Fibrous Dysplasia, Polyostotic
Reagent Kits, Diagnostic
Reproducibility of Results
Sensitivity and Specificity
Enzyme-Linked Immunosorbent Assay
Stress-level cortisol treatment impairs inhibitory control of behavior in monkeys. (1/78)Most studies of cortisol-induced cognitive impairments have focused on hippocampal-dependent memory. This study investigates a different aspect of cognition in a randomized placebo-controlled experiment with monkeys that were treated with cortisol according to a protocol that simulates a prolonged stress response. Young adult and older adult monkeys were assigned randomly to placebo or chronic treatment with cortisol in a 2 x 2 factorial design (n = 8 monkeys per condition). Inhibitory control of behavior was assessed with a test shown previously in primates to reflect prefrontal cortical dysfunction. Failure to inhibit a specific goal-directed response was evident more often in older adults. Treatment with cortisol increased this propensity in both older and young adult monkeys. Age-related differences in response inhibition were consistent across blocks of repeated test trials, but the treatment effects were clearly expressed only after prolonged exposure to cortisol. Aspects of performance that did not require inhibition were not altered by age or treatment with cortisol, which concurs with effects on response inhibition rather than nonspecific changes in behavior. These findings lend support to related reports that cortisol-induced disruptions in prefrontal dopamine neurotransmission may contribute to deficits in response inhibition and play a role in cognitive impairments associated with endogenous hypercortisolism in humans. (+info)
Glucocorticoid and mineralocorticoid resistance/hypersensitivity syndromes. (2/78)Glucocorticoids and mineralocorticoids regulate diverse functions important to maintain central nervous system, cardiovascular, metabolic, and immune homeostasis. The actions of these hormones are mediated by their specific intracellular receptors: the glucocorticoid (GR) and mineralocorticoid (MR) receptors. Pathologic conditions associated with changes of tissue sensitivity to these hormones have been described. The syndrome of familial glucocorticoid resistance is characterized by hypercortisolism without Cushing's syndrome stigmata. The molecular defects of four kindreds and one sporadic case have been elucidated as inactivating mutations in the ligand-binding domain of GR. Two cases developed glucocorticoid resistance at the heterozygous state. In these patients, mutant receptors possessed transdominant negative activity upon the wild type receptor. Insensitivity to mineralocorticoids (which may also be caused by loss of function mutations of the MR gene) was found in one sporadic case and four autosomal dominant cases of Pseudohypoaldosteronism type 1. These included two frameshift mutations and a premature termination codon in exon 2, leading to gene products lacking the entire DNA- and ligand-binding domains, and a single base-pair deletion in the intron-5 splice donor site. Tissue hypersensitivity to glucocorticoids was recently hypothesized in patients with Human Immunodeficiency Virus (HIV) type-1 infection via the accessory proteins Vpr and Tat which enhance GR transactivation. Since HIV-1 long terminal repeat (LTR) and glucocorticoid-responsive promoters use the same set of coactivators, these proteins may stimulate HIV-1-LTR and glucocorticoid-inducible genes concurrently. The former may directly stimulate viral proliferation, while the latter may indirectly enhance viral propagation by suppressing the host immune system through glucocorticoid-mediated mechanisms. (+info)
Uptake ratio of (19-1311) cholesterol by adrenal glands as observed by a scintigraphic method. (3/78)The adrenal scintigram was performed after administration of [19-131I] cholesterol. A high/low ratio of both adrenal glands was calculated to evaluate whether there is a difference between the left and right sides in adrenal diseases. During scanning, information was stored in a 64 X 64 matrix and then punched out on a computer compatible paper tape. This paper tape was processed with a small digital computer. The areas of interest were selected over adrenal glands. The computer decided mean counts per unit area. After subtraction of background counts, a high/low ratio of adrenal gland was calculated. In five patients with Cushing's syndrome due to bilateral hyperplasia, a high/low ratio ranged from 1.0 to 2.0. In four patients with primary aldosteronism due to adenoma, a high/low ratio ranged from 1.33 to 4.0. This method may be useful to differentiate bilateral hyperplasia from unilateral adrenocortical adenoma. (+info)
From open to laparoscopic adrenalectomy: a review of 16-year experience. (4/78)OBJECTIVE: To review the experience with adrenal surgery which was associated with significant morbidity and notable mortality in the past, although laparoscopic approach is beginning to be accepted as the procedure of choice. METHODS: The indications and results of adrenalectomy in 104 patients (36 men, 68 women) over the past 16 years were reviewed. Any potential improvement of surgical results over time was analyzed. RESULTS: Ninety-three patients (89%) had functional problems while malignancy was present in 11 patients (11%). Anterior approach was employed in 27 patients, posterior in 56, lateral in 10, and laparoscopic in 11. One patient required conversion from laparoscopic to anterior approach. No operative mortality was seen, but the morbidity occurred in 16.7%. Complication rate decreased significantly in this study period (1981-1990 versus 1991-1996, 22% versus 5%; P = 0.02). Laparoscopic adrenalectomy was successfully performed for 59% of the patients requiring adrenalectomy recently, compared to 68% of posterior adrenalectomy in the past. CONCLUSIONS: Adrenal surgery is a safe procedure, associated with acceptable morbidity, which has decreased over time. Laparoscopic adrenalectomy is becoming the preferred approach for the majority of patients requiring adrenalectomy. (+info)
Parathyroid hormone secretion in chronic human endogenous hypercortisolism. (5/78)Osteoporosis is a common manifestation of Cushing's syndrome, but the mechanisms responsible for this abnormality have not been defined. With the objective of analyzing parathyroid hormone (PTH) secretion in chronic hypercortisolism (CH), we evaluated 11 healthy subjects and 8 patients with CH, 6 with Cushing's disease and 2 with adrenal adenoma. These volunteers were submitted to tests of PTH stimulation through hypocalcemia (EDTA), PTH suppression through hypercalcemia (iv and oral calcium), and evaluation of bone mineral density (BMD) by DEXA. During the test of PTH stimulation, the calcium and magnesium concentrations of the normal and CH groups were similar. Patients with CH showed an increased PTH response to the hypocalcemic stimulus compared to controls. PTH values were significantly higher in the CH group at 70 (17.5 +/- 3.5 vs 10.2 +/- 1.3 pmol/l, P = 0.04), and 120 min (26.1 +/- 5.9 vs 11.3 +/- 1.9 pmol/l, P = 0.008) of EDTA infusion. The area under the curve for PTH during EDTA infusion was also significantly higher in patients with CH than in normal subjects (1867 +/- 453 and 805 +/- 148 pmol l(-1) 2 h(-1), P = 0.02). During the test of PTH suppression, calcium, magnesium and PTH levels of the patients with hypercortisolism and controls were similar. BMD was decreased in patients with hypercortisolism in the spine (0.977 +/- 0.052 vs 1.205 +/- 0.038 g/cm2 in controls, P<0.01). In conclusion, our results show that subjects with CH present decreased bone mass mainly in trabecular bone. The use of dynamic tests permitted the detection of increased PTH secretion in response to a hypocalcemic stimulus in CH patients that may probably be involved in the occurrence of osteoporosis in this state. (+info)
Arterial lesions in repeatedly bred spontaneously hypertensive rats. (6/78)Repeatedly bred male and female rats of many strains develop hyperglycemia, hyperlipidemia, hypertension, and arteriosclerosis spontaneously. The intensity of their arterial disease and related metabolic derangements appear to be related to their reproductive activity. Repeatedly bred spontaneously hypertensive rats (SHR) were found to have severe hypertension, hyperglycemia, hyperlipidemia, elevated creatine phosphokinase (CPK), serum glutamic oxaloacetic and glutamic pyruvic transaminase (SGOT, SGPT), and lactic dehydrogenase (LDH), as well as high circulating corticosterone levels. Despite these atherogenic metabolic derangements and their severe hypertension, the breeder SHR did not develop the severe, generalized arteriosclerosis found in other strains of breeder rats. Instead, the arterial lesions, consisting of intimal hyalinization and fibrosis, medial hypertrophy, and occlusion of the lumen, were found only in male breeder SHR and were confined to the intratubular arteries of the testes. It is suggested that the severe hypertension, genetic influences, or differences in hypothalamic-pituitary-adrenal-gonadal function in breeder SHR may not have been conducive to the development of arteriosclerosis in this particular strain of rats. (+info)
Osteoporosis is more prevalent in adrenal than in pituitary Cushing's syndrome. (7/78)Osteoporosis is the most common complication of Cushing's syndrome. We retrospectively examined the prevalence and risk factors for osteoporosis in 42 female patients with Cushing's syndrome. Osteoporosis and atraumatic fractures were assessed by bone mineral density of the lumbar vertebral spine (L2-L4) using dual energy X-ray absorptiometry (DXA) and X-ray examination. The prevalence of osteoporosis and fracture were 54.8% and 21.4%, respectively. The prevalence of osteoporosis (69.6% vs. 37.8%) and atraumatic bone fracture (26.1% vs. 15.8%) were significantly higher in patients with adrenal Cushing's than in those with pituitary Cushing's. AP and lateral BMD was significantly higher in patients with pituitary origin than in those with adrenal origin. Among several variables examined by multiple logistic regression, the etiology of Cushing's syndrome (adrenal vs. pituitary origin) was a significant factor affecting the prevalence of osteoporosis. Neither age, body mass index, duration of amenorrhea, nor extent of hypercortisolism were significant factors in this analysis. Plasma DHEA-S and urinary 17-KS excretion were significantly higher in pituitary Cushing's than in adrenal Cushing's. The present study shows that the prevalence of osteoporosis in patients with Cushing's syndrome is influenced by its etiology. A factor associated with pituitary Cushing's syndrome, such as adrenal androgen, may protect these patients from glucocorticoid-induced osteoporosis. (+info)
CARCINOMA OF LUNG WITH ADRENAL HYPERFUNCTION AND HYPERCALCEMIA TREATED BY PARATHYROIDECTOMY. (8/78)A case of severe hypercalcemia secondary to carcinoma of the lung is described in which hypokalemic alkalosis, renal failure and pancreatitis were also present. The relative importance of the few bone metastases found at autopsy is considered, and a probable endocrine-like effect of the tumour in the development of the hypercalcemia is postulated. Treatment of the hypercalcemia included administration of corticosteroids and disodium EDTA, peritoneal dialysis and subtotal parathyroidectomy; the most effective of these was peritoneal dialysis. Subtotal parathyroidectomy failed to produce a further decrease in serum calcium values. The occurrence of hypokalemic alkalosis in the presence of increased adrenocortical function and its relationship to the carcinoma of the lung are discussed. The possibility that this neoplasm produced two factors which caused systemic effects ordinarily associated with the function of endocrine glands must be considered. (+info)
Adrenocortical hyperfunction can be caused by a variety of factors, including:
1. Cushing's syndrome: This is a rare hormonal disorder caused by excessive production of cortisol by the adrenal glands. It can be caused by a benign tumor in the pituitary gland or an adrenal gland, or by taking too much corticosteroid medication.
2. Adrenocortical carcinoma: This is a rare and aggressive type of cancer that affects the adrenal glands. It can cause excessive production of cortisol and other hormones.
3. Familial Cushing's syndrome: This is a genetic disorder that causes excessive production of cortisol by the adrenal glands.
4. Glucocorticoid-remediable aldosteronism (GRA): This is a rare genetic disorder that affects the production of hormones by the adrenal glands, leading to excessive production of cortisol and aldosterone.
5. Licorice ingestion: Consuming large amounts of licorice can cause an increase in the production of cortisol and other hormones by the adrenal glands.
6. Primary aldosteronism (PA): This is a group of rare genetic disorders that affect the production of hormones by the adrenal glands, leading to excessive production of aldosterone and cortisol.
7. Secondary adrenocortical hyperfunction: This can occur due to various conditions such as thyroid disorders, pituitary tumors, or other endocrine disorders that affect the regulation of hormone production by the adrenal glands.
Symptoms of adrenocortical hyperfunction may include:
1. Weight gain and central obesity
2. Increased appetite and food cravings
3. Fatigue and weakness
4. Mood changes, such as anxiety or depression
5. Insomnia and sleep disturbances
6. High blood pressure and cardiovascular risk factors
7. Easy bruising and poor wound healing
8. Muscle weakness and fatigue
9. Thinning of the skin and bones (osteoporosis)
10. Increased risk of infections and decreased immune function.
If you suspect that you or someone you know may have adrenocortical hyperfunction, it is essential to consult with a healthcare professional for proper diagnosis and treatment. A doctor may perform several tests, including:
1. Blood tests to measure hormone levels in the body, such as cortisol and aldosterone.
2. Saliva tests to measure cortisol levels throughout the day.
3. Urine tests to measure cortisol levels over a 24-hour period.
4. Imaging tests, such as CT scans or MRI scans, to examine the adrenal glands and look for any signs of tumors or other abnormalities.
5. Other tests to assess the body's response to stress, such as a corticotropin (ACTH) stimulation test.
Treatment options for adrenocortical hyperfunction depend on the underlying cause of the condition and may include:
1. Medications to reduce hormone production in the adrenal glands, such as metyrapone or ketoconazole.
2. Surgery to remove any tumors or cysts in the adrenal glands.
3. Radiation therapy to shrink tumors and reduce hormone production.
4. Lifestyle changes, such as weight loss, stress management techniques, and regular exercise.
5. Monitoring of hormone levels and other health markers to ensure that the condition is under control.
Adrenocortical carcinoma can be subdivided into three main types based on their histological features:
1. Typical adrenocortical carcinoma: This is the most common type and accounts for about 70% of all cases. It is characterized by a large, irregular tumor that grows in the cortex of the adrenal gland.
2. Adenomatous adrenocortical carcinoma: This type is less aggressive than typical adrenocortical carcinoma and accounts for about 20% of cases. It is characterized by a small, well-circumscribed tumor that grows in the cortex of the adrenal gland.
3. Adrenocortical sarcoma: This is the least common type and accounts for about 10% of cases. It is characterized by a rare, malignant tumor that grows in the cortex of the adrenal gland.
Adrenocortical carcinoma can cause a variety of symptoms, including abdominal pain, weight loss, fatigue, and skin changes. The diagnosis is typically made through a combination of imaging studies, such as CT scans and MRI, and tissue biopsy. Treatment options include surgery, chemotherapy, and radiation therapy, and the prognosis depends on the stage and aggressiveness of the tumor.
Overall, adrenocortical carcinoma is a rare and aggressive cancer that requires prompt diagnosis and treatment to improve patient outcomes.
Types of Adrenal Cortex Neoplasms:
1. Adrenocortical carcinoma (ACC): A rare and aggressive malignant tumor that originates in the adrenal cortex. It is often associated with virilization (excessive masculinization) in women.
2. Adrenocortical adenoma (ACA): A benign tumor that originates in the adrenal cortex. It is less common than ACC and may not cause any symptoms.
3. Pheochromocytoma: A rare tumor that originates in the adrenal medulla, which is the inner part of the adrenal gland. It can secrete excessive amounts of hormones that regulate blood pressure and heart rate.
4. Paraganglioma: A rare tumor that originates in the paraganglia, which are clusters of cells located near the adrenal glands. These tumors can produce excessive amounts of hormones and cause similar symptoms as pheochromocytoma.
Symptoms of Adrenal Cortex Neoplasms:
1. Virilization (excessive masculinization) in women, such as deepening of the voice, excessive body hair growth, and clitoral enlargement.
2. Headache, fatigue, and weight gain due to excessive production of steroid hormones.
3. High blood pressure and heart rate due to excessive production of catecholamines (hormones that regulate blood pressure and heart rate).
4. Abdominal pain, nausea, and vomiting due to the tumor's size and location.
Diagnosis of Adrenal Cortex Neoplasms:
1. Imaging tests such as CT scans or MRI to visualize the tumor and determine its size and location.
2. Laboratory tests to measure hormone levels in the blood, including cortisol, aldosterone, and catecholamines.
3. Biopsy to obtain a tissue sample for further examination under a microscope.
Treatment of Adrenal Cortex Neoplasms:
1. Surgery to remove the tumor, which is usually curative.
2. Medications to control symptoms such as high blood pressure and hormone levels.
3. Radiation therapy may be used in cases where surgery is not feasible or if there is a risk of recurrence.
Prognosis of Adrenal Cortex Neoplasms:
The prognosis for adrenal cortex neoplasms depends on the type and size of the tumor, as well as the extent of hormone production. In general, the prognosis is good for patients with benign tumors that are removed surgically. However, malignant tumors can have a poorer prognosis and may require additional treatments such as radiation therapy or chemotherapy.
Prevention of Adrenal Cortex Neoplasms:
There is no known prevention for adrenal cortex neoplasms, but early detection and treatment can improve outcomes. Regular monitoring of hormone levels and imaging tests can help detect tumors at an early stage.
1. Reduce stress: High levels of cortisol can be caused by stress, so finding ways to manage stress can help prevent adrenal cortex neoplasms.
2. Maintain a healthy diet: Eating a balanced diet that includes plenty of fruits, vegetables, and whole grains can help support overall health and well-being.
3. Exercise regularly: Regular physical activity can help reduce stress and improve overall health.
4. Get enough sleep: Aim for 7-8 hours of sleep per night to help regulate hormone levels.
5. Limit caffeine and alcohol: Both substances can disrupt hormone levels and contribute to the development of adrenal cortex neoplasms.
Dysphonia can manifest in different ways, including:
1. Hoarseness: A raspy, strained, or rough quality to the voice.
2. Breathy voice: A weak, airy, or faint voice.
3. Harsh voice: A loud, screeching, or grating voice.
4. Rough voice: A scratchy, raw, or bumpy voice.
5. Stuttering: Repetition or prolongation of sounds, syllables, or words.
6. Slurred speech: Difficulty articulating words or speaking clearly.
7. Monotone speech: Speaking in a flat, emotionless tone.
Dysphonia can be acute or chronic, and it can affect individuals of all ages and backgrounds. In some cases, dysphonia may be a symptom of an underlying medical condition, such as a viral infection, allergies, or a neurological disorder. In other cases, it may be caused by overuse or misuse of the voice, such as shouting, singing, or speaking loudly for extended periods.
Treatment options for dysphonia depend on the underlying cause and severity of the condition. Some common treatments include:
1. Voice therapy: Techniques to improve breath support, vocal technique, and speech clarity.
2. Medications: To reduce inflammation, allergies, or other underlying conditions that may be contributing to dysphonia.
3. Surgery: In some cases, surgery may be necessary to correct structural problems in the vocal cords or other areas of the voice box.
4. Laryngeal electromyography (LEMG): A test used to evaluate the function of the vocal cords and surrounding muscles.
5. Speech therapy: To improve communication skills and address any language or cognitive impairments that may be contributing to dysphonia.
6. Botulinum toxin injections (Botox): Injected into the vocal cords to reduce spasms and improve voice quality.
7. Vocal cord paralysis: In some cases, injection of a local anesthetic or botulinum toxin may be used to paralyze one or both vocal cords, allowing for rest and healing.
It's important to seek medical attention if you experience any persistent or severe changes in your voice, as early diagnosis and treatment can improve outcomes and reduce the risk of long-term vocal cord damage. A healthcare professional will be able to assess your symptoms and recommend appropriate treatment options based on the underlying cause of your dysphonia.
Some common types of voice disorders include:
1. Dysphonia: A term used to describe difficulty speaking or producing voice sounds.
2. Aphonia: A complete loss of voice.
3. Spasmodic dysphonia: A neurological disorder characterized by involuntary movements of the vocal cords, causing a strained or breaking voice.
4. Vocal fold paralysis: A condition in which the muscles controlling the vocal cords are weakened or paralyzed, leading to a hoarse or breathy voice.
5. Vocal cord lesions: Growths, ulcers, or other injuries on the vocal cords that can affect voice quality and volume.
6. Laryngitis: Inflammation of the voice box (larynx) that can cause hoarseness and loss of voice.
7. Chronic laryngitis: A persistent form of laryngitis that can last for months or even years.
8. Acid reflux laryngitis: Gastroesophageal reflux disease (GERD) that causes stomach acid to flow up into the throat, irritating the vocal cords and causing hoarseness.
9. Vocal fold nodules: Growths on the vocal cords that can cause hoarseness and other voice changes.
10. Vocal cord polyps: Growths on the vocal cords that can cause hoarseness and other voice changes.
Voice disorders can significantly impact an individual's quality of life, as they may experience difficulty communicating effectively, loss of confidence, and emotional distress. Treatment options for voice disorders depend on the underlying cause and may include voice therapy, medications, surgery, or a combination of these approaches.
Adrenocortical adenomas are typically slow-growing and may not cause any symptoms in the early stages. However, as they grow, they can begin to produce excessive amounts of hormones such as cortisol and aldosterone, which can lead to a variety of symptoms including:
* Weight gain and central obesity
* Buffalo hump (a fat deposit on the back of the neck)
* Moon face (a rounded, full face)
* Stretch marks and thin skin
* Easy bruising and poor wound healing
* Fatigue, weakness, and decreased muscle mass
* Increased blood pressure and salt craving
* Decreased potassium levels
If the adenoma becomes large enough, it can also cause compression of nearby structures such as the surrounding blood vessels and nerves, leading to additional symptoms such as:
* Pain in the abdomen or flank
* Nausea and vomiting
* Feeling of fullness after eating only a small amount
* Fever and chills
If left untreated, adrenocortical adenomas can continue to grow and potentially lead to complications such as:
* Adrenal crisis (a life-threatening condition caused by the sudden release of large amounts of hormones into the bloodstream)
* Heart problems, such as hypertension and cardiac arrhythmias
* Kidney damage and failure
* Osteoporosis and bone fractures
The exact cause of adrenocortical adenomas is not known, but they are believed to be related to genetic mutations that occur during fetal development. They can also be associated with certain medical conditions such as familial adenomatous polyposis (FAP) and Li-Fraumeni syndrome.
The diagnosis of an adrenocortical adenoma is based on a combination of imaging studies, such as CT scans or MRI, and laboratory tests to assess hormone levels in the blood and urine. The imaging studies can help identify the size and location of the adenoma, while the laboratory tests can help confirm the presence of excess hormones in the body.
Treatment options for adrenocortical adenomas include:
* Surgery to remove the adenoma: This is the primary treatment for most adrenocortical adenomas. The surgery may be performed through a laparoscope (a thin tube with a camera and light on the end) or through an open incision in the abdomen.
* Radiation therapy: This may be used in cases where the adenoma cannot be removed completely by surgery or if it has spread to other parts of the body.
* Hormone therapy: Medications such as metyrapone or ketoconazole can be used to reduce hormone production by the adrenal gland.
It is important to note that not all adrenocortical adenomas are cancerous, and some may not require treatment. Your doctor will discuss the best course of treatment for you based on the specific characteristics of your adenoma and your overall health.
In summary, the diagnosis of an adrenocortical adenoma is based on a combination of imaging studies and laboratory tests, and treatment options include surgery, radiation therapy, and hormone therapy. It is important to work closely with your doctor to determine the best course of treatment for you.
The exact cause of fibrous dysplasia is unknown, but genetic factors are suspected to play a role. It can occur sporadically or as part of certain inherited medical conditions. Fibrous dysplasia is more common in males than females and typically affects children and young adults.
The symptoms of fibrous dysplasia depend on the bones affected and may include pain, limb deformity, and difficulty moving or using affected limbs. Diagnosis is based on a combination of clinical evaluation, imaging studies such as X-rays, CT scans or MRI, and biopsy to confirm the presence of fibrous tissue in affected bones.
Treatment for fibrous dysplasia depends on the severity of symptoms and the specific bones involved, but may include medications such as bisphosphonates to slow bone growth, surgery to remove affected bone tissue or correct deformities, or radiation therapy to reduce pain and improve function. In some cases, surgical removal of affected bone tissue may be necessary.
Prognosis for fibrous dysplasia varies depending on the severity of symptoms and the specific bones involved, but in general, with appropriate treatment, most individuals with this condition can achieve significant improvement in symptoms and function. However, some individuals may experience chronic pain or disability despite treatment.
In summary, fibrous dysplasia is a developmental disorder that affects multiple bones in the body, causing pain, deformity, and impaired function of affected limbs. Diagnosis is based on clinical evaluation, imaging studies, and biopsy, and treatment options include medications, surgery, or radiation therapy. Prognosis varies depending on severity and specific bones involved.
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- may be used as additional codes to indicate either functional activity by neoplasms and ectopic endocrine tissue or hyperfunction and hypofunction of endocrine glands associated with neoplasms and other conditions classified elsewhere. (icd10data.com)
- Purified Cortrophin Gel is the anterior pituitary hormone which stimulates the functioning adrenal cortex to produce and secrete adrenocortical hormones. (nih.gov)
- Adrenal cortex: hypo- and hyperfunction. (salimetrics.com)
- 12. Clinical features, risk of mass enlargement, and development of endocrine hyperfunction in patients with adrenal incidentalomas: a long-term follow-up study. (nih.gov)
- Dexamethasone sodium phosphate, a synthetic adrenocortical steroid, is a white or slightly yellow crystalline powder. (nih.gov)
- Purified Cortrophin Gel is contraindicated in patients with primary adrenocortical insufficiency or adrenocortical hyperfunction. (nih.gov)
- 1987). Assessment of adrenocortical activity in term newborn infants using salivary cortisol determinations. (salimetrics.com)
- Preoperatively, and in the event of serious trauma or illness, in patients with known adrenal insufficiency or when adrenocortical reserve is doubtful. (nih.gov)
- Purified Cortrophin Gel is the anterior pituitary hormone which stimulates the functioning adrenal cortex to produce and secrete adrenocortical hormones. (nih.gov)
- McCune-Albright syndrome (MAS) consists of at least two of the following three features: (1) polyostotic fibrous dysplasia (PFD), (2) café-au-lait skin pigmentation (see the image below), and (3) autonomous endocrine hyperfunction (eg, gonadotropin-independent precocious puberty ). (medscape.com)