+ Author Affiliations
Erciyes University Medical School, 38039 Kayseri, Turkey
(Correspondence should be addressed to F Kelestimur; Email: fktimur@erciyes.edu.tr)
The life and times of a pituitary Cushing's survivor (1987) AND a kidney cancer (Renal Cell Carcinoma) survivor (2006). I must be a Super-Woman...NOT!
Sharmyn McGraw writes:
Hey Everyone!!! I’d like to invite all of you to help me spread the word about our Hormonal & Pituitary Health Symposium Oct. 22, 2011, Santa Monica CA. It’s free and a continental breakfast and box lunch is included and the best part is hearing from our team of neuroendocrine experts and meeting many new friends. To register and for a copy of the events schedule www.brain-tumor.org or call Pat Fitzwater at (805) 300-9154 I hope to see many of you there!
Peace and great health all!
Sharmyn
Learn about your Master Gland
This symposium aims to educate patients, their families and the public about the importance of the "Master Gland" in health and in illness.
Topics covered will include: the basics of pituitary gland function and malfunction; signs, symptoms and treatment of hormonal excess and hormonal deficiency; epidemiology of pituitary adenomas and related brain tumors; treatment options for pituitary tumors (acromegaly, Cushing's disease, prolactinoma and non-functional adenomas, craniopharyngioma) including endonasal endoscopic surgery, radiotherapy and non-surgical therapies.
Additional topics will include optimizing your access to care, insurance issues and finding the appropriate pituitary specialists, as well as information about clinical trials in pituitary hormonal disorders
More information and registration
He's known as the neurosurgeon who successfully operated on U.S. Rep. Gabrielle Giffords after she was shot in the head, but Dr. G. Michael Lemole Jr. is building a reputation in an entirely different area of brain surgery - removing hard-to-reach tumors through the nose.
Lemole and an ear, nose and throat surgeon at Tucson's University Medical Center have established a new center for benign and malignant tumors that occur in the sinus cavities and at the base of the brain. Among other things distinguishing the center is the surgeons' ability to remove large tumors like craniopharyngiomas through the nose, eliminating a need to open up the skull.
Rather than using a microscope as surgeons have done in the past for such surgeries, Lemole uses an instrument called an endoscope, which allows a broader view inside the brain. It's like the difference between looking at a room through a keyhole versus opening the door and getting a panoramic view, he said.
"It's not that through-the-nose surgery is new. It's the new tools and expertise that allow us to put the camera right up front and center at the pituitary level or wherever the target is," Lemole said. "And with those special tools, we're able to reach around corners, and this allows us to take out tumors that we couldn't in the past."
Tumors at the base of the skull are particularly difficult, he said in a recent interview, pulling out a model of a brain and pointing to one section in the bottom.
"Just down here, just in this little tight area, you have the nerves for your hearing, for your facial strength, the nerves for sensation over your face and, of course, your brain stem, which is critical to passing all the information from the brain all the way down the spinal cord. So I have to work in a very tight space and if I have a large tumor that is wrapping around all the structures, it becomes much more complex."
Of about 3,000 board-certified neurosurgeons in the country, only 200 or so specialize in skull-base tumors.
With the advanced technology of the endoscope and using a technique of breaking the tumor down called debulking, they are able to remove tumors through patients' nasal passages.
Lemole and UMC's otolaryngology division chief Dr. Alexander G. Chiu have done about 15 of the minimally invasive nasal surgeries together since establishing the local Center for Sinonasal and Skull Base Tumors four months ago.
Benign pituitary tumors are the most common, but they've also done surgeries together to remove craniopharyngiomas, as well as benign and malignant sinus tumors. They hope to do at least 100 such minimally invasive surgeries per year.
Lemole and Chiu hope their center, unique for its collaboration in an academic setting, will attract patients from across the Southwestern U.S. and eventually become a medical tourism destination for people from other parts of the country and even the world.
They say the key to the center is teamwork. Most neurosurgeons aren't comfortable operating on tumors when they move into the eye orbit or into the nasal space - it's beyond where they typically go. That's where having a specialist like Chiu as reinforcement is a tremendous help.
"Your nose and your sinuses border your brain. So a lot of the tumors that go from the nose can actually go up into the brain," Chiu said. "And a lot of the tumors at the base of the brain can actually hang down into the nose."
Traditionally, to remove a sinus tumor, surgeons would split a patient's lip and pull the face aside.
"You'd be left with a big scar," Chiu said.
The nasal surgeries often take much longer than when the skull is opened up, but the surgery is still more advantageous to the patient, the doctors say.
One of the center's first patients was 49-year-old Tucson aircraft mechanic Eugene Vasquez. The father of three and grandfather of four had a growing brain tumor that he said looked like a peach. It was pressing on his eyes, causing double vision, dizziness and headaches. The whole left side of his face eventually went numb. He'd first been diagnosed in September 2009 when he went to a local emergency room for what he thought was a sinus infection. He was told there might be nothing that could be done.
"It scared the crap out of me," said Vasquez, who had the tumor removed through his nose by Chiu and Lemole Nov. 20. He was released from UMC on Thanksgiving and went back to work a month later. "I got lucky. I was blessed that Dr. Chiu got here at the right time."
Chiu came to Tucson from a 1,000-bed hospital at the University of Pennsylvania six months ago. While UMC, at 487 beds, is less than half the size of the hospital he came from, Chiu said establishing a Center for Sinonasal and Skull Base Tumors in Tucson was an opportunity he wanted to pursue. And working with Lemole, who operated a skull-base tumor center at the University of Illinois in Chicago, was a big part of the reason he took the job, he said. Lemole moved from Chicago to Tucson to become chief of neurosurgery at UMC in October 2009.
Vasquez's tumor was benign, but the terms "benign" and "malignant" can be misleading when it comes to brain growths. Many benign tumors are fatal because of the damage they cause to critical parts of the brain. Chiu told Vasquez his tumor was dangerously large and performed the surgery almost immediately after seeing him.
"When things go beautifully and everything goes well, it's very common for patients to not feel like they've had much surgery," Chiu said. "The biggest advantage we have is that patients will spend a lot less time in the hospital and have a lot less pain."
Not all patients qualify for the surgery. A glioma, for example, would be too high in the brain to qualify. "It has to be at the bottom of the brain so that we can access it through the nose," Chiu said. Such tumors are rare and affect less than 1 percent of the population, Lemole said.
Lemole stressed that the center he's established with Chiu is not solely about removing tumors through the nose. It's about treating all tumors at the base of the skull, he said. The center also works with plastic surgeons, oculoplastic surgeons, radiology, radiation oncology, endocrinologists and neurologists.
"It's a multidisciplinary group," he said. "If the patient needs the minimally invasive approach and we can offer that, we'd love to. If they need the maximally invasive approach where we literally take down their face or take down their skulls in the old traditional ways, we can do that, too."
Lemole still performs trauma surgeries like he did Jan. 8, the day of Tucson's mass shootings, but the skull-base work now comprises most of what he does.
On StarNet: Stephanie Innes brings you the latest health information in her blog, Tucson Health and Wellness, at go.azstarnet.com/health
Reporter Stephanie Innes is at sinnes@azstarnet.com
From http://azstarnet.com/news/science/health-med-fit/article_64800a3e-9389-563f-9854-44089944cffa.html
The author: Professor Yasser Metwally
INTRODUCTION
October 8, 2010 — The most concerning cause of acquired hypopituitarism is a tumor in the hypothalamic-pituitary region. The most common tumor that arises in this region in childhood is a craniopharyngioma. While craniopharyngiomas are derived from epithelial remnants of Rathke’s pouch, the same tissue that forms the anterior pituitary gland, they are not usually found exclusively within the pituitary gland, but more likely they are confined to the suprasellar region or are found in both suprasellar and intrasellar locations.[1] The presenting symptoms are dependent both on the main location of the tumor and on the direction(s) that the tumor grows. For example, if the tumor grows downward, it may cause alterations in the anterior and posterior clinoid bones or in the floor of the sella turcica and/or compress the pituitary gland. If the tumor grows upward, it may compromise vision by effects on the optic nerves.
While medical textbooks typically describe the most common visual change in patients with craniopharyngioma as "bitemporal hemianopsia" (loss of the outer visual fields of both eyes) due to compression of the optic chiasm, this rarely occurs so precisely. More likely is the development of "quadrianopsias," which are smaller, more irregular field cuts. If the tumor grows even farther upward beyond the visual tracts, it may block the third ventricle and cause obstructive hydrocephalus, leading to headaches, vomiting, and/or blurry vision (in association with papilledema). Craniopharyngiomas are benign tumors histologically, but they are often described as "geographically malignant" based on their location and ability to wrap around vital structures (eg, optic nerves) precluding complete surgical removal. As stated previously, tumors originating in the pituitary gland are uncommon causes of acquired hypopituitarism in children. However, any surgery to remove a tumor in the hypothalamic-pituitary region may lead to hypopituitarism if it is not already present.
Figure 1. A, Craniopharyngioma, compressing the optic chiasma, hypothalamus and extending upward into the lateral ventricle. The tumour is partially cystic with calcified material. B, A sagittal section of the brain shows a large craniopharyngioma below the cerebral ventricle. Note the stippled pattern of the tumor.
Another cause of acquired hypopituitarism is radiation treatment of a cancerous tumor in the head or neck region. More specifically, the radiation that is required to cure the child’s tumor may, of necessity, damage normal tissue in its path or beyond. When hypopituitarism ensues in this situation, it is usually the result of radiation-induced damage to the hypothalamus, as the pituitary gland is relatively resistant to radiation. Different hypothalamic-pituitary axes have different sensitivities to radiation. Doses as low as 18 Gy using conventional fractionation can interfere with GH dynamics; doses higher than 40 Gy can cause deficiencies of gonadotropins, TSH, and ACTH, while >50 Gy may cause hyperprolactinemia, especially among young women.
Other causes of acquired hypopituitarism in childhood include previous brain infection (encephalitis and/or meningitis), hydrocephalus (even without an underlying tumor), vascular abnormalities (such as a varix in the hypothalamic-pituitary area)[2], and major head trauma usually associated with a significant loss of consciousness.[3]
Potential Anterior Pituitary Hormone Deficiencies
In childhood hypopituitarism, GH is the most commonly underproduced pituitary hormone, often as the result of loss of hypothalamic GH-releasing hormone (GHRH) (Table 2). The deficiency of GH primarily leads to short stature and slow height velocity. Untreated GH deficiency in children also causes disturbed body composition, with a reduction in lean body mass (ie, muscle) and an excess of fat, the latter accumulating predominantly in the cheeks of the face and in the abdomen, creating a cherubic or angel-like appearance.[4]
Table 2. Hierarchy of Hypothalamic-Pituitary-Target Organ Hormones
Hypothalamus
Pituitary
Target Organ
Hormone/Function
Growth hormone-releasing hormone (GHRH)
Anterior:
Growth hormone (GH)
Cartilage/liver
Insulin-like growth factor-1 (IGF-1)
Thyrotropin-releasing hormone (TRH)
Anterior:
Thyroid-stimulating hormone (TSH)
Thyroid gland
T4/T3
Gonadotropin-releasing hormone (GnRH)
Anterior:
Luteinizing hormone (LH)
Ovary
Estradiol
Follicle-stimulating hormone (FSH)
Testicle
Testosterone
Corticotropin-releasing hormone (CRH)
Anterior:
Corticotropin (ACTH)
Adrenal glands
Cortisol
Prolactin-inhibitory factor
Anterior:
Prolactin
Breast
Milk
Hypothalamic factors
Posterior:
Antidiuretic hormone (ADH)
Kidney
Urine concentration
Deficiency of hypothalamic thyrotropin-releasing hormone (TRH) or pituitary TSH causes central hypothyroidism. Unlike children whose hypothyroidism is due to thyroid gland damage, those with hypopituitarism typically have somewhat higher thyroid hormone levels and thus may have few or no symptoms. In other cases, as occurs in patients with primary thyroid disease, short stature and slow height velocity, relative weight excess, constipation, dry skin, cold intolerance, and fatigue may be present.
Younger children with deficiencies of either hypothalamic gonadotropin-releasing hormone (GnRH) or the pituitary gonadotropins typically show no abnormalities since luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels are normally low prior to puberty. In contrast, adolescent-aged children with deficiencies of the gonadotropins present with failure to start or progress through puberty (breast development and menstrual periods in girls and enlargement of the testicles and penis in boys). Infrequently and paradoxically, central sexual precocity can be seen in the setting of hypopituitarism.
Loss of hypothalamic corticotropin-releasing hormone (CRH) or pituitary ACTH results in an ability of the adrenal zonas fasciculata and reticularis to manufacture normal amounts of cortisol (central adrenal insufficiency). If deficient, this hormone is most likely to place a child in a life-threatening situation. While there would likely be no symptoms under normal circumstances, except maybe mild fatigue, lack of cortisol in the setting of infection, fever, surgery, trauma, etc, may cause vomiting, dehydration, shock, and even death. Biochemical correlates of cortisol deficiency include hypoglycemia and hyponatremia (with normokalemia). In this setting, mineralocorticoid function is completely normal, as aldosterone production by the zona glomerulosa of the adrenal cortex is regulated by the renin-angiotensin and not the CRH-ACTH system.
Potential Anterior Pituitary Hormone Excess
Serum levels of prolactin are usually normal or only mildly increased (if there is disruption of the hypothalamic-pituitary stalk) secondary to the loss of a normally predominant inhibitory signal from the hypothalamus. Although there are typically no symptoms in this situation, in rare cases a small amount of galactorrhea might occur.
Potential Posterior Pituitary Hormone Excess
As stated previously, a deficiency of ADH causes central or neurogenic DI. Infants and toddlers manifest DI with excessively wet diapers. If unrecognized and hence untreated, dehydration with elevated serum sodium concentrations will ensue in this age group as young children cannot report and easily satisfy heightened thirst. Older children with DI typically present with excessive day-and night-time urination, new onset of bed-wetting, and increased thirst. DI most often occurs unintentionally as a result of surgical treatment of a hypothalamic-pituitary tumor, such as a craniopharyngioma. In some cases, DI is temporary due to local postsurgical edema, but it will be permanent if surgical sacrifice close to the hypothalamus or of the stalk itself is required for complete cure of a brain tumor in the suprasellar region.[5] DI may also occur in association with a diencephalic germinoma.
Figure 2. Craniopharyngioma. (A) Sagittal T1-weighted image shows a cystic mass in the suprasellar region. (B) Coronal T1-weighted image shows a large cystic mass in the suprasellar region with compression of the optic chiasm. (C) Coronal postcontrast T1-weighted image shows enhancement of the irregular cyst wall. (D) Sagittal postcontrast T1-weighted image demonstrates enhancement of the cyst wall with a nodular area on the right side.
Figure 3. Craniopharyngioma. (A) Axial postcontrast CT scan shows a cystic mass with rim enhancement in the suprasellar region. (B) Sagittal T1-weighted image shows a large cystic mass involving the sellar and suprasellar regions. The mass shows high signal intensity on T1-weighted imaging, consistent with high protein content. A fluid-fluid level is seen within the cystic lesion. (C) Coronal T2-weighted image demonstrates a high signal intensity mass with suprasellar extension and slight parasellar extension into the cavernous sinuses.
Figure 4. Sarcoidosis. (A) Coronal T1-weighted image demonstrates a suprasellar isointense mass. (B) Coronal postcontrast T1-weighted image shows intense enhancement of the mass just inferior to the optic chiasm.
Figure 5. Histiocytosis. (A) Sagittal postcontrast T1-weighted image demonstrates an enhancing mass in the suprasellar region involving the infundibulum. (B) Coronal postcontrast T1-weighted image shows an enhancing mass in the suprasellar region along the infundibulum. Compression of the optic chiasm is seen. (C) Coronal postcontrast T1-weighted image obtained 3 months later after treatment shows a significant decrease in the size of the mass lesion along the infundibulum.
Figure 6. A, Postmortem case of hypothalamic tuberculoma. B, Tuberculous infection of the hypothalamus (arrow)
References
Lafferty AR, Chrousos GP. Pituitary tumors in children and adolescents. J Clin Endocrinol Metab. 1999;84:4317-4323.
Martin NA, Macagba-Crain CL, Geffner ME, et al. Isolated growth hormone deficiency associated with a giant arteriovenous varix. Neurosurgery. 1990;27:295-298.
Benvenga S, Campenni A, Ruggeri RM, et al. Clinical review 113: hypopituitarism secondary to head trauma. J Clin Endocrinol Metab. 2000;85:1353-1361.
Carrel AL,Allen DB. Effects of growth hormone on body composition and bone metabolism. Endocrine. 2000;12:163-172.
Blevins LS Jr, Wand GS. Diabetes insipidus. Crit Care Med. 1992;20:69-79.
From http://yassermetwally.wordpress.com/2010/10/08/acquired-hypopituitarism-2/
Patients with long-term chronic conditions, such as Cushing’s disease or Klinefelter’s syndrome, appear to be at increased risk for long-term unemployment related to their disease.
Researchers compared unemployment rates with re-employment rates for 130 patients (81 women) aged 65 years or younger with Addison’s disease, Cushing’s disease, craniopharyngioma or Klinefelter’s syndrome. The researchers presented the results at the Annual Society for Endocrinology BES 2010 in Manchester, England.
Based on telephone questionnaires, 83 patients (63.8%) were employed at the time of diagnosis. However, 79 patients (60.8%) were later unemployed, related to their long-term chronic condition.
Seventy-seven patients (59.2%) reported being satisfied with their current working status and ability to work. Among those unemployed, nine of 53 patients (40.8%) said they would like to work but did not feel supported.
Although the study was small and did not include all chronic endocrine conditions, the researchers said data show a high rate of unemployment for this patient population.
“Long-term unemployment is a significant problem for people with chronic diseases,” John Wass, MD, professor of endocrinology at Oxford University and consultant endocrinologist at Oxford Radcliffe Hospitals, said in a press release. “More people should consider returning to work following diagnosis, and more doctors need to encourage and support their patients in this. While a return to work may not be suitable for all patients, it can significantly improve their well-being and quality of life.”
Wass J. Poster #116. Presented at: The Annual Society for Endocrinology BES meeting; March 15-18, 2010; Manchester, England.
Mark Sherlock, John Ayuk, Jeremy W. Tomlinson, Andrew A. Toogood, Aurora Aragon-Alonso, Michael C. Sheppard, Andrew S. Bates, and Paul M. Stewart*
Centre for Endocrinology, Diabetes, and Metabolism (M.S., J.A., J.W.T., A.A.T., A.A.-A., M.C.S., P.M.S.), School of Clinical and Experimental Medicine, College of Medical and Dental Sciences, University of Birmingham, Birmingham B15 2TH, United Kingdom; and Birmingham Heartlands and Solihull National Health Service Trust (A.S.B.), Birmingham B9 5SS, United Kingdom
* To whom correspondence should be addressed. E-mail: P.M.Stewart@bham.ac.uk.
Pituitary disease is associated with increased mortality predominantly due to vascular disease. Control of cortisol secretion and GH hypersecretion (and cardiovascular risk factor reduction) is key in the reduction of mortality in patients with Cushing's disease and acromegaly, retrospectively.
For patients with acromegaly, the role of IGF-I is less clear-cut. Confounding pituitary hormone deficiencies such as gonadotropins and particularly ACTH deficiency (with higher doses of hydrocortisone replacement) may have a detrimental effect on outcome in patients with pituitary disease. Pituitary radiotherapy is a further factor that has been associated with increased mortality (particularly cerebrovascular). Although standardized mortality ratios in pituitary disease are falling due to improved treatment, mortality for many conditions are still elevated above that of the general population, and therefore further measures are needed.
Craniopharyngioma patients have a particularly increased risk of mortality as a result of the tumor itself and treatment to control tumor growth; this is a key area for future research in order to optimize the outcome for these patients.
From http://edrv.endojournals.org/cgi/content/abstract/er.2009-0033v1
INTRODUCTION
Adrenal insufficiency can be caused by diseases of the adrenal gland (primary), interference with corticotropin (ACTH) secretion by the pituitary gland (secondary), or interference with corticotropin-releasing hormone (CRH) secretion by the hypothalamus (tertiary). This topic will review the major causes of the latter two disorders; the causes of primary adrenal insufficiency, and the clinical manifestations and approach to diagnosis are discussed separately. (See "Causes of primary adrenal insufficiency (Addison's disease)" and "Clinical manifestations of adrenal insufficiency in adults" and "Diagnosis of adrenal insufficiency in adults".)
SECONDARY ADRENAL INSUFFICIENCY
Any process that involves the pituitary and interferes with ACTH secretion can cause secondary adrenal insufficiency. The ACTH deficiency may be isolated, or occur in conjunction with other pituitary hormone deficiencies (panhypopituitarism).
Panhypopituitarism — Pituitary tissue can be destroyed and hormone secretion reduced by large pituitary tumors or craniopharyngiomas, infectious diseases such as tuberculosis or histoplasmosis, infiltrative diseases, lymphocytic hypophysitis, head trauma, and large intracranial artery aneurysms. Pituitary infarction can occur at the time of delivery if excessive blood is lost and hypotension occurs (Sheehan's syndrome), and hemorrhage may occur into a pituitary tumor (pituitary apoplexy). Pituitary metastases are frequently (about 5 percent) found in patients with disseminated cancer at autopsy; however, these metastases rarely reduce hormone secretion [1]. (See "Causes of hypopituitarism".)
ACTH deficiency due to genetic pituitary abnormalities is rare. ACTH and cortisol deficiency have been described in patients with multiple pituitary hormone deficiencies due to mutations in the PROP-1 (Prophet of Pit-1) gene, even though PROP-1 is not expressed in corticotropes. The onset of cortisol deficiency, which may be severe, ranges from childhood to late adulthood [2-5]. Mutations in other transcription factors involved in early pituitary development (HESX1, LHX4) also can result in variable degrees of hypopituitarism that include ACTH deficiency [6,7]. (See "Causes of hypopituitarism".)
Isolated ACTH deficiency — Isolated ACTH deficiency is a rare disorder [8]. The defect is probably at the pituitary level because there is no ACTH secretory response to CRH or vasopressin, as there usually is in hypothalamic disorders [9-11]. Occasional patients may have hypothyroxinemia and hyperprolactinemia that are corrected with glucocorticoid replacement [12,13].

In recent years, brain tumor removal through smaller and less invasive techniques has become possible. These newer “keyhole” approaches can now be used to approach a majority of both benign and malignant brain tumors, including those that arise from the brain itself, from the coverings of the brain and skull base, from the pituitary gland and from metastatic brain tumors arising from cancers elsewhere in the body. The increasing success of keyhole surgery over the last decade has been accelerated by technological advances in micro-instrumentation, surgical navigation (like GPS for the brain), and endoscopy providing a more panoramic view of the intracranial space. The shift away from traditional large craniotomies has multiple advantages including less disruption of normal anatomy, including smaller incisions, less muscle manipulation, less bone removal and minimal or no brain retraction, all of which translate into a more rapid and less painful recovery with a lower risk of complications. Keyhole approaches have been shown safe and effective for a wide spectrum of brain, skull base and pituitary tumors. Common keyhole craniotomies include the endonasal route (through a nostril), the supra-orbital route (through an eyebrow incision), the retro-sigmoid route (through an incision behind the ear) and the navigation-guided keyhole craniotomy for removal of deeply situated brain tumors.
The endonasal route uses the nostril as its entry point. Using the operating microscope and endoscope, the approach passes through the back of the nasal cavity to the skull base without facial incisions, brain retraction or post-operative nasal packing. It allows direct access to the midline skull base, undersurface of the frontal lobes and brainstem, optic nerves, other cranial nerves and pituitary gland. The endonasal route is used for removing pituitary adenomas and for many other brain and skull base tumors that arise in and around the pituitary gland including craniopharyngiomas, clival chordomas, Rathke’s cleft cysts and meningiomas.
This approach is performed through an incision in the eyebrow and a small craniotomy (bony opening) above the eyebrow measuring approximately 2 x 3 cm. It differs from the traditional fronto-temporal craniotomies in that it requires minimal temporalis muscle dissection (the chewing muscle), involves much less bone removal and minimal to no brain retraction. It is ideal for many meningiomas, some craniopharyngiomas and some frontal tumors such as gliomas and metastatic tumors.
This approach is performed through an incision directly behind the ear and a bony opening that allows access to the posterior fossa which is an area of the cranium where the cerebellum (for balance and coordination), brainstem and many important nerves reside. This approach is ideal for many schwannomas (acoustic neuroma), meningiomas and tumors of the cerebellum.
This approach is used for reaching tumors within the brain, typically below the brain surface. Using surgical navigation, a small incision is marked on the scalp and the underlying craniotomy usually is 2 to 3 cm in maximal diameter. A trajectory through the brain is then chosen that avoids or minimizes damage to critical brain areas (speech, comprehension, reading, motor, sensory areas). This approach is used for removal of gliomas, metastatic brain tumors and tumors in the ventricles (fluid filled brain chambers).
Keyhole craniotomies provide a minimally invasive approach for many intracranial tumors, typically yielding a rapid patient recovery and excellent cosmetic result compared to traditional larger craniotomies. However, these are technically demanding surgeries, require specialized instrumentation and are certainly not appropriate for all brain tumors. Some brain tumors still require a large bony opening for safe and effective removal. Additionally, some tumors that could be removed by a “keyhole approach” can also be removed by a traditional approach with an excellent outcome. Thus, it is important that the neurosurgeon performing a craniotomy for tumor removal select the best approach based upon his/her own judgment and clinical experience.
Below is a list of common brain, skull base and pituitary tumors often treated by keyhole approaches. This list is by no means exhaustive. Most such tumors are diagnosed by MRI with and without contrast or with CT scans; MRI’s generally provide more information. Other diagnostic tests are often needed depending upon tumor type and location.
These are locally invasive tumors that arise in the skull base typically which are typically slow-growing. However, a minority of chordomas behave aggressively like a malignancy. Symptoms may include headaches and double vision as well as visual loss, hearing loss and difficulty swallowing, in-coordination and motor weakness. Initial treatment is with surgical removal and most can be approached by an endonasal route. However, some extensive and/or laterally placed chordomas may require different skull base approaches. Because chordomas typically invade the bone and dura of the skull base, complete removal is often not possible and many chordomas also require treatment with focused radiotherapy (radiosurgery, stereotactic radiotherapy or proton beam radiation).
These benign tumors arise along the undersurface of the brain near the pituitary gland and pituitary stalk. They occur most commonly in childhood, adolescence and later adult life. They often become adherent to brain structures and can cause a variety of symptoms depending upon their location including loss of pituitary hormonal function (low cortisol, low thyroid, growth failure, loss of sexual function and menstrual periods, diabetes insipidus, obesity), visual loss and headache. Craniopharyngiomas may become quite large (over 4 cm). Initial treatment is surgical removal by the endonasal route or a supra-orbital or other craniotomy. Because of their tendency to be adherent to the optic chiasm, other nerves and important blood vessels, complete tumor removal may not be possible in up to 50% of patients. Patients with incomplete tumor removal typically require focused radiotherapy with radiosurgery or stereotactic radiotherapy. Many patients require hormone replacement therapy.
Gliomas are the most common type of primary brain tumor. They can occur at any age and in any part of the brain. The 3 major types include astrocytomas, ependymomas and oligodendrogliomas. The most common glioma is the high grade glioblastoma multiforme which generally carries a poor prognosis. Symptoms from a glioma are variable and depend on tumor location and size; common complaints include headache, seizures, confusion, weakness, numbness, incoordination and personality changes. Because gliomas are infiltrative into the brain, they typically cannot be removed completely. Treatment may involve surgical debulking through a craniotomy, radiosurgery or whole brain radiation plus chemotherapy. In many instances, all 3 treatments are needed.
Meningiomas are the most common benign brain tumor although up to 5% can be aggressive or malignant. The occur mostly in adults, are more common in women and arise from the brain coverings. They are typically attached to the dura (outer layer of the meninges); common locations include the undersurface of the cranium, frontal fossa (under the frontal lobes), tuberculum sella (near the optic nerves), sphenoid wing (near the temporal lobes) and the posterior fossa (near the cerebellum). Meningiomas may produce a variety of symptoms depending upon their location including visual loss, hearing loss, headaches, seizures, weakness, imbalance and personality changes. Symptomatic meningiomas are typically treated by surgical removal. The approach depends upon tumor location and may include a craniotomy (convexity, temporal, supra-orbital or retrosigmoid) or an endonasal approach. Some meningiomas also require focused radiation treatment (radiosurgery).
These tumors arise from a cancer from another part of the body and are the most common brain tumor type. Cancer commonly associated with metastatic brain tumors are lung, breast, melanoma, colon, renal and thyroid. When diagnosed, patients may have one or multiple metastatic brain tumors. Symptoms depend upon tumor location and may include headache, seizures, weakness, numbness, incoordination, confusion and personality changes. Treatment for larger tumors may involve surgical removal through a keyhole craniotomy. Smaller tumors (under 3 cm) can often be treated with radiosurgery, whole brain radiation and/or chemotherapy. In many patients, chemotherapy, radiation and surgery are all needed. Although the prognosis for patients with a metastatic brain tumor can be poor, treatments are continually improving and there are new therapies in development.
These benign tumors arise from the pituitary gland and account for 15-20% of primary brain tumors. Adenomas are classified by size and whether they produce pituitary hormones; those less than 1 cm in diameter are called microadenomas those over 1 cm in diameter are called macroadenomas. The four common types of adenomas include prolactinomas, adrenocorticotropic hormone (ACTH) secreting adenomas causing Cushing’s disease, growth hormone (GH) secreting adenomas causing acromegaly, and endocrine-inactive adenomas. Pituitary adenomas may cause problems because of hormonal excess (acromegaly, Cushing’s disease, prolactinoma), pituitary hormonal failure, vision loss, headaches and/or bleeding into the tumor (pituitary apoplexy). In addition to an MRI of the pituitary, detailed pituitary hormonal testing is also part of the initial evaluation. Endonasal surgery is considered the first-line treatment for all pituitary adenomas except prolactinomas which can often be treated with medication (cabergoline or bromocriptine). Some patients with a pituitary adenoma also require focused radiation (radiosurgery) and/or hormonal replacement.
These benign tumors arise from the nerve sheath (covering) of cranial nerves. The most common types arise from the 8th (vestibulo-cochlear nerve) or 5th cranial nerve (trigeminal nerve). Vestibular (acoustic) schwannomas cause hearing loss and tinnitus (ringing in the ear). As they enlarge they can compress the brainstem, cerebellum and other cranial nerves, resulting incoordination, vertigo, facial numbness, facial weakness and difficulty swallowing. Trigeminal schwannomas are less common and can cause facial pain (trigeminal neuralgia), double vision and incoordination. Treatment for acoustic schwannomas is by surgical removal through a retro-sigmoid craniotomy or other skull base approach. Smaller acoustic tumors can be treated with radiosurgery (focused radiation). Treatment for trigeminal schwannomas is typically by surgery.
1. Fatemi N, Dusick JR, de Paiva N, Kelly DF: The endonasal microscopic approach for pituitary adenomas and other parasellar tumors: a 10-year experience. Neurosurgery, 63 [ONS Suppl 2]; ONS 63:244-256, 2008
2. Fatemi N, Dusick JR, de Paiva N, Malkasian D, Kelly DF: Endonasal versus supra-orbital keyhole removal of craniopharyngiomas and tuberculum sellae meningiomas. Neurosurgery, 64 [ONS Suppl 2]:ONS 64:269–287, 2009
Dr. Kelly completed Neurosurgical Residency training at George Washington University Medical Center in 1993. He joined UCLA and Harbor-UCLA Medical Centers that same year and in 1998 became director of the UCLA Pituitary Tumor and Neuroendocrine Program. Before leaving UCLA in June 2007, he was Professor of Neurosurgery and Vice-Chief of Clinical Affairs for the Division of Neurosurgery and Co-Director of the UCLA Clinical Brain Injury Program. As Director of the newly formed Brain Tumor Center at the John Wayne Cancer Institute and Saint John’s Health Center, Dr. Kelly will continue to focus his efforts on developing innovative treatments for patients with brain and pituitary tumors and providing fellowship training in minimally invasive intracranial surgery. Dr. Kelly is the author or co-author of over 50 peer-reviewed publications and a dozen book chapters. He is a member of the editorial board of the journal Neurosurgery. He is an active member of the American Association of Neurological Surgeons, the Congress of Neurological Surgeons and the Pituitary Society. He is also a member of the recently appointed Pituitary Adenoma Treatment Guidelines Committee of the American Association of Neurological Surgeons.
The Brain Tumor Center at Saint John’s Health Center in Santa Monica, California provides comprehensive care and minimally invasive neurosurgery for patients with brain, skull base and pituitary tumors. With colleagues in Endocrinology, Oncology, Radiation-Oncology, Head & Neck Surgery, Neurology and Neuro-Ophthalmology, we provide a multidisciplinary approach to these complex problems. The Brain Tumor Center serves the Los Angeles region and beyond, treating many patients from out of California and from abroad. For additional information: www.brain-tumor.org.
From http://medicaltourismmag.com/detail.php?Req=222&issue=10
A pituitary tumor is an abnormal growth in the pituitary gland, the part of the brain that regulates the body's balance of hormones.
The pituitary gland is a pea-sized endocrine gland located at the base of the brain. The pituitary regulates and controls the release of hormones from other endocrine glands, which in turn regulate many body processes. These hormones include:
- Adrenocorticotropic hormone (ACTH)
- Growth hormone (GH)
- Prolactin
- Thyroid-stimulating hormone (TSH)
About 75% of pituitary tumors release hormones. When a tumor produces too much of one or more hormones, the following conditions may occur:
- Central hypothyroidism (excess thyroid-stimulating hormone)
- Cushing syndrome (excess adrenocorticotropic hormone)
- Gigantism or acromegaly (excess growth hormone)
- Prolactinoma (excess prolactin)
As the tumor grows, hormone-secreting cells of the pituitary may be damaged, causing hypopituitarism.
The causes of pituitary tumors are unknown, although some are a part of a hereditary disorder called multiple endocrine neoplasia I (MEN I).
There are other types of tumors that can be found in the same area of the head as a pituitary tumor:
- Craniopharyngiomas
- Cysts
- Germinomas
- Tumors that have spread from cancer in another part of the body (metastatic tumors)
About 15% of tumors in the skull are pituitary tumors. Most pituitary tumors are located in the anterior pituitary lobe and are usually noncancerous (benign).
Pituitary tumors develop in about 20% of people, although many of the tumors do not cause symptoms and the condition is never diagnosed during the person's lifetime...
~~~~~~~
This article also includes causes; a comprehensive symptoms list; treatments and much more. Read it at http://health.nytimes.com/health/guides/disease/pituitary-tumor/overview.html?scp=1&sq=pituitary%20tumours&st=cse
~~~~~~~~~~~~~~~~~~~~~~~
MaryONote: It's so nice to see articles like this getting out into the mainstream press. For so many years pituitary tumors weren't talked about. As a matter of fact, often when I've told people about my surgery they didn't even know where the pituitary gland was located. Many would indicate the abdominal area and think it was there.
Hopefully, with more news items in papers and on TV the general public will be more aware of the pituitary (and adrenal) and their various locations.
Someday...I wish...that people will be aware of Cushing's like they are of thyroid issues or diabetes. not that I wish that more people had Cushing's, of course, but I'd just like to see more awareness, knowledge and understanding.
Someday, I hope that people will be tested more routinely for these "orphan diseases", doctors won't automatically decide that the patient is causing his/her own symptoms and get to the diagnostic and treatment phases more quickly.
A statistic I've seen many times over the years, that 20% of all people have a pituitary tumor was mentioned in this article:
Pituitary tumors develop in about 20% of people, although many of the tumors do not cause symptoms and the condition is never diagnosed during the person's lifetime.
The last part is especially scary: "the condition is never diagnosed during the person's lifetime."
How about getting people diagnosed - and cured - while they're still alive?
From http://www.dailyherald.com/story/?id=262733&src=1
By Kimberly Pohl
Bernie Pedersen was growing, just not vertically.
As an 8-year-old, he stood about 4-foot-3 and weighed 52 pounds. Four years later, he was 4-foot-5 and 125 pounds.
Doctors brushed it off. With a 4-foot-11 mother, he'd probably be small as an adult, they said.
Then came the anxiety, emotional outbursts, muscle pains, depression, even suicidal thoughts. It took two years, but the proper diagnoses finally came: Pedersen had the endocrine disorder Cushing's disease and craniopharyngioma, a benign tumor associated with the pituitary gland. He'd need to have surgery and get all his hormones replaced artificially.
Now 29, the 6-foot-4 Palatine resident and Lake Zurich High School grad hovers over most and helps guide others through similar growth disorders. He volunteers with the Oak Park-based Major Aspects of Growth in Children, also known as the Magic Foundation.
The Safeco Insurance Foundation recently recognized Pedersen, an insurance agent, with its 2008 Community Hero award. In his name, the group donated $15,000 to the Magic Foundation, which provides support to more than 25,000 people and families affected by a variety of medical conditions affecting growth.
"I have 18 years experience with this and can provide a lot of insight," said Pedersen. "Adults, kids and their parents are scared seeing this for the first time. I try to support them and show them they're not alone."
Kids often share their fears about puberty with Pedersen, whose own adolescence was nightmarish. Before surgery at age 11 to remove his walnut-sized brain tumor, he played sports and took honors classes.
"He was a handsome, athletic kid who came back to junior high with 52 staples across his head and wandering eyes," said his mother, Susan.
Pedersen said he lost all his friends and ballooned to nearly 300 pounds by the end of his freshman year at Lake Zurich High. Surgery damaged his hypothalamus, which helps regulate appetite and metabolism. Other symptoms included impaired vision, short-term memory impairment, mood swings and fatigue. He did poorly at college.
In the past few years, however, he's found an effective cocktail of replacement hormones and medications. He graduated from Harper College, is studying for certification in the IT field and works at the Palatine insurance agency founded in 1952 by his grandfather, Bernard Pedersen, a longtime state lawmaker from Palatine who died in 1996.
The younger Pedersen is activities coordinator at the Magic Foundation's biannual conventions, which can draw up to 500 people. He leads discussion groups and speaks on panels.
"I show them that people can live a normal life on replacement hormones," he said.
Added his mom: "Bernie gives parents confidence that their child can also grow up and live a normal life."
For more information, go to magicfoundation.org.
From NIH (July 12, 2008)
| 1 | Recruiting | Prevalence of Pituitary Incidentaloma in Relatives of Patients With Pituitary Adenoma | ||||
| Condition: | Pituitary Adenoma | |||||
| Intervention: | ||||||
| 2 | Recruiting | Pituitary Tumor Surveillance: Pathogenic Correlation | ||||
| Condition: | Pituitary Tumor | |||||
| Intervention: | ||||||
| 3 | Recruiting | Temozolomide in Treating Patients With Invasive Pituitary Tumors | ||||
| Condition: | Brain and Central Nervous System Tumors | |||||
| Interventions: | Drug: temozolomide; Procedure: DNA methylation analysis; Procedure: gene expression profiling; Procedure: laboratory biomarker analysis; Procedure: protein expression analysis; Procedure: proteomic profiling | |||||
| 4 | Recruiting | Rosiglitazone in Treating Patients With Pituitary Tumors | ||||
| Condition: | Brain and Central Nervous System Tumors | |||||
| Intervention: | Drug: rosiglitazone maleate | |||||
| 5 | Recruiting | An Investigation of Pituitary Tumors and Related Hypothalmic Disorders | ||||
| Conditions: | Abnormalities; Craniopharyngioma; Cushing's Syndrome; Endocrine Disease; Pituitary Neoplasm | |||||
| Intervention: | ||||||
| 6 | Recruiting | Study of Thyrotropin-Releasing Hormone in Normal Volunteers and in Patients With Thyroid or Pituitary Abnormalities | ||||
| Conditions: | Healthy; Pituitary Disease; Thyroid Disease | |||||
| Intervention: | Drug: TRH (Thyrotropin Releasing Hormone) | |||||
| 7 | Recruiting | Assessment of Cardiovascular Risk Markers in Growth Hormone Deficient Patients With Nonsecreting Pituitary Adenomas | ||||
| Conditions: | Growth Hormone Deficiency; Pituitary Tumor | |||||
| Intervention: | ||||||
| 8 | Recruiting | Effect of Diazoxide on the Obesity Secondary to Hypothalamic-Pituitary Lesions | ||||
| Conditions: | Hypothalamic-Pituitary Lesions; Craniopharyngiomas | |||||
| Intervention: | Drug: DIAZOXIDE | |||||
| 9 | Recruiting | Rosiglitazone in Treating Patients With Newly Diagnosed ACTH-Secreting Pituitary Tumor (Cushing's Disease) | ||||
| Condition: | Brain and Central Nervous System Tumors | |||||
| Interventions: | Drug: rosiglitazone maleate; Procedure: laboratory biomarker analysis | |||||
| 10 | Recruiting | Evaluation of Patients With Thyroid Disorders | ||||
| Conditions: | Hyperthyroidism; Hypothyroidism; Pituitary Neoplasm | |||||
| Intervention: | ||||||
| 11 | Recruiting | Effects of Growth Hormone Administration on Cardiovascular Risk in Cured Acromegalics With Growth Hormone Deficiency | ||||
| Conditions: | Acromegaly; Growth Hormone Deficiency; Pituitary Disease | |||||
| Interventions: | Drug: Somatropin; Drug: Placebo | |||||
| 12 | Recruiting | Pituitary Functions After Traumatic Brain Injury (TBI) and/or Subarachnoid Hemorrhage (SAH) | ||||
| Conditions: | Traumatic Brain Injury; Subarachnoid Hemorrhage; Hypopituitarism | |||||
| Intervention: | ||||||
| 13 | Recruiting | The Treatment and Natural History of Acromegaly | ||||
| Conditions: | Acromegaly; Pituitary Neoplasm | |||||
| Intervention: | ||||||
| 14 | Recruiting | Lanreotide as Primary Treatment for Acromegalic Patients With Pituitary Gland Macroadenoma | ||||
| Condition: | Acromegaly Associated With Pituitary Gland Macroadenoma | |||||
| Intervention: | Drug: Lanreotide autogel | |||||
| 15 | Recruiting | Does Topical Steroid Treatment Impair the Adrenal Function? | ||||
| Conditions: | Hypothalamus-Pituitary-Adrenal Axis Assessement; Topical Steroid Therapy in Chronic Skin Diseases | |||||
| Intervention: | ||||||
| 16 | Recruiting | Pituitary Derived-Intermedin is an Estrogen-Modulated Factor for Reducing Blood Pressure | ||||
| Conditions: | Menopause; Hypertension | |||||
| Intervention: | Behavioral: intermedin | |||||
| 17 | Recruiting | Genetics of Endocrine Tumours | ||||
| Condition: | Acromegaly | |||||
| Intervention: | ||||||
| 18 | Recruiting | Hypothalamus-Pituitary-Adrenal Axis and Use of Mifepristone for Psychotic Depression | ||||
| Condition: | Depression | |||||
| Interventions: | Drug: Mifepristone; Drug: Placebo | |||||
| 19 | Recruiting | Testosterone Gel Applied to Women With Pituitary Gland Problems | ||||
| Condition: | Panhypopituitarism | |||||
| Intervention: | Drug: Transdermal Testosterone gel | |||||
| 20 | Recruiting | Detection and Treatment of Endocrine Abnormalities in Childhood Cancer Survivors | ||||
| Conditions: | Hypopituitarism; Hypogonadism; Thyroid Dysfunction; Bone Diseases, Metabolic | |||||
| Intervention: | ||||||
| 21 | Recruiting | National Cooperative Growth Study (NCGS) of Optimal Nutropin AQ and Nutropin Dosing in Pubertal Growth Hormone-Deficient (GHD) Patients | ||||
| Condition: | Dwarfism, Pituitary | |||||
| Intervention: | ||||||
| 22 | Recruiting | Bone Mineral Density (BMD) in Adolescents With Growth Hormone Deficiency (GHD) | ||||
| Conditions: | Dwarfism, Pituitary; Turner Syndrome | |||||
| Intervention: | ||||||
| 23 | Recruiting | Inter-Assay Growth Hormone and IGF-I Variability | ||||
| Conditions: | Acromegaly; Growth Hormone Deficiency | |||||
| Intervention: | ||||||
| 24 | Recruiting | A Phase I Study in Asthma Patients Evaluating the Effect of Doses of FlutiForm™ on the Amount, if Any, of Cortisol Produced by the Adrenal Glands | ||||
| Condition: | Asthma | |||||
| Interventions: | Drug: FlutiForm 250/10 ug; Drug: FlutiForm 100/10 ug; Drug: Oral Prednisone 10mg; Drug: Placebo | |||||
| 25 | Recruiting | Study to Define Optimal IGF-1 Monitoring in Children Treated With NutropinAq | ||||
| Conditions: | Turner Syndrome; Renal Insufficiency, Chronic; Pituitary Diseases; Dwarfism | |||||
| Intervention: | Drug: Somatropin (rDNA origin) | |||||
| 26 | Recruiting | Endocrine and Psychological Evaluation of Adopted Children | ||||
| Condition: | Psychosocial Adjustment | |||||
| Intervention: | ||||||
| 27 | Recruiting | Evaluation and Treatment of Neurosurgical Disorders | ||||
| Condition: | Neurologic Disorders | |||||
| Intervention: | ||||||
| 28 | Recruiting | Screening Patients With Central Nervous System Tumors for Participation in National Cancer Institute Clinical Trials | ||||
| Conditions: | Brain and Central Nervous System Tumors; Lymphoma | |||||
| Interventions: | Procedure: cytology specimen collection procedure; Procedure: physiologic testing | |||||
| 29 | Recruiting | Effects of Corticotropin Releasing Hormone (CRH) on the Sleep in Patients With Hypopituitarism | ||||
| Condition: | Hypopituitarism | |||||
| Interventions: | Other: corticotropin releasing hormone (CRH); Other: Placebo | |||||
| 30 | Recruiting | Effect of Calcipotriol Plus Hydrocortisone Ointment on the Adrenal Hormone Balance and Calcium Metabolism in Patients With Psoriasis Vulgaris on the Face and Skin Folds | ||||
| Condition: | Psoriasis Vulgaris | |||||
| Intervention: | Drug: Calcipotriol plus hydrocortisone (LEO 80190) | |||||
| 31 | Recruiting | Testosterone-Driven Growth-Hormone (GH) Secretion in Aging Men | ||||
| Condition: | Aging | |||||
| Intervention: | Drug: anastrazole or dutasteride | |||||
| 32 | Recruiting | Endocrine Studies in Health and Disease | ||||
| Condition: | Endocrine Diseases | |||||
| Intervention: | ||||||
| 33 | Recruiting | New Imaging Techniques in the Evaluation of Patients With Ectopic Cushing Syndrome | ||||
| Condition: | Cushing Syndrome | |||||
| Intervention: | ||||||
| 34 | Recruiting | Hypothalamic-Pituitary-Adrenal (HPA) Axis in Psychotic Depression | ||||
| Conditions: | Psychotic Disorders; Depression; Depressive Disorder, Major | |||||
| Intervention: | Drug: Mifepristone | |||||
| 35 | Not yet recruiting | Cortisol Response to ACTH in Acute Stress | ||||
| Condition: | Aortic Aneurysm, Abdominal | |||||
| Intervention: | Drug: Adrenocorticotrophic hormone | |||||
| 36 | Recruiting | Antineoplaston Therapy in Treating Patients With Brain Tumors | ||||
| Condition: | Brain and Central Nervous System Tumors | |||||
| Interventions: | Drug: antineoplaston A10; Drug: antineoplaston AS2-1 | |||||
| 37 | Recruiting | Studying the Effects of 7 Days of Gonadotropin Releasing Hormone (GnRH) Treatment in Men With Hypogonadism | ||||
| Conditions: | Kallmann Syndrome; Idiopathic Hypogonadotropic Hypogonadism | |||||
| Intervention: | Drug: gonadotropin releasing hormone (GnRH) | |||||
| 38 | Recruiting | Decreased Testosterone Levels in Men Over 65 | ||||
| Conditions: | Aging; Hypogonadism; Andropause | |||||
| Interventions: | Drug: Anastrozole; Drug: Testosterone Gel | |||||
| 39 | Recruiting | Does Inhaled Busedonide or Fluticasone Impair Adrenal Function? | ||||
| Condition: | Adrenal Insufficency | |||||
| Intervention: | ||||||
| 40 | Recruiting | Does Intravitreal Injection of Triamcinolone Acetonide Impairs the Adrenal Function | ||||
| Condition: | Secondary Adrenal Insuffisency | |||||
| Intervention: | ||||||
| 41 | Recruiting | Efficacy of Octreotide Acetate and Cabergoline in Patients With Acromegaly | ||||
| Condition: | Acromegaly | |||||
| Intervention: | Drug: Octreotide acetate and cabergoline | |||||
| 42 | Recruiting | Steady-State Feedback Actions of Testosterone on Luteinizing Hormone Secretion in Young and Older Men | ||||
| Condition: | Hypogonadism | |||||
| Intervention: | Drug: Ketoconazole, Dexamethesone, Androgel,GnRH | |||||
| 43 | Recruiting | Cutivate Lotion HPA Axis Pediatric Study | ||||
| Condition: | Atopic Dermatitis | |||||
| Intervention: | Drug: Fluticasone propionate 0.05% lotion | |||||
| 44 | Recruiting | Defining the Genetic Basis for the Development of Primary Pigmented Nodular Adrenocortical Disease (PPNAD) and the Carney Complex | ||||
| Conditions: | Cushing's Syndrome; Hereditary Neoplastic Syndrome; Lentigo; Neoplasm; Testicular Neoplasm | |||||
| Intervention: | ||||||
| 45 | Not yet recruiting | Influence of Administration Route of Testosterone on Male Fertility | ||||
| Condition: | Hypogonadism | |||||
| Interventions: | Drug: MPP10, testosterone; Drug: Testosterone | |||||
| 46 | Recruiting | Pulsatile GnRH in Anovulatory Infertility | ||||
| Conditions: | Hypogonadotropic Hypogonadism; Amenorrhea; Kallman's Syndrome | |||||
| Interventions: | Drug: GnRH; Device: Mini-infusion pump | |||||
| 47 | Recruiting | Hydrocortisone in Patients of Out-of-Hospital Cardiac Arrest | ||||
| Condition: | Heart Arrest | |||||
| Intervention: | Drug: Hydrocortisone | |||||
| 48 | Recruiting | Effect of Race on Gonadotropin Responses | ||||
| Condition: | Premenopause | |||||
| Interventions: | Drug: Estradiol steroid infusion; Drug: Progesterone steroid infusion | |||||
| 49 | Not yet recruiting | Risperidone-Induced Hyperprolactinemia Treated With Bromocriptine | ||||
| Conditions: | Schizophrenia; Hyperprolactinemia | |||||
| Intervention: | Drug: Bromocriptin | |||||
| 50 | Recruiting | Consequence of Lifetime Isolated Growth Hormone Deficiency | ||||
| Condition: | Growth Hormone Deficiency | |||||
| Intervention: | Drug: growth hormone administration for 6 months | |||||
| | ||||||
| 51 | Not yet recruiting | Cardiac and Skeletal Muscle Energy Metabolism in Abnormal Growth Hormone States | ||||
| Conditions: | Acromegaly; Growth Hormone Deficiency | |||||
| Intervention: | ||||||
| 52 | Recruiting | Safety and Biological Activity of C2L-OCT-01 PR in Acromegalic Patients | ||||
| Condition: | Acromegaly | |||||
| Interventions: | Drug: C2L-OCT-01 PR, 10 or 20 mg; Drug: C2L-OCT-01 PR, 20 mg | |||||
| 53 | Recruiting | A Study of the Efficacy and Safety of CORLUX in the Treatment of Endogenous Cushing's Syndrome | ||||
| Condition: | Cushing's Syndrome | |||||
| Intervention: | Drug: mifepristone | |||||
| 54 | Recruiting | Physiopathology of Sodium Retention in Acromegaly | ||||
| Condition: | Acromegaly | |||||
| Intervention: | Drug: furosemide | |||||
| 55 | Recruiting | Investigation of the Genetic Causes of Kallmann Syndrome and Reproductive Disorders | ||||
| Conditions: | Hypogonadism; Kallmann Syndrome; Puberty, Delayed; Puberty, Precocious; Hypothalamic Amenorrhea; Anosmia | |||||
| Intervention: | ||||||
| 56 | Recruiting | Characterizing Psychological Consequences of Childhood Trauma | ||||
| Condition: | Major Depressive Disorder | |||||
| Interventions: | Drug: DEX-CRF stimulation test; Behavioral: Psychosocial stress induction; Procedure: Brain imaging of sad mood , self-reference, reward; Behavioral: Acoustic startle | |||||
| 57 | Recruiting | Insulin Sensitivity and Substrate Metabolism in Patients With Cushing's Syndrome | ||||
| Conditions: | Cushing's Syndrome; Insulin Resistance | |||||
| Intervention: | Procedure: Surgery | |||||
| 58 | Recruiting | Exercise Amenorrhea Stress and Bone Health in Adolescents | ||||
| Condition: | Healthy | |||||
| Intervention: | ||||||
| 59 | Recruiting | Dexamethasone Treatment of Congenital Adrenal Hyperplasia | ||||
| Condition: | Adrenal Hyperplasia, Congenital | |||||
| Intervention: | Drug: dexamethasone | |||||
| 60 | Recruiting | Leuprolide in Determining the Cause of Gonadotropin Deficiency | ||||
| Condition: | Hypogonadism | |||||
| Interventions: | Drug: gonadotropin releasing hormone; Drug: leuprolide | |||||
| 61 | Not yet recruiting | Neuroendocrine Dysfunction in Traumatic Brain Injury: Correlation With Cognitive Dysfunction and Repair | ||||
| Condition: | Traumatic Brain Injury | |||||
| Intervention: | ||||||
| 62 | Recruiting | Study of Depression, Peptides, and Steroids in Cushing's Syndrome | ||||
| Condition: | Cushing's Syndrome | |||||
| Intervention: | ||||||
| 63 | Recruiting | Study of Recombinant Human Insulin-Like Growth Factor I in Patients With Severe Insulin Resistance | ||||
| Conditions: | Insulin Resistance; Hyperglycemia | |||||
| Intervention: | Drug: insulin-like growth factor I | |||||
| 64 | Recruiting | Safety and Efficacy of Different Dose Levels of Pasireotide in Patients With de Novo, Persistent or Recurrent Cushing's Disease | ||||
| Condition: | Cushing's Disease | |||||
| Intervention: | Drug: Pasireotide | |||||
| 65 | Recruiting | Cardiovascular Risk Factors and LCH in Adults | ||||
| Condition: | Histiocytosis, Langerhans-Cell | |||||
| Intervention: | ||||||
| 66 | Recruiting | Polycystic Ovary Syndrome (PCOS) and Sleep Apnea | ||||
| Conditions: | Polycystic Ovary Syndrome; Obstructive Sleep Apnea | |||||
| Interventions: | Device: continuous positive airway pressure (CPAP); Drug: depot leuprolide plus estrogen/progestin replacement; Drug: pioglitazone | |||||
| 67 | Recruiting | Involvement of Endogenous Digitalis-Like Compounds in Breast Cancer | ||||
| Conditions: | Breast Neoplasms; Fibrocystic Disease of Breast; Mammaplasty | |||||
| Intervention: | ||||||
| 68 | Recruiting | Study of GnRH (Gonadotropin Releasing Hormone) Treatment for Idiopathic Hypogonadotropic Hypogonadism (IHH) | ||||
| Condition: | Hypogonadism | |||||
| Intervention: | Drug: Gonadotropin Releasing Hormone (GnRH) | |||||
| 69 | Recruiting | Effects of Testosterone in Women With Depression | ||||
| Condition: | Depression | |||||
| Intervention: | Drug: Testosterone | |||||
| 70 | Recruiting | RU-486 in the Treatment of Bipolar Depression | ||||
| Condition: | Bipolar Depression | |||||
| Intervention: | Drug: mifepristone (RU-486) | |||||
| 71 | Recruiting | Prazosin to Reduce Stress-Induced Cocaine/Alcohol Craving and Relapse | ||||
| Conditions: | Cocaine Dependence; Alcohol Dependence | |||||
| Interventions: | Drug: Prazosin; Drug: placebo | |||||
| 72 | Recruiting | Obesity and Weight Loss on Reproductive Function | ||||
| Condition: | Obesity | |||||
| Intervention: | ||||||
| 73 | Recruiting | Baselines in Reproductive Disorders | ||||
| Conditions: | Amenorrhea; Hypogonadotropic Hypogonadism; Kallmann's Syndrome | |||||
| Intervention: | Procedure: Frequent baseline blood sampling | |||||
| 74 | Recruiting | rhGH and rhIGF-1 Combination Therapy in Children With Short Stature Associated With IGF-1 Deficiency | ||||
| Condition: | Insulin-Like Growth Factor-1 Deficiency | |||||
| Interventions: | Drug: somatropin; Drug: mecasermin and somatropin; Drug: mecasermin and somatropin; Drug: mecasermin and somatropin | |||||
| 75 | Recruiting | Adrenal Function in Critical Illness | ||||
| Condition: | Adrenal Insufficiency | |||||
| Intervention: | ||||||
| 76 | Recruiting | Feasibility Study Into the Contraceptive Effect of Estetrol | ||||
| Condition: | Healthy | |||||
| Interventions: | Drug: estetrol; Drug: estetrol; Drug: estetrol and desogestrel; Drug: estetrol and progesterone | |||||
| 77 | Recruiting | Ethylvinyl Acetate (EVA) Vaginal Ring Delivery System Study | ||||
| Condition: | Healthy | |||||
| Intervention: | Drug: Ethylvinyl Acetate (EVA) Vaginal Ring Delivery System | |||||
| 78 | Recruiting | Guanfacine to Reduce Stress-Induced Cocaine/Alcohol Craving and Relapse | ||||
| Conditions: | Cocaine Dependent; Alcohol Dependent | |||||
| Interventions: | Drug: Guanfacine; Drug: Placebo | |||||
| 79 | Recruiting | Pelvic Pain in Women With Endometriosis | ||||
| Conditions: | Endometriosis; Pelvic Pain; Healthy; Tubal Ligation | |||||
| Intervention: | ||||||
| 80 | Not yet recruiting | FHA: Metabolism and Stress Reactivity | ||||
| Conditions: | Anovulation; FHA; Eumenorrhea | |||||
| Intervention: | ||||||
| 81 | Recruiting | The Effect of Ethanol on Overnight Glucose Regulation in Type 2 | ||||
| Condition: | Type 2 Diabetes, Insulin Requiring | |||||
| Interventions: | Other: oral ethanol, overnight; Other: IV ethanol; Other: soda water; Other: soda water | |||||
| 82 | Recruiting | Prospective, Open-Label, Multicenter, International Study of Mifepristone for Symptomatic Treatment of Cushing's Syndrome Caused by Ectopic Adrenal Corticotrophin Hormone (ACTH) Secretion | ||||
| Condition: | Cushing's Syndrome | |||||
| Intervention: | Drug: Mifepristone | |||||
| 83 | Recruiting | Dexamethasone to Prevent Oral Chronic Graft-Versus-Host Disease | ||||
| Condition: | Graft vs Host Disease | |||||
| Intervention: | Drug: Dexamethasone 0.01% Solution | |||||
| 84 | Recruiting | Effect of Lithium Carbonate on Low-Dose Radioiodine Therapy in Early Thyroid Cancer | ||||
| Conditions: | Thyroid Cancer; Differentiated Thyroid Carcinoma | |||||
| Intervention: | Drug: Lithium Carbonate | |||||
| 85 | Recruiting | Sex Differences in Progesterone Effects on Responses to Stress and Drug Cues | ||||
| Condition: | Cocaine Dependence | |||||
| Interventions: | Drug: Progesterone; Drug: Placebo | |||||
| 86 | Recruiting | Measurement of Outcome of Surgical Treatment in Patients With Acromegaly | ||||
| Condition: | Acromegaly | |||||
| Intervention: | ||||||
| 87 | Recruiting | Glucose Tolerance in Acromegaly: The Influence of GH-Excess on Glucose Metabolism and Insulin Resistance | ||||
| Conditions: | Acromegaly; Diabetes; Insulin Resistance; Impaired Glucose Tolerance | |||||
| Intervention: | ||||||
| 88 | Recruiting | Baseline Sexual Function, Cognitive Function, Body Composition and Muscle Parameters and Pharmacokinetics of Transdermal Testosterone Gel in Women With Hypopituitarism | ||||
| Condition: | Panhypopituitarism | |||||
| Intervention: | Drug: Transdermal Testosterone Gel | |||||
| 89 | Recruiting | Estrogen Treatment in Acromegalic Women | ||||
| Condition: | Acromegaly | |||||
| Intervention: | Drug: Alesse | |||||
| 90 | Recruiting | Endocrine Dysfunction and Growth Hormone Deficiency in Children With Optic Nerve Hypoplasia | ||||
| Conditions: | Growth Hormone Deficiency; Septo-Optic Dysplasia; Hypopituitarism | |||||
| Intervention: | Drug: Nutropin AQ | |||||
| 91 | Recruiting | Predictive Factors of Response to Somatostatin Analogues in Acromegalic Patients With Persistent Disease Following Surgery | ||||
| Condition: | Acromegaly | |||||
| Intervention: | ||||||
| 92 | Recruiting | Androgen Replacement Therapy in Women With Hypopituitarism | ||||
| Condition: | Hypopituitarism | |||||
| Intervention: | Drug: TheraDerm | |||||
| 93 | Recruiting | Substrate Metabolism and Insulin Sensitivity in Patients With Hyperprolactinemia Before and After Treatment | ||||
| Conditions: | Hyperprolactinemia; Insulin Resistance | |||||
| Intervention: | Drug: Cabergoline | |||||
| 94 | Not yet recruiting | Use of Somatostatin Analogue Therapy as Primary Medical Treatment of Acromegaly | ||||
| Condition: | Acromegaly | |||||
| Intervention: | Drug: Somatuline Autogel | |||||
| 95 | Recruiting | Pharmacologic Treatment of Congenital Nephrogenic Diabetes Insipidus | ||||
| Condition: | Nephrogenic Diabetes Insipidus | |||||
| Interventions: | Drug: sildenafil; Drug: calcitonin; Drug: hydrochlorothiazide/amiloride; Drug: indomethacin; Drug: Placebo for sildenafil; Drug: placebo for calcitonin | |||||
| 96 | Recruiting | Somatuline® Depot (Lanreotide) for Acromegaly Post-Marketing Observational Study | ||||
| Condition: | Acromegaly | |||||
| Intervention: | ||||||
| 97 | Recruiting | Endometriosis Patients Undergoing Quinagolide Treatment | ||||
| Conditions: | Hyperprolactinemia; Endometriosis | |||||
| Intervention: | Procedure: ENDOMETRIAL BIOPSY | |||||
| 98 | Recruiting | Changes of Left Ventricular Mass and Cardiac Function in Patients With Active Acromegaly During Treatment With the Growth Hormone Receptor Antagonist Pegvisomant | ||||
| Conditions: | Acromegaly; Heart Failure; Hypertrophy, Left Ventricular | |||||
| Intervention: | Drug: pegvisomant | |||||
| 99 | Not yet recruiting | Reversal of Antipsychotic-Induced Hyperprolactinemia, Weight Gain, Hyperglycemia and Dyslipidemia | ||||
| Conditions: | Hyperprolactinemia; Weight Gain; Dyslipidemia | |||||
| Intervention: | Drug: Abilify (aripiprazole) | |||||
| 100 | Not yet recruiting | Open Label Study to Assess the Efficacy of an Extended Injection Interval Schedule of Lanreotide Autogel 120 mg in Acromegalic Subjects Who Are Biochemically Controlled on Long Term Treatment With Octreotide LAR 10 or 20 mg | ||||
| Condition: | Acromegaly | |||||
| Intervention: | Drug: Lanreotide Autogel 120 mg | |||||
| | ||||||
| 101 | Recruiting | Open Label Extension Study Evaluating Safety and Biological Activity of C2L-OCT-01 PR in Acromegalic Patients | ||||
| Condition: | Acromegaly | |||||
| Intervention: | Drug: C2L-OCT-01 PR 30 mg | |||||
| 102 | Recruiting | Ultrasound Guided Sandostatin LAR Injection in Acromegaly | ||||
| Condition: | Acromegaly | |||||
| Interventions: | Drug: Sandostatin LAR; Drug: Sandostatin LAR | |||||
| 103 | Recruiting | Substrate Metabolism and Insulin Sensitivity in Acromegalic Patients Before and After Treatment | ||||
| Conditions: | Acromegaly; Growth Hormone; Insulin Resistance | |||||
| Intervention: | Procedure: Transsphenoidal adenomectomy | |||||
| 104 | Recruiting | Co-Treatment With Pegvisomant and a Somatostatin Analogue (SA) in SA-Responsive Acromegalic Patients | ||||
| Conditions: | Acromegaly; Insulin Resistance; Impaired Glucose Tolerance | |||||
| Interventions: | Drug: Pegvisomant; Drug: Somatostatin analog (Lanreotid or Octreotid) | |||||
| 105 | Recruiting | Testosterone and Growth Hormone for Bone Loss in Men | ||||
| Conditions: | Hypopituitarism; Hypogonadism; Growth Hormone Deficiency | |||||
| Interventions: | Drug: Testosterone plus somatropin; Drug: testosterone | |||||
| 106 | Recruiting | Safety and Efficacy of Pasireotide Long Acting Release (LAR) vs. Octreotide LAR in Patients With Active Acromegaly | ||||
| Condition: | Acromegaly | |||||
| Intervention: | Drug: Pasireotide | |||||