthood onset forms.
The growth hormone deficiency (GHD) syndrome is associated with a cluster of cardiovascular-risk factors such as central adiposity, increased visceral fat, insulin resistance, dyslipoproteinemia and decreased plasma fibrinolytic activity. GH administration has effects on a number of these factors, but it is unknown which mechanisms are implicated in GH action on the process of atherosclerosis. In addition to alterations in atherosclerotic markers, abnormalities in cardiac function and structure have been reported among patients with GHD possibly contributing to the increased cardiovascular mortality. In addition, GHD is associated with cardiac autonomic dysfunction that may also contribute to cardiovascular mortality and improves with GH replacement therapy.
The vast majority of studies have focused primarily on men and the gender-specific effects of GH replacement on cardiovascular risk factors remain unknown. In addition to being of interest in terms of understanding the physiologic effects of GH therapy, there are important therapeutic implications regarding data in women. Cardiovascular disease is the leading cause of mortality in women. Effects of GH replacement on bone density may be less pronounced in women and because specific GH effects on cardiovascular risk factors in women are unknown, many adult women with GHD are untreated.
Long-term GH treatment decreases total body fat including visceral fat. Decreases in central fat as assessed by waist to hip ratio have been reported in some studies, but not in others. Administration of GH causes insulin resistance acutely but long-term therapy may restore glucose sensitivity. GH treatment increases lipoprotein (a) (Lp (a)) levels but its effects on other lipoproteins are still controversial. Some studies have reported decreases in LDL cholesterol with or without increases in HDL cholesterol with GH administration, while others have not. Twelve months of GH replacement improves left ventricular mass and cardiac performance in young adults with GHD. Key factors likely involved in the discrepant findings include heterogeneity of patients studied in terms of age of onset of the GH deficiency (childhood versus adulthood), gender, severity of GHD and methodologic issues such as dose and duration of GH administration. In addition, many of the studies have no control period.
Inflammation plays a central role in the pathophysiology of atherosclerosis. Each atherosclerotic lesion represents a different stage of a chronic inflammatory process in the arterial wall and different markers along the inflammatory cascade have been reported to predict cardiovascular risk [34]. Among those, high-sensitivity testing for C-reactive protein (CRP) is one of the best validated. Several prospective studies support a strong link between levels of CRP and future risk of coronary events. CRP adds considerable value to the total and HDL cholesterol measurement in the prediction of cardiovascular risk. Other distal indicators of inflammation such as serum-amyloid polypeptide A (SAA) likewise predict coronary risk. These distal markers reflect the consequences of elevated proinflammatory cytokines like interleukin-6 (IL-6). GH is known to have important immunomodulatory effects. We therefore hypothesized that the effects of GH on the process of atherosclerosis might be mediated through the cytokine-inflammatory pathway. We have recently investigated the effects of physiologic GH replacement in cardiovascular risk markers in men with GHD. In this study we found that CRP and IL-6 levels decreased in GH treated men compared to controls despite no significant change in serum lipid levels. We also recently have investigated levels of inflammatory markers in women with hypopituitarism compared with healthy controls. We found that women with hypopituitarism have increased levels of IL-6 and CRP suggesting that chronic inflammation may be involved in the pathogenesis of atherosclerosis in this population. It will be critical to determine whether physiologic GH replacement has beneficial effects in women, and whether these effects are influenced by estrogen.
We will investigate the effect of long-term physiologic GH administration on IL-6, CRP, SAA as well as other classic cardiovascular risk factors in women with GHD in a randomized, placebo-controlled study. In addition, we will evaluate structural/function correlates in women by measuring arterial wall distensibility and heart rate variability in parallel with cardiovascular risk markers.
We will establish the gender-specific effects of physiologic GH replacement on cardiovascular risk in women with GHD by investigating whether this therapy:
- has gender-specific effects on cardiovascular risk markers
- has gender-specific effects on lipid profiles
- alters heart rate variability and arterial distensibility in parallel with changes in cardiovascular risk markers
- has different effects depending upon gonadal status
- Conditions
- Growth Hormone Deficiency
- Being tested
- Somatropin, Placebo
- Keywords
- Growth Hormone, Cardiovascular risk, Pituitary, Hypothalamic, GH Deficiency, Pituitary Tumor, Pituitary Disease
- Medical subject headings
- Dwarfism, Pituitary, Pituitary Diseases, Pituitary Neoplasms
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
SomatropinDrug
Also called Genotropin
Stratified based on age and estrogen status from 3 to 6 mcg/kg/day
PlaceboDrug
Dosage based on age and estrogen status ranging from 3 to 6 mcg/kg/day
| Study group | Role | What they receive |
|---|---|---|
| 1 | Active comparator | Not described Receives: Drug: Somatropin |
| 2 | Placebo comparator | Not described Receives: Drug: Placebo |
What is being measured
The primary outcome is the main question the study is designed to answer.
Gender specific effects on cardiovascular risk markers
Measured: baseline, 1, 3, 6, 7, 9, and 12 months
Secondary outcomes (2)
Heart Rate Variability
Measured: baseline, 3, 6, 9, and 12 months
Quality of Life
Measured: baseline, 1, 3, 6, 7, 9, and 12 months
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted26 Aug 2005 (estimated)
- Study startJan 2002
- Primary completionNov 2006
- Study completionNov 2006
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (45)Papers the sponsor has linked to this study.
- Other trials for Growth Hormone DeficiencyStudies of the same condition, open and under way.
- More trials run by Massachusetts General HospitalThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase N/A
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- Double blind
- Who is masked
- Participant, Investigator
- Enrolment
- 63 participants (actual)
Sponsor and investigators
- Lead sponsor
- Massachusetts General Hospital
- Sponsor type
- University, hospital or other
- Investigators
- Anne Klibanski, M.D, Principal investigator, Massachusetts General Hospital
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT00136032
- Sponsor's protocol ID
- 2001p-001761
- Status last verified
- Feb 2008
- First submitted
- 24 Aug 2005
- Last updated
- 18 Feb 2008
- Results posted
- No
- Data monitoring committee
- Yes
Publications
Rosen T, Bengtsson BA. Premature mortality due to cardiovascular disease in hypopituitarism. Lancet. 1990 Aug 4;336(8710):285-8. doi: 10.1016/0140-6736(90)91812-o.
PubMed 1973979Bulow B, Hagmar L, Eskilsson J, Erfurth EM. Hypopituitary females have a high incidence of cardiovascular morbidity and an increased prevalence of cardiovascular risk factors. J Clin Endocrinol Metab. 2000 Feb;85(2):574-84. doi: 10.1210/jcem.85.2.6346.
PubMed 10690858Wuster C, Slenczka E, Ziegler R. [Increased prevalence of osteoporosis and arteriosclerosis in conventionally substituted anterior pituitary insufficiency: need for additional growth hormone substitution?]. Klin Wochenschr. 1991 Oct 18;69(16):769-73. doi: 10.1007/BF01797616. German.
PubMed 1762381Tomlinson JW, Holden N, Hills RK, Wheatley K, Clayton RN, Bates AS, Sheppard MC, Stewart PM. Association between premature mortality and hypopituitarism. West Midlands Prospective Hypopituitary Study Group. Lancet. 2001 Feb 10;357(9254):425-31. doi: 10.1016/s0140-6736(00)04006-x.
PubMed 11273062Markussis V, Beshyah SA, Fisher C, Sharp P, Nicolaides AN, Johnston DG. Detection of premature atherosclerosis by high-resolution ultrasonography in symptom-free hypopituitary adults. Lancet. 1992 Nov 14;340(8829):1188-92. doi: 10.1016/0140-6736(92)92892-j.
PubMed 1359261Pfeifer M, Verhovec R, Zizek B, Prezelj J, Poredos P, Clayton RN. Growth hormone (GH) treatment reverses early atherosclerotic changes in GH-deficient adults. J Clin Endocrinol Metab. 1999 Feb;84(2):453-7. doi: 10.1210/jcem.84.2.5456.
PubMed 10022400Evans LM, Davies JS, Goodfellow J, Rees JA, Scanlon MF. Endothelial dysfunction in hypopituitary adults with growth hormone deficiency. Clin Endocrinol (Oxf). 1999 Apr;50(4):457-64. doi: 10.1046/j.1365-2265.1999.00671.x.
PubMed 10468904Capaldo B, Patti L, Oliviero U, Longobardi S, Pardo F, Vitale F, Fazio S, Di Rella F, Biondi B, Lombardi G, Sacca L. Increased arterial intima-media thickness in childhood-onset growth hormone deficiency. J Clin Endocrinol Metab. 1997 May;82(5):1378-81. doi: 10.1210/jcem.82.5.3951.
PubMed 9141519Cuneo RC, Salomon F, McGauley GA, Sonksen PH. The growth hormone deficiency syndrome in adults. Clin Endocrinol (Oxf). 1992 Nov;37(5):387-97. doi: 10.1111/j.1365-2265.1992.tb02347.x. No abstract available.
PubMed 1486686De Boer H, Blok GJ, Voerman HJ, De Vries PM, van der Veen EA. Body composition in adult growth hormone-deficient men, assessed by anthropometry and bioimpedance analysis. J Clin Endocrinol Metab. 1992 Sep;75(3):833-7. doi: 10.1210/jcem.75.3.1517374.
PubMed 1517374Binnerts A, Deurenberg P, Swart GR, Wilson JH, Lamberts SW. Body composition in growth hormone-deficient adults. Am J Clin Nutr. 1992 May;55(5):918-23. doi: 10.1093/ajcn/55.5.918.
PubMed 1570798Weaver JU, Monson JP, Noonan K, John WG, Edwards A, Evans KA, Cunningham J. The effect of low dose recombinant human growth hormone replacement on regional fat distribution, insulin sensitivity, and cardiovascular risk factors in hypopituitary adults. J Clin Endocrinol Metab. 1995 Jan;80(1):153-9. doi: 10.1210/jcem.80.1.7829604.
PubMed 7829604Johansson JO, Fowelin J, Landin K, Lager I, Bengtsson BA. Growth hormone-deficient adults are insulin-resistant. Metabolism. 1995 Sep;44(9):1126-9. doi: 10.1016/0026-0495(95)90004-7.
PubMed 7666785Rosen T, Eden S, Larson G, Wilhelmsen L, Bengtsson BA. Cardiovascular risk factors in adult patients with growth hormone deficiency. Acta Endocrinol (Copenh). 1993 Sep;129(3):195-200. doi: 10.1530/acta.0.1290195.
PubMed 8212983Johansson JO, Landin K, Tengborn L, Rosen T, Bengtsson BA. High fibrinogen and plasminogen activator inhibitor activity in growth hormone-deficient adults. Arterioscler Thromb. 1994 Mar;14(3):434-7. doi: 10.1161/01.atv.14.3.434.
PubMed 8123648
Study at a glance
From the registry record, last updated by the sponsor on 18 Feb 2008. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Gender-Specific Effects of Physiologic GH Administration on Cardiovascular Risk Factors in Women With Growth Hormone Deficiency
- ClinicalTrials.gov ID
- NCT00136032
- Acronym / sponsor ID
- 2001p-001761
- Conditions
- Growth Hormone Deficiency
- Keywords
- Growth Hormone, Cardiovascular risk, Pituitary, Hypothalamic, GH Deficiency, Pituitary Tumor, Pituitary Disease
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 63 participants (actual)
- Lead sponsor
- Massachusetts General HospitalUniversity, hospital or other
- Study start
- Jan 2002
- Primary completion
- Nov 2006 (actual)
- Study completion
- Nov 2006 (actual)
- First posted
- 26 Aug 2005 (estimated)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
The purpose of the study is to evaluate the effects of growth hormone replacement on women with growth hormone deficiency. Growth hormone deficiency means the body no longer produces growth hormone due to a tumor or some kind of disease of the brain in an area called the pituitary/hypothalamic region. This is the area of the brain where growth hormone is normally produced. We, the researchers at Massachusetts General Hospital, will establish the effects of growth hormone replacement on cardiovascular parameters (laboratory tests, the flexibility of the arteries, changes in heart rate) in women with growth hormone deficiency. Our goal is to see if this therapy:
- has effects on women's cardiovascular risk markers (special blood tests which indicate how healthy the heart and arteries are)
- has effects on women's types and levels of various substances circulating in their blood
- in women affects the stiffness of their arteries and heart rate variability in parallel with changes in cardiovascular risk markers
- has different effects depending on whether women are pre or post menopausal.
Participation in this study is expected to last approximately 12 months.
Detailed description
The aim of the study is to evaluate the gender specific effects of physiologic Growth Hormone (GH) replacement in women with GH deficiency on the basis of pituitary/hypothalamic region tumors, radiation, or surgery on cardiovascular risk markers and arterial distensibility. Cardiovascular mortality in growth hormone (GH) deficient adults has been shown to be increased in a number of retrospective studies. Increased arterial intima-media thickness, increased prevalence of atherosclerotic plaques and endothelial dysfunction have been reported in growth hormone deficient adults both in childhood and adulthood onset forms.
The growth hormone deficiency (GHD) syndrome is associated with a cluster of cardiovascular-risk factors such as central adiposity, increased visceral fat, insulin resistance, dyslipoproteinemia and decreased plasma fibrinolytic activity. GH administration has effects on a number of these factors, but it is unknown which mechanisms are implicated in GH action on the process of atherosclerosis. In addition to alterations in atherosclerotic markers, abnormalities in cardiac function and structure have been reported among patients with GHD possibly contributing to the increased cardiovascular mortality. In addition, GHD is associated with cardiac autonomic dysfunction that may also contribute to cardiovascular mortality and improves with GH replacement therapy.
The vast majority of studies have focused primarily on men and the gender-specific effects of GH replacement on cardiovascular risk factors remain unknown. In addition to being of interest in terms of understanding the physiologic effects of GH therapy, there are important therapeutic implications regarding data in women. Cardiovascular disease is the leading cause of mortality in women. Effects of GH replacement on bone density may be less pronounced in women and because specific GH effects on cardiovascular risk factors in women are unknown, many adult women with GHD are untreated.
Long-term GH treatment decreases total body fat including visceral fat. Decreases in central fat as assessed by waist to hip ratio have been reported in some studies, but not in others. Administration of GH causes insulin resistance acutely but long-term therapy may restore glucose sensitivity. GH treatment increases lipoprotein (a) (Lp (a)) levels but its effects on other lipoproteins are still controversial. Some studies have reported decreases in LDL cholesterol with or without increases in HDL cholesterol with GH administration, while others have not. Twelve months of GH replacement improves left ventricular mass and cardiac performance in young adults with GHD. Key factors likely involved in the discrepant findings include heterogeneity of patients studied in terms of age of onset of the GH deficiency (childhood versus adulthood), gender, severity of GHD and methodologic issues such as dose and duration of GH administration. In addition, many of the studies have no control period.
Inflammation plays a central role in the pathophysiology of atherosclerosis. Each atherosclerotic lesion represents a different stage of a chronic inflammatory process in the arterial wall and different markers along the inflammatory cascade have been reported to predict cardiovascular risk [34]. Among those, high-sensitivity testing for C-reactive protein (CRP) is one of the best validated. Several prospective studies support a strong link between levels of CRP and future risk of coronary events. CRP adds considerable value to the total and HDL cholesterol measurement in the prediction of cardiovascular risk. Other distal indicators of inflammation such as serum-amyloid polypeptide A (SAA) likewise predict coronary risk. These distal markers reflect the consequences of elevated proinflammatory cytokines like interleukin-6 (IL-6). GH is known to have important immunomodulatory effects. We therefore hypothesized that the effects of GH on the process of atherosclerosis might be mediated through the cytokine-inflammatory pathway. We have recently investigated the effects of physiologic GH replacement in cardiovascular risk markers in men with GHD. In this study we found that CRP and IL-6 levels decreased in GH treated men compared to controls despite no significant change in serum lipid levels. We also recently have investigated levels of inflammatory markers in women with hypopituitarism compared with healthy controls. We found that women with hypopituitarism have increased levels of IL-6 and CRP suggesting that chronic inflammation may be involved in the pathogenesis of atherosclerosis in this population. It will be critical to determine whether physiologic GH replacement has beneficial effects in women, and whether these effects are influenced by estrogen.
We will investigate the effect of long-term physiologic GH administration on IL-6, CRP, SAA as well as other classic cardiovascular risk factors in women with GHD in a randomized, placebo-controlled study. In addition, we will evaluate structural/function correlates in women by measuring arterial wall distensibility and heart rate variability in parallel with cardiovascular risk markers.
We will establish the gender-specific effects of physiologic GH replacement on cardiovascular risk in women with GHD by investigating whether this therapy:
- has gender-specific effects on cardiovascular risk markers
- has gender-specific effects on lipid profiles
- alters heart rate variability and arterial distensibility in parallel with changes in cardiovascular risk markers
- has different effects depending upon gonadal status
Study design
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- Double blind (participant, investigator)
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| 1 | Active comparator | Drug: Somatropin |
| 2 | Placebo comparator | Drug: Placebo |
Who may qualify
- Ages
- 18 to 65 years
- Sex
- Female only
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (4 listed)
- GH deficiency due to pituitary or hypothalamic tumors or disease affecting this area. Subjects will have been treated with medication, surgery, radiation, or a combination of these. GH deficiency will be defined as a peak plasma GH of less than 5 ng/ml in response to insulin tolerance testing or growth hormone releasing hormone (GHRH) plus arginine stimulation test. In subjects with suspected hypothalamic dysfunction the arginine plus L-dopa stimulation test may be used, with a cutoff of 1.7 ng/ml for diagnosis of GH deficiency. Partial GH deficiency will be defined as a GH peak of 5 to 9 ng/ml (inclusive) during insulin tolerance testing or GHRH plus arginine testing.
- GH deficiency will also be diagnosed if insulin-like growth factor-I (IGF-I) levels are below 2 standard deviations for the age-sex normal range in a patient with at least two documented hormone deficiencies.
- Subjects must have evidence of a stable pituitary mass (for at least 12 months) if there is a history of a tumor except in the case of ACTH-producing microadenomas, where no follow-up imaging is required after cure.
- Subjects age 40 and over must have a screening mammogram if they have not already had one within one year prior to their baseline visit
Key exclusion criteria (11 listed)
- Active Cushing's disease within 1 year
- History of acromegaly
- Untreated thyroid or adrenal insufficiency. Subjects on replacement therapy must be stable for at least 3 months prior to entry into the study.
- History of malignancy except for skin cancer and except for childhood solid malignancy with documented cure for > 10 years prior to starting the study
- Hemoglobin <10.0 gm/dl
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| SomatropinAlso: GenotropinStratified based on age and estrogen status from 3 to 6 mcg/kg/day | Drug | 1 |
| PlaceboDosage based on age and estrogen status ranging from 3 to 6 mcg/kg/day | Drug | 2 |
Primary outcome
Gender specific effects on cardiovascular risk markers
Time frame: baseline, 1, 3, 6, 7, 9, and 12 months
2 secondary outcomes
Heart Rate Variability
Time frame: baseline, 3, 6, 9, and 12 months
Quality of Life
Time frame: baseline, 1, 3, 6, 7, 9, and 12 months
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 18 Feb 2008.
- Background: PubMed 1973979Rosen T, Bengtsson BA. Premature mortality due to cardiovascular disease in hypopituitarism. Lancet. 1990 Aug 4;336(8710):285-8. doi: 10.1016/0140-6736(90)91812-o.
- Background: PubMed 10690858Bulow B, Hagmar L, Eskilsson J, Erfurth EM. Hypopituitary females have a high incidence of cardiovascular morbidity and an increased prevalence of cardiovascular risk factors. J Clin Endocrinol Metab. 2000 Feb;85(2):574-84. doi: 10.1210/jcem.85.2.6346.
- Background: PubMed 1762381Wuster C, Slenczka E, Ziegler R. [Increased prevalence of osteoporosis and arteriosclerosis in conventionally substituted anterior pituitary insufficiency: need for additional growth hormone substitution?]. Klin Wochenschr. 1991 Oct 18;69(16):769-73. doi: 10.1007/BF01797616. German.
- Background: PubMed 11273062Tomlinson JW, Holden N, Hills RK, Wheatley K, Clayton RN, Bates AS, Sheppard MC, Stewart PM. Association between premature mortality and hypopituitarism. West Midlands Prospective Hypopituitary Study Group. Lancet. 2001 Feb 10;357(9254):425-31. doi: 10.1016/s0140-6736(00)04006-x.
- Background: PubMed 1359261Markussis V, Beshyah SA, Fisher C, Sharp P, Nicolaides AN, Johnston DG. Detection of premature atherosclerosis by high-resolution ultrasonography in symptom-free hypopituitary adults. Lancet. 1992 Nov 14;340(8829):1188-92. doi: 10.1016/0140-6736(92)92892-j.
- Background: PubMed 10022400Pfeifer M, Verhovec R, Zizek B, Prezelj J, Poredos P, Clayton RN. Growth hormone (GH) treatment reverses early atherosclerotic changes in GH-deficient adults. J Clin Endocrinol Metab. 1999 Feb;84(2):453-7. doi: 10.1210/jcem.84.2.5456.
- Background: PubMed 10468904Evans LM, Davies JS, Goodfellow J, Rees JA, Scanlon MF. Endothelial dysfunction in hypopituitary adults with growth hormone deficiency. Clin Endocrinol (Oxf). 1999 Apr;50(4):457-64. doi: 10.1046/j.1365-2265.1999.00671.x.
- Background: PubMed 9141519Capaldo B, Patti L, Oliviero U, Longobardi S, Pardo F, Vitale F, Fazio S, Di Rella F, Biondi B, Lombardi G, Sacca L. Increased arterial intima-media thickness in childhood-onset growth hormone deficiency. J Clin Endocrinol Metab. 1997 May;82(5):1378-81. doi: 10.1210/jcem.82.5.3951.
- Background: PubMed 1486686Cuneo RC, Salomon F, McGauley GA, Sonksen PH. The growth hormone deficiency syndrome in adults. Clin Endocrinol (Oxf). 1992 Nov;37(5):387-97. doi: 10.1111/j.1365-2265.1992.tb02347.x. No abstract available.
- Background: PubMed 1517374De Boer H, Blok GJ, Voerman HJ, De Vries PM, van der Veen EA. Body composition in adult growth hormone-deficient men, assessed by anthropometry and bioimpedance analysis. J Clin Endocrinol Metab. 1992 Sep;75(3):833-7. doi: 10.1210/jcem.75.3.1517374.
- Background: PubMed 1570798Binnerts A, Deurenberg P, Swart GR, Wilson JH, Lamberts SW. Body composition in growth hormone-deficient adults. Am J Clin Nutr. 1992 May;55(5):918-23. doi: 10.1093/ajcn/55.5.918.
- Background: PubMed 7829604Weaver JU, Monson JP, Noonan K, John WG, Edwards A, Evans KA, Cunningham J. The effect of low dose recombinant human growth hormone replacement on regional fat distribution, insulin sensitivity, and cardiovascular risk factors in hypopituitary adults. J Clin Endocrinol Metab. 1995 Jan;80(1):153-9. doi: 10.1210/jcem.80.1.7829604.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Anne Klibanski, M.D principal investigator
Massachusetts General Hospital
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing Somatropin in people with Growth Hormone Deficiency, run by Massachusetts General Hospital at 1 site in United States.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 4 inclusion and 11 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 18 Feb 2008. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in United States. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. Some participants in this study may receive a placebo. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Gender specific effects on cardiovascular risk markers (time frame: baseline, 1, 3, 6, 7, 9, and 12 months). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT00136032, which also lists 45 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 18 Feb 2008.