Neoplasms

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Pituitary Neoplasms

Neoplasms, Glandular and Epithelial

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Endocrine Gland Neoplasms

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Nervous System Neoplasms

Growth Hormone Deficiency

Isolated Growth Hormone Deficiency

All Drugs and Chemicals

Hormones

Adult patients with GH deficiency due to a nonsecreting pituitary tumor

Adult patients with a nonsecreting pituitary tumor but without GH deficiency

Pamela U Freda, MD

The purpose of this study is to determine if patients with a history of nonsecreting pituitary adenomas with untreated GH deﬁcient patients have proﬁles consistent with increased cardiovascular risk compared to patients without GH deficiency who have undergone similar surgery.

PROJECT TITLE: Assessment of Cardiovascular Risk in Patients with Growth Hormone Deficiency Following Transsphenoidal Surgery for Nonsecreting Pituitary Adenomas.

BACKGROUND Recently, an awareness of the risks of hypopituitarism in adults has been raised by epidemiological studies demonstrating its association with increased mortality, likely from cardiovascular (CV) causes. In particular, untreated growth hormone deficiency has been implicated as a possible cause of this increased mortality. A 2004 clinical review of growth hormone deficiency in adults highlights the plausibility of this argument by citing studies potentially linking GHD to the following: elevated CRP, LDL and coagulation factor levels, increased abdominal obesity, increased insulin resistance, increased prevalence of structural and functional heart disease and increased rates of endothelial cell and large artery dysfunction. Furthermore, therapy for GH deficiency has been shown to lower total and LDL cholesterol and reduce visceral fat mass, reduce signs of early atherosclerosis and perhaps decrease overall risk of myocardial infarction. While these studies suggest that GHD is an important cardiovascular risk factor, we believe the data are imperfect since some of the studies chose comparison groups too dissimilar (allowing for the possibility of unrecognized confounding). Previous studies have assessed cardiovascular risk in patients with hypopituitarism in comparison to the general population or much younger GH replaced subjects or GHD patients before and after GH therapy. In contrast, we plan to compare cardiovascular risk among adult patients rendered growth hormone deficient following surgery for a non secreting pituitary adenoma versus patients who have undergone the same surgery but who remain growth hormone sufficient. We plan to test for growth hormone deficiency using the Arginine/GHRH stimulation test in 80 subjects. We will divide the patients into two groups: growth hormone deficient and growth hormone sufficient. Once we have recruited enough patients in each group (thirty), we will compare known CV risk markers and endothelial function in carefully matched patients from each group. This approach will allow us to compare similar patients (i.e. all will have undergone surgery, some in each group will have undergone radiation) whose primary difference will be the GH status. In addition, from each group we will identify patients with additional pituitary deficiencies in the hope of comparing patients with either isolated GHD or patients with multiple endocrinopathies to similar matched controls.

At least two other novel aspects of our study include the use of magnetic resonance spectroscopy to measure intramyocellular and intrahepatic lipids and venous endothelial cell biopsy to assess endothelial function. Regarding the first modality, elevated levels of intramyocellular and intrahepatic lipids have been associated with insulin resistance in other populations. It is our hypothesis that subtle abnormalities in these lipid stores may correlate with insulin resistance in patients with apparent occult GH deficiency. With regard to endothelial function, previous work has linked GHD with endothelial cell dysfunction but typically through indirect measures including serum markers and arterial flow mediated dilatation. However, a technique has been recently developed to safely sample venous endothelial cells which in turn will enable us to assess directly at the level of endothelial cells, oxidative stress, cell activation and nitric oxide synthesis. It is our belief that this new method will help confirm the contention that GHD alters the basic function of endothelial cells.

STUDY DESIGN This study will assess the level of cardiovascular risk in two patient populations: those patients who are GHD following transsphenoidal surgery for nonsecreting pituitary adenomas and those patients who are not GHD following similar surgery. The primary outcome will be serum markers of cardiovascular risk including lipids, CRP, IL6 and homocysteine.

Experimental Protocol:

Subjects for this study will have all undergone transsphenoidal surgery for a nonsecreting pituitary adenoma. In addition, there may be some additional subjects, who have also undergone transsphenoidal surgery for a nonsecreting pituitary adenoma, recruited by word of mouth from the cohort of patients described above. Only patients who are not receiving GH therapy will be considered. Of those patients who have received RT, only those at least 5 years from radiotherapy will be recruited in order to lessen the likelihood of a false positive Arginine/GHRH stimulation test which can occur in the early years post RT.

The remaining respondents will be stratified into two groups based on the presence or absence of a history of other hypopituitarism: 1) those with \> 1 known pituitary hormone deficiency (other than GH) and who are on replacement for these and 2) those with no known pituitary hormone deficits. The status of other pituitary hormone replacement therapies will be verified prior to the arrival of the subjects for further testing. Patients will need to be on stable doses of replacement therapy for at least 3 months prior to the study visit and if on hormone replacements they must be on hydrocortisone \< 30 mg/day or equivalent and physiological doses of thyroid and sex steroid replacements. If possible, patients will be asked to provide copies of their most recent endocrine studies if these were not available from the chart review to verify the adequacy of their replacement therapy. Any woman known to be pregnant or any woman of childbearing age with a positive urinary HCG will not be considered for the study (we will screen all woman of childbearing age at the first visit prior to initiation of any testing). In addition, any woman actively nursing cannot be included in the study (we will ask all women of childbearing age at the first visit). We will recruit equal numbers from these two groups, inviting subjects to our Neuroendocrine Unit for an initial visit where they will undergo a clinical exam with vital signs, anthropometric measurements and skin fold thickness assessments. Subjects will also undergo GH stimulation testing with Arginine/GHRH to identify GH deficient (peak GH \< 4 µg/L) and nonGH de•cient (peak GH \> 10 µg/L) groups. Lastly, all subjects will have an endothelial cell biopsy performed.

Thirty matched pairs of patients from the GHD and GH sufficient groups will be contacted further for an additional visit to our unit for some or all of the following tests:

* Fasting blood sampling for CV risk markers including CRP, homocysteine, lipoproteins, IL6 IGFI and IGFBP3 (all subjects, n=30 pairs)
* 75 gm OGTT; Insulin and glucose (all subjects, n=30 pairs)
* DEXA scan to assess body composition and bone density (all subjects, n=30 pairs)
* Ultrasound to assess carotid intimal medial thickness and brachial artery flowmediated dilatation (subset of subjects, n=10 pairs).
* Magnetic resonance spectroscopy assessment of intramyocellular lipids and intrahepatic lipids in a subset of each group of the cohort (subset of subjects, n=10 pairs). Subjects will be studied within 6 months of their initial GH stimulation test.

STUDY DRUGS Subjects will undergo an Arginine/GHRH stimulation test. They will receive Rgene (Upjohn) a 10% Arginine Hydrochloride solution in water and Geref Diagnostic (Serono).

STUDY SUBJECTS Subjects for the study will include adult patients who have undergone transsphenoidal pituitary surgery for a nonsecreting pituitary adenoma.

STUDY LOCATION This study will take place out of the Neuroendocrine Unit, Columbia University.

POTENTIAL RISKS Participation in this study will involve minimal standard risks associated with blood draws. In addition there is a potential risk from exposure to radiation from DEXA scans. However, the amount of radiation exposure from DEXA scanning is only one percent of a chest xray and it is in accordance with federal guidelines for this type of research. Given the risk posed to a fetus from radiation exposure, pregnant or nursing mothers will be excluded from the study. To assess for pregnancy we will chec a urine HCG on all women of childbearing age prior to initiating any testing. In addition, women of childbearing age will be asked if they actively nursing and if so they will be excluded from the study. Since the risk to pregnant or nursing mothers is present only at the time of testing, no additional precautions against pregnancy need to be taken in the days following our testing. Ultrasound (for IMT and flow mediated dilatation studies) poses minimal risk beyond mild discomfort from the gel and probe. MRI also poses minimal risk beyond mild discomfort from the enclosed space and noise of the machine as long as there is no metal within the scanner room. The subjects will be asked a series of questions by the MRI technicians to ensure that they are safe to proceed with MRI. In addition, pregnant woman cannot undergo MRI. The risks of endothelial biopsy are thought to include pain, inflammation, infection and clots. In a previous study it was found to be safe but patients will be asked to return one week after the biopsy for evaluation of the site. If any symptoms arise prior to one week follow up patients will be advised to call or proceed to the emergency room.

The most common adverse reactions from the administration of arginine include nausea, vomiting, headache, flushing, numbness, local venous irritation. Systemic allergic reaction is rare but patients with highly allergic tendencies will not be included. Pregnant or nursing subjects will also be excluded as mentioned above. For GHRH, common side effects include transient warmth/flushing of face, injection site pain, redness/swelling at site of injection, nausea, headache, vomiting, strange taste in mouth, paleness, tightness in chest. A physician will be present throughout the administration of these two drugs.

POTENTIAL BENEFITS The results of the growth hormone stimulation test will be made available to subjects and their doctors. Therefore, if a subject is found to be growth hormone deficient, he or she might benefit from growth hormone therapy which has been shown, in some studies, to improve body composition, cholesterol levels and other factors associated with an increased risk for cardiovascular disease. A decision to initiate therapy, however should only occur after a careful discussion between the subject and his or her personal physician occurs. There may also be some benefit from DEXA scanning as it might identify previously undiagnosed osteoporosis. This condition has effective treatment options. Lastly, participation in the study will help further contribute to our understanding of the risk of heart disease in growth hormone deficient patients.

Assessment of Cardiovascular Risk Markers in Growth Hormone Deficient Patients With Nonsecreting Pituitary Adenomas

Assessment of Cardiovascular Risk Markers in GH Deficient Patients With Nonsecreting Pituitary Adenomas

EMD Serono

Genentech, Inc.

Columbia University

Pamela U. Freda MD

Musculoskeletal Diseases

Diseases and Abnormalities at or Before Birth

Dwarfism

Dwarfism, Pituitary

Bone Diseases

Bone Diseases, Developmental

Bone Diseases, Endocrine

Hypopituitarism

Estrogens

Stratified based on age and estrogen status from 3 to 6 mcg/kg/day

Somatropin

Dosage based on age and estrogen status ranging from 3 to 6 mcg/kg/day

Placebo

Anne Klibanski, M.D

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.

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:

1. has gender-specific effects on cardiovascular risk markers
2. has gender-specific effects on lipid profiles
3. alters heart rate variability and arterial distensibility in parallel with changes in cardiovascular risk markers
4. has different effects depending upon gonadal status

Growth Hormone Administration and Its Effects on Cardiovascular Risk Factors in Growth Hormone Deficient Women

Gender-Specific Effects of Physiologic GH Administration on Cardiovascular Risk Factors in Women With Growth Hormone Deficiency

Massachusetts General Hospital

Anne Klibanski, MD

Nutritional and Metabolic Diseases

Bone Diseases, Metabolic

Metabolic Diseases

Bone Density Conservation Agents

Micronutrients

Gastrointestinal Agents

Channel Blockers

Vitamins

Mineral

Vitamin D

Cholecalciferol

Calcium

Calcium Carbonate

Calcium, Dietary

Diphosphonates

Risedronic Acid

Ergocalciferols

Trace Elements

Calcium Channel Blockers

Vitamin D3

Calciferol

Calcium Supplement

Ergocalciferol

Vitamin D2

No bisphosphonate therapy given, participants will take Vitamin D 400 IU daily for 18 months, as well as calcium carbonate 500 mg twice a day for 18 months.

Bisphosphonate Therapy-Risedronate 35 mg once a week for 18 months, Vitamin D 400 IU daily for 18 months and calcium carbonate 500 mg twice daily for 18 months

Bisphosphonate therapy given to patients with growth hormone deficiency

bisphosphonate therapy (risedronate)

Vitamin D given to patients with growth hormone deficiency

Vitamin D supplement

calcium supplement given to patients with growth hormone deficiency

Timothy A Damron, MD

The purpose of this project is to evaluate the hypothesis that bisphosphonate treatment given to growth hormone deficient patients (regardless of current growth hormone replacement therapy status and without changing that status) significantly increases total body bone mineral density during an eighteen month period of treatment combined with calcium and Vitamin D when compared to calcium and Vitamin D treatment alone.

Adult patients with Dexa scan (bone scan) z-scores \< -1.0 (meaning low bone density) in at least one site will be selected for randomization. All patients who qualify for randomization will undergo baseline bloodwork for serum bone specific alkaline phosphatase (BSAP) and n-terminal telopeptides of collagen (NTX) levels. Recent bloodwork obtained as part of their ongoing long-term Pediatric Oncology and/or Endocrine clinic follow-up evaluation will be reviewed to exclude any baseline correctable confounding causes of osteopenia (low bone density). All women of childbearing potential will have a pregnancy test.

For those patients already on growth hormone replacement therapy, growth hormone will be administered as per standard of care, with standard dose ranges adjusted based upon IGF-1(Insulin like growth factor) monitoring. Those patients not currently receiving growth hormone replacement therapy will not be placed on therapy as a part of this study. Patients on and off growth hormone replacement therapy will be randomized in a block design to the two treatment arms to assure equal numbers in each treatment arm. The bisphosphonate to be utilized will be provided to the Arm II patients at no charge. All Arm II patients will receive the same bisphosphonate regimen, Risedronate 35 mg per oral once weekly for 18 months. All patients on arms I and II will also receive Vitamin D (400 IU p.o. daily) and calcium carbonate (500 mg p.o. twice daily) free of charge for eighteen months.

Study of Adults With Low Growth Hormone Who Survived Childhood Cancer Where Treatment Caused Low Bone Density

Treatment of Childhood Cancer Therapy-induced Osteopenia in Growth Hormone Deficient Adult Survivors: Does Bisphosphonate Treatment Improve Bone Mineral Density?

For those patients already on growth hormone replacement therapy, growth hormone will be administered as per standard of care, with standard dose ranges adjusted based upon IGF-1 monitoring. Those patients not currently receiving growth hormone replacement therapy will not be placed on therapy as a part of this study. Patients on and off growth hormone replacement therapy will be randomized in a block design to the two treatment arms to assure equal numbers in each treatment arm. The bisphosphonate to be utilized will be provided to the Arm II patients at no charge. All Arm II patients will receive the same bisphosphonate regimen, Risedronate 35 mg per oral once weekly for 18 months. All patients on arms I and II will also receive Vitamin D (400 IU p.o. daily) and calcium carbonate (500 mg p.o. twice daily) free of charge for eighteen months.

State University of New York - Upstate Medical University

Professor

bisphosphonate use and growth hormone use

Bisphosphonate and Growth Hormone Use

Growth hormone use only, no bisphosphonate used

Growth Hormone Only

Total

Age Continuous

Sex: Female, Male

Early termination due to low enrollment, and lost to follow up of three subjects. Data was limited and therefore not reviewed/analyzed

Timothy A. Damron

Data analyis halted, due to low enrollment,no outcomes to report

Change in Total Body Bone Mineral Density During an 18 Month Period

Bisphosphonate and Growth Hormone

Growth hormone only, no bisphosphonate will be used

Overall Study

Symptoms and General Pathology

Heart and Blood Diseases

Syndrome

Atherosclerosis

Metabolic Syndrome

Insulin Resistance

Arteriosclerosis

Arterial Occlusive Diseases

Vascular Diseases

Hypoglycemic Agents

Insulin

Insulin, Globin Zinc

Hormone Antagonists

Recombinant Growth Hormone, Genotropin (Pfizer)

Annamaria AL Colao, Prof.

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).

This is an observational,5-yr prospective, controlled study. At study entry, all subjects underwent serum assay of IGF-I, systolic and diastolic blood pressure (SBP, DBP) measurement, total-, and HDL-cholesterol, triglycerides, glucose, and insulin level after an overnight fasting, and common carotid arteries ultrasonography. The oral glucose load (oGTT) was performed by measuring blood glucose every 30 minutes for 2 hours after the oral administration of 75 g of glucose diluted in 250 ml of saline solution. The conversion factors (mg/dl to mmol/l) for lipids and glucose were as follows: cholesterol 0.02586, triglycerides 0.01129, and glucose 0.05551. According with previous studies (13,19-21) blood pressure was measured at the right arm, with the subjects in relaxed sitting position. The average of six measurements (three taken by each of two examiners, in the same day, between 8.00-9.00 in the morning) with a mercury sphygmomanometer was used in all analysis.

In the patients, all parameters and carotid ultrasonography were re-evaluated after 12, 24, 36, 48 and 60 months while in controls they were re-evaluated after 60 months.

At study entry and at study end, in all of the patients and controls the prevalence of insulin-resistance syndrome (IRS) was evaluated according with the American College of Endocrinology (14) based on the presence of at least two criteria of the following: triglycerides levels ≥1.7 mmol/liter, HDL-cholesterol levels ≤1.0 mmol/liter, blood pressure above 130/85 mmHg, fasting glucose between 6.1 and 7 mmol/liter or 2 hr after oGTT between 7.7 and 11.1 mmol/liter.

Effect of 5 Years of GH Replacement on Atherosclerosis

Phase 4 Study of Recombinant GH on Intima-Media Thickness at Common Carotids and on Cardiovascular Risk Factors in Hypopituitary Patients

Federico II University

Study title	NCT ID	Conditions	Interventions	Eligibility	Organization
Assessment of Cardiovascular Risk Markers in Growth Hormone Deficient Patients With Nonsecreting Pituitary Adenomas	NCT00646308	Growth Hormone ... Pituitary Tumor		18 Years - 75 Years	Columbia University
Growth Hormone Administration and Its Effects on Cardiovascular Risk Factors in Growth Hormone Deficient Women	NCT00136032	Growth Hormone ...	Somatropin Placebo	18 Years - 65 Years	Massachusetts General Hospital
Study of Adults With Low Growth Hormone Who Survived Childhood Cancer Where Treatment Caused Low Bone Density	NCT00145704	Osteopenia	bisphosphonate ... Vitamin D suppl... Calcium	18 Years -	State University of New York - Upstate Medical University
Study of Adults With Low Growth Hormone Who Survived Childhood Cancer Where Treatment Caused Low Bone Density	NCT00145704	Osteopenia	bisphosphonate ... Vitamin D suppl... Calcium	18 Years -	State University of New York - Upstate Medical University
Study of Adults With Low Growth Hormone Who Survived Childhood Cancer Where Treatment Caused Low Bone Density	NCT00145704	Osteopenia	bisphosphonate ... Vitamin D suppl... Calcium	18 Years -	State University of New York - Upstate Medical University
Study of Adults With Low Growth Hormone Who Survived Childhood Cancer Where Treatment Caused Low Bone Density	NCT00145704	Osteopenia	bisphosphonate ... Vitamin D suppl... Calcium	18 Years -	State University of New York - Upstate Medical University
Assessment of Cardiovascular Risk Markers in Growth Hormone Deficient Patients With Nonsecreting Pituitary Adenomas	NCT00646308	Growth Hormone ... Pituitary Tumor		18 Years - 75 Years	Columbia University
Effect of 5 Years of GH Replacement on Atherosclerosis	NCT00462475	Hypopituitarism Pituitary Tumor... Growth Hormone ...	Recombinant Gro...	18 Years - 50 Years	Federico II University

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