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Corticotropin Stimulation Test

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161. Osteoporosis (Primary) (Follow-up)

and patients" can lead to increased bone mineral density (BMD) testing and greater use of osteoporosis medications. [ ] In addition, a physician reminder in conjunction with a patient risk assessment strategy apparently can result in a reduction in patient fractures and an increase in osteoporosis therapy. The authors concluded that multicomponent tools aimed at doctors and patients may support clinical decision making in the management of osteoporosis. A 2009 study indicated that the use of a case manager (...) modalities such as moist hot packs and transcutaneous electrical nerve stimulation should also be considered. During this period, monitoring the patient carefully for signs of constipation, urinary retention, and respiratory depression, which can occur with the use of narcotic analgesics, is essential. A comfortable mechanical support for the spine and, in some cases, a thoracic orthosis may need to be prescribed. The primary reason for the application of a thoracic orthosis is to limit motion

2014 eMedicine.com

162. Osteoporosis in Solid Organ Transplantation (Follow-up)

are indicated in the pretransplant evaluation of all patients awaiting solid organs [ , ] : Serum calcium level Phosphorus level Bicarbonate level Alkaline phosphatase level BUN/creatinine levels Intact PTH assay, to assess for hyperparathyroidism (primary or secondary) 25-Hydroxyvitamin D value to assess total body vitamin D stores Thyroid function tests (eg, thyroid-stimulating hormone, free levothyroxine) Testosterone level (males only), to ensure eugonadism Estradiol and FSH levels (in females (...) hormone, thereby decreasing gonadal hormone production; may also directly decrease gonadal hormone production Suppress corticotropin, thereby suppressing the adrenal production of androstenedione, a substrate for both testosterone and estrone production Decrease osteoblast-mediated bone formation Increase bone resorption Glucocorticoids result in a disproportionate loss of cancellous or trabecular bone, possibly because trabecular bone has an inherently greater rate of turnover than cortical bone

2014 eMedicine.com

163. Osteoporosis (Secondary) (Follow-up)

and patients" can lead to increased bone mineral density (BMD) testing and greater use of osteoporosis medications. [ ] In addition, a physician reminder in conjunction with a patient risk assessment strategy apparently can result in a reduction in patient fractures and an increase in osteoporosis therapy. The authors concluded that multicomponent tools aimed at doctors and patients may support clinical decision making in the management of osteoporosis. A 2009 study indicated that the use of a case manager (...) modalities such as moist hot packs and transcutaneous electrical nerve stimulation should also be considered. During this period, monitoring the patient carefully for signs of constipation, urinary retention, and respiratory depression, which can occur with the use of narcotic analgesics, is essential. A comfortable mechanical support for the spine and, in some cases, a thoracic orthosis may need to be prescribed. The primary reason for the application of a thoracic orthosis is to limit motion

2014 eMedicine.com

164. Pseudo-Cushing Syndrome (Follow-up)

cortisol with an automated immunoassay system. Clinical Chemistry & Laboratory Medicine . 2006. 44(12):1441-5. . Alwani RA, Schmit Jongbloed LW, de Jong FH, van der Lely AJ, de Herder WW, Feelders RA. Differentiating between Cushing's disease and pseudo-Cushing's syndrome: comparison of four tests. Eur J Endocrinol . March/2014. 170(4):477-86. . Yanovski JA, Cutler GB Jr, Chrousos GP, Nieman LK. Corticotropin-releasing hormone stimulation following low-dose dexamethasone administration. A new test (...) cortisol concentrations. [ ] PCS can occur at any age; it can develop in infants exposed to alcohol in breast milk. [ ] Next: Causes and Complications Etiology The mechanism behind PCS is unclear. Most evidence suggests central stimulation of a corticotropin-releasing hormone (CRH), either at the hypothalamic or suprahypothalamic level. [ , ] Rats given 15% alcohol for 3 months showed a greater number of corticotropin-producing cells with increased secretory activity. [ ] A two-hit hypothesis has been

2014 eMedicine.com

165. Epileptic and Epileptiform Encephalopathies (Follow-up)

epilepticus or worsen cognitive function. Additionally, adrenocorticotropic hormone (ACTH) or corticosteroids may be used, usually after standard AEDs have failed. A ketogenic diet and intravenous immunoglobulin (IVIG) may also be helpful. Vagus nerve stimulation and epilepsy surgery may be appropriate in select cases. The degree of correlation between EEG abnormalities and neuropsychological deficits requires better description in most of these syndromes. However, often a goal of treatment is to improve (...) , ACTH and vigabatrin are usually used in practice. There is no consensus on ACTH dosing for infants. In infantile spasms, a prospective single-blind study showed no difference in the effectiveness of high-dose, long-duration corticotropin (150 U/m 2 /d for 3 wk then taper over 9 wk) versus low-dose, short-duration corticotropin (20-30 U/d for 2-6 wk then taper over 1 wk) with respect to spasm cessation and improvement in patient's EEG; hypertension was more common with larger doses. Corticosteroids

2014 eMedicine.com

166. Tourette Syndrome and Other Tic Disorders (Follow-up)

dyskinesia. Dopamine agonist therapy Paradoxically, several mixed dopamine agonists have also been proven effective in reducing tic frequency. [ , , ] To date, they have been tested exclusively in relatively low doses, partly because of a theory that, at these doses, they must antagonize dopamine function by selective action at presynaptic receptors. Accumulating evidence suggests that this rationale is faulty, however, and trials with higher doses may be expected. Habit reversal therapy Five RCTs have (...) demonstrated the efficacy of a specific form of behavior therapy for tics. [ , , , , , ] The originally tested treatment consisted of a package of interventions called habit reversal therapy, [ ] which comprises monitoring, relaxation, and other nonspecific elements of behavior therapy. The most important element is application of a competing response whenever the patient notices either a tic or the urge to tic. Initially, heavy effort on the part of the patient may be needed. However, in all 4 reported

2014 eMedicine.com

167. Carney Syndrome (Follow-up)

See for more detail. Diagnosis Laboratory studies used in the diagnosis of Carney complex include the following: Complete blood count (CBC) Glucose/electrolytes Erythrocyte sedimentation rate Thyroxine/thyroid-stimulating hormone Adrenocorticotropic hormone Growth hormone Twenty-four–hour urinary cortisol excretion test and dexamethasone stimulation test: To evaluate for primary pigmented nodular adrenocortical disease (PPNAD) as part of Carney complex [ ] Echocardiography is the investigation (...) . (See Pathophysiology and Etiology.) Endocrine overactivity is one of the characteristics of this syndrome. [ ] In fact, corticotropin hormone–independent due to primary pigmented nodular adrenocortical disease is an important characteristic of Carney complex. (See Workup and Treatment.) Patient education The family should be aware that this is an autosomal dominant disorder with a 50% chance that the offspring of an affected individual will have the disorder. Previous Next: Pathophysiology Carney

2014 eMedicine.com

168. Hyperaldosteronism, Primary (Follow-up)

benefit. [ ] Next: Pharmacologic Therapy Calcium channel blockers By inhibiting the intracellular calcium flux in the adrenocortical cells, the dihydropyridine calcium channel blockers reduce the production of aldosterone in response to a variety of stimulants, including potassium, corticotropin, and angiotensin-II. Nifedipine is the most extensively studied of these medications; however, although nifedipine causes a significant improvement in patients with hypertension (HTN), it does not address (...) following chronic corticotropin suppression by exogenous steroids. However, if significant develops, potassium supplements should be discontinued, and the patient can be started on furosemide at doses of 80-160 mg daily. Previous Next: Diet A low-salt diet, although helpful in achieving blood pressure control in primary aldosteronism, may be associated with false-negative results on biochemical testing. A high-salt diet makes the achievement of blood pressure control more difficult and may cause false

2014 eMedicine.com

169. Hypopituitarism (Diagnosis)

produced in the hypothalamus. These regulatory hormones are transported to the anterior pituitary via the pituitary portal system circulation. The release-stimulating hormones produced by the hypothalamus include the following: Growth hormone–releasing hormone (GHRH) Corticotropin-releasing hormone (CRH) Thyrotropin-releasing hormone (TRH) Gonadotropin-releasing hormone (GnRH) PRL secretion is distinct from that of the other anterior pituitary hormones, being inhibited by hypothalamic dopamine (...) from the anterior pituitary include the following: Growth hormone (GH) Adrenocorticotropic hormone (ACTH) Thyroid-stimulating hormone (TSH) Luteinizing hormone (LH) Follicle-stimulating hormone (FSH) Prolactin (PRL) The pathway from embryogenesis to the full differentiation of specific functional cell types within the pituitary is controlled by numerous genes that encode transcription factors. (See the diagram below.) Mutations in these genes are causes of congenital hypopituitarism and have

2014 eMedicine Pediatrics

170. Hypothermia, Circulatory Arrest and Cardiopulmonary Bypass (Diagnosis)

catecholamines, cortisol, growth hormone, Glucagon, corticotropin (or adrenocorticotropic hormone [ACTH]), thyroid-stimulating hormone (TSH), and endorphins. levels of thyroid hormone decreases the first few days after CPB. Decreased renal and hepatic function after CPB leads to decreased clearance of vasoactive inflammatory mediators from the kidneys and liver. The lung is normally responsible for metabolizing and clearing many of these hormones, particularly catecholamines. Exclusion of the lungs from (...) surfaces of the bypass circuit are associated with activation of inflammatory mediators. Effects include activation of the complement system, including plasma-activated complement 3 (C3a). A potent stimulator of platelet aggregation, C3a causes the release of from mast cells and basophils, increases vascular permeability, and stimulates WBCs to release oxygen free radicals and lysosomal enzymes. Elevated levels of C3a are linked to the duration of CPB. Neutrophil activation has been linked

2014 eMedicine Pediatrics

171. Hyposomatotropism (Diagnosis)

requiring comprehensive clinical and auxologic assessment combined with biochemical testing of the GH-insulinlike growth factor (IGF) axis and radiologic evaluation. Biochemical testing of the GH-IGF axis includes radioimmunoassays (RIAs) of GH, IGF, and insulinlike growth factor binding proteins (IGFBPs) [ , , ] Next: Background Human pituitary-derived growth hormone In the 1950s, growth hormone isolated from the pituitaries of humans and anthropoid apes was discovered to stimulate growth in children (...) , Thompson JQ. Human growth hormone release. Comparison of provocative test procedures. Am J Med . 1974 Feb. 56(2):179-85. . Lanes R, Hurtado E. Oral clonidine-an effective growth hormone-releasing agent in prepubertal subjects. J Pediatr . 1982 May. 100(5):710-4. . Collu R, Leboeuf G, Letarte J, Ducharme JR. Stimulation of growth hormone secretion by levodopa-propranolol in children and adolescents. Pediatrics . 1975 Aug. 56(2):262-6. . Merimee TJ, Rabinowtitz D, Fineberg SE. Arginine-initiated release

2014 eMedicine Pediatrics

172. Adrenal Hypoplasia (Treatment)

to restore blood pressure. This can be repeated if the blood pressure remains low. Once samples for serum electrolytes, blood sugar, cortisol, 17-hydroxyprogesterone, and adrenocorticotropic hormone (ACTH) concentrations are obtained, treat the patient with glucocorticoids. This therapy is based on suspicion of adrenal insufficiency because it may be life preserving. A cosyntropin stimulation test confirms the diagnosis of adrenocortical insufficiency. Dexamethasone may be given prior to the cosyntropin (...) in relation to growth and illness: a noninvasive prospective study using gas chromatography-mass spectrometry. J Clin Endocrinol Metab . 2005 Oct. 90(10):5737-42. . Kazlauskaite R, Evans AT, Villabona CV, et al. Corticotropin tests for hypothalamic-pituitary- adrenal insufficiency: a metaanalysis. J Clin Endocrinol Metab . 2008 Nov. 93(11):4245-53. . Schurmeyer TH, Avgerinos PC, Gold PW, et al. Human corticotropin-releasing factor in man: pharmacokinetic properties and dose-response of plasma

2014 eMedicine Pediatrics

173. Adrenal Insufficiency (Treatment)

, Polonsky KS, Larson PR, eds. Williams Textbook of Endocrinology . 11th ed. Philadelphia, PA: Saunders; 2008. 229. Iwanaga K, Yamamoto A, Matsukura T, Niwa F, Kawai M. Corticotrophin-releasing hormone stimulation tests for the infants with relative adrenal insufficiency. Clin Endocrinol (Oxf) . 2017 Dec. 87 (6):660-4. . Kazlauskaite R, Evans AT, Villabona CV, et al. Corticotropin tests for hypothalamic-pituitary- adrenal insufficiency: a metaanalysis. J Clin Endocrinol Metab . 2008 Nov. 93(11):4245-53 (...) . . Thaler LM. Comment on the low-dose corticotropin stimulation test is more sensitive than the high-dose test. [letter]. J Clin Endocrinol Metab . 1998 Dec. 83(12):4530-1; author reply 4532-3. . Tordjman K, Jaffe A, Greenman Y, Stern N. Comments on the comparison of low and high dose corticotropin stimulation tests in patients with pituitary disease. J Clin Endocrinol Metab . 1998 Dec. 83(12):4530; author reply 4532-3. . Mayenknecht J, Diederich S, Bahr V, Plockinger U, Oelkers W. Comparison of low

2014 eMedicine Pediatrics

174. Adrenal Glands (Treatment)

entirely controlled by the secretion of ACTH by the anterior pituitary gland, which is controlled by corticotropin-releasing hormone (CRH) secreted by the hypothalamus. In normal situations, CRH, ACTH, and cortisol secretory rates demonstrate a circadian rhythm, with a zenith in the early morning and a nadir in the evening. Various stresses also stimulate increased ACTH and, thus, cortisol secretion. A negative feedback effect of cortisol on the anterior pituitary and the hypothalamus help control (...) test for distinguishing between Cushing disease and ectopic ACTH production is the metyrapone stimulation test. Because metyrapone blocks 11-hydroxylase, which is responsible for conversion of 11-deoxycortisol to cortisol, administration at 15 mg/kg (or 750 mg for adolescents) PO every 4 hours for 24 hours decreases plasma cortisol and increases ACTH. The normal response is an increase in plasma 11-deoxycortisol levels to more than 10 μg/dL and an increase in 24-hour urine 17-OHCS levels to twice

2014 eMedicine Pediatrics

175. Panhypopituitarism (Diagnosis)

: Apr 29, 2018 Author: Robert P Hoffman, MD; Chief Editor: Sasigarn A Bowden, MD Share Email Print Feedback Close Sections Sections Panhypopituitarism Overview Practice Essentials The pituitary gland is called the master endocrine gland of the body because it controls the function of other endocrine organs. The anterior pituitary produces the hormones thyrotropin (thyroid-stimulating hormone [TSH]), corticotropin (adrenocorticotropic hormone [ACTH]), luteinizing hormone (LH), follicle-stimulating (...) of the cause. Genetic testing is available at various commercial and academic laboratories for mutations associated with hypopituitarism. Cortisol deficiency requires prompt recognition and treatment. This is particularly true for the child who may be facing surgery or experiencing other significant stresses related to the cause of hypopituitarism. In TSH deficiency, the dose of L-thyroxine replacement is age dependent. In cases of gonadotropin deficiency, sex steroid replacement should begin at puberty

2014 eMedicine Pediatrics

176. Adrenal Disease and Pregnancy (Diagnosis)

replacement. Patients with previously undiagnosed adrenocortical deficiency may present with an acute addisonian crisis during labor or postpartum. Fetal growth restriction Maternal cortisol deficiency has been suggested as a possible cause of fetal intrauterine growth restriction. Clinical suspicion should arise if fetal growth restriction is associated with abnormally low maternal blood pressure and an unusual increase in skin pigmentation due to maternal corticotropin and melanocyte-stimulating hormone (...) , and interpretation of suppression of 24-hour urine cortisol and plasma cortisol levels seems to yield reliable results. Corticotropin levels Once hypercortisolemia is established, corticotropin levels should be measured. For all forms of Cushing syndrome in pregnancy, corticotropin levels are normal or they are high secondary to placental corticotropin production or owing to placental corticotropin-releasing hormone–stimulated pituitary corticotropin production. Therefore, corticotropin levels are not useful

2014 eMedicine.com

177. Adrenal Glands (Follow-up)

entirely controlled by the secretion of ACTH by the anterior pituitary gland, which is controlled by corticotropin-releasing hormone (CRH) secreted by the hypothalamus. In normal situations, CRH, ACTH, and cortisol secretory rates demonstrate a circadian rhythm, with a zenith in the early morning and a nadir in the evening. Various stresses also stimulate increased ACTH and, thus, cortisol secretion. A negative feedback effect of cortisol on the anterior pituitary and the hypothalamus help control (...) test for distinguishing between Cushing disease and ectopic ACTH production is the metyrapone stimulation test. Because metyrapone blocks 11-hydroxylase, which is responsible for conversion of 11-deoxycortisol to cortisol, administration at 15 mg/kg (or 750 mg for adolescents) PO every 4 hours for 24 hours decreases plasma cortisol and increases ACTH. The normal response is an increase in plasma 11-deoxycortisol levels to more than 10 μg/dL and an increase in 24-hour urine 17-OHCS levels to twice

2014 eMedicine Pediatrics

178. Adrenal Hypoplasia (Follow-up)

spectrometry. J Clin Endocrinol Metab . 2005 Oct. 90(10):5737-42. . Kazlauskaite R, Evans AT, Villabona CV, et al. Corticotropin tests for hypothalamic-pituitary- adrenal insufficiency: a metaanalysis. J Clin Endocrinol Metab . 2008 Nov. 93(11):4245-53. . Schurmeyer TH, Avgerinos PC, Gold PW, et al. Human corticotropin-releasing factor in man: pharmacokinetic properties and dose-response of plasma adrenocorticotropin and cortisol secretion. J Clin Endocrinol Metab . 1984 Dec. 59(6):1103-8. . Peter M (...) , cushingoid features, hypertension, hyperglycemia, cataracts, osteopenia, and growth failure. Growth failure is one of the more sensitive indicators of excess exposure in children. Blood pressure and plasma renin activity provides a guide for adequacy of mineralocorticoid therapy. If no signs of puberty are seen by age 14-15 years, suspect hypogonadotropic hypogonadism. This is associated with low serum concentrations of gonadotropins (eg, leuteinizing hormone [LH] and follicle-stimulating hormone [FSH

2014 eMedicine Pediatrics

179. Adrenal Insufficiency (Follow-up)

, Polonsky KS, Larson PR, eds. Williams Textbook of Endocrinology . 11th ed. Philadelphia, PA: Saunders; 2008. 229. Iwanaga K, Yamamoto A, Matsukura T, Niwa F, Kawai M. Corticotrophin-releasing hormone stimulation tests for the infants with relative adrenal insufficiency. Clin Endocrinol (Oxf) . 2017 Dec. 87 (6):660-4. . Kazlauskaite R, Evans AT, Villabona CV, et al. Corticotropin tests for hypothalamic-pituitary- adrenal insufficiency: a metaanalysis. J Clin Endocrinol Metab . 2008 Nov. 93(11):4245-53 (...) . . Thaler LM. Comment on the low-dose corticotropin stimulation test is more sensitive than the high-dose test. [letter]. J Clin Endocrinol Metab . 1998 Dec. 83(12):4530-1; author reply 4532-3. . Tordjman K, Jaffe A, Greenman Y, Stern N. Comments on the comparison of low and high dose corticotropin stimulation tests in patients with pituitary disease. J Clin Endocrinol Metab . 1998 Dec. 83(12):4530; author reply 4532-3. . Mayenknecht J, Diederich S, Bahr V, Plockinger U, Oelkers W. Comparison of low

2014 eMedicine Pediatrics

180. Maternal Chorioamnionitis (Diagnosis)

refill time, cool and clammy skin, pale or mottled appearance, and/or oliguria Gastrointestinal: Abdominal distention, vomiting, diarrhea, and/or bloody stools Central nervous system: Thermal regulatory abnormalities, behavioral abnormalities, apnea, and/or seizures Hematologic and/or hepatic: Pallor, petechiae or purpura, and overt bleeding Laboratory tests During the intrapartum period, the diagnosis of chorioamnionitis is usually based on clinical criteria, particularly for pregnancies at term (...) . Laboratory studies for asymptomatic pregnant mothers who present with premature labor or PROM include the following: Examination of amniotic fluid Maternal blood studies Maternal urine studies Maternal group B streptococcal (GBS) screening test Testing in febrile pregnant women with suspected chorioamnionitis may include the following: White blood cell (WBC) counts C-reactive protein (CRP) levels Alpha1-proteinase inhibitor (A1PI) complex measurement Serum interleukin-6 (IL-6) or ferritin levels Studies

2014 eMedicine Pediatrics

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