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Corticotropin Stimulation Test

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161. 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

162. 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

163. 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

164. 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

165. 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

166. 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

167. 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

168. 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

169. 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

170. 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

171. 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

172. 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

173. 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

174. 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

175. Menkes Kinky Hair Disease (Diagnosis)

cloning has enabled molecular diagnosis of females who carry the gene and at-risk fetuses in certain families, enhancing preventive efforts. Evidence that the gene encodes a highly conserved copper-transporting adenosine triphosphatase (ATPase) has stimulated investigation of the molecule's normal function in prokaryotic and eukaryotic systems. [ ] Knowledge gleaned from such efforts may ultimately suggest the novel therapeutic strategies needed to achieve normal neurologic outcomes in patients (...) abnormality, was excluded from direct consideration by localization to chromosome 16 in somatic cell hybrid studies. Experience with prenatal detection increased, and biochemical tests that used chorionic villus samples were developed to enable earlier diagnosis in at-risk pregnancies. A Menkes parents and professionals association was formed in the United States. In 1987, a female with classic Menkes kinky hair disease caused by an X-autosome chromosomal translocation was reported. This critical

2014 eMedicine Pediatrics

176. Conduct Disorder (Follow-up)

in the anterior cingulate cortex (ACC), orbitofrontal cortices (OFC), and dorsolateral prefrontal cortex (DLPFC) that worsens over time due to dysphoria activation of brain stress systems and increases in corticotropin-releasing factor (CRF). [ ] Areas deep in the brain, especially the amygdala and insula, appear to exhibit abnormal function reflected in overall decreases in resting state connectivity and smaller overall size. [ ] This decrease in brain structure and functionality is also seen in youth (...) and community. Parents become reluctant to take their child with CD out in public because they fear an uncontrollable incident with the child. After increased negative interaction with the child, parental stimulation may decrease as the parent spends less time with the child. In these situations, children with CD do not have sufficient opportunities to learn to accurately identify their strong emotions or to develop necessary self-control skills. Elementary school progression As the children advance

2014 eMedicine Pediatrics

177. Congenital Adrenal Hyperplasia (Diagnosis)

, hyperkalemia, and elevated plasma renin activity (PRA), indicating hypovolemia Hypertensive forms of adrenal hyperplasia (ie, 11-beta-hydroxylase deficiency and 17-alpha-hydroxylase deficiency) are associated with suppressed PRA and, often, hypokalemia Subtle forms of adrenal hyperplasia (as in nonclassic forms of 21-hydroxylase deficiency and nonclassic 3-beta-hydroxysteroid dehydrogenase deficiency): Synthetic corticotropin (Cortrosyn) stimulation testing demonstrates the abnormal accumulation (...) (eg, mixed gonadal dysgenesis, Denys-Drash syndrome) Urogenitography is often helpful in defining the anatomy of the internal genitalia A bone-age study is useful in evaluating for advanced skeletal maturation in a child who develops precocious pubic hair, clitoromegaly, or accelerated linear growth Other tests A karyotype is essential in an infant with ambiguous genitalia, to establish the chromosomal sex Genetic testing is essential for genetic counseling and prenatal diagnosis of adrenal

2014 eMedicine Pediatrics

178. Conduct Disorder (Diagnosis)

in the anterior cingulate cortex (ACC), orbitofrontal cortices (OFC), and dorsolateral prefrontal cortex (DLPFC) that worsens over time due to dysphoria activation of brain stress systems and increases in corticotropin-releasing factor (CRF). [ ] Areas deep in the brain, especially the amygdala and insula, appear to exhibit abnormal function reflected in overall decreases in resting state connectivity and smaller overall size. [ ] This decrease in brain structure and functionality is also seen in youth (...) and community. Parents become reluctant to take their child with CD out in public because they fear an uncontrollable incident with the child. After increased negative interaction with the child, parental stimulation may decrease as the parent spends less time with the child. In these situations, children with CD do not have sufficient opportunities to learn to accurately identify their strong emotions or to develop necessary self-control skills. Elementary school progression As the children advance

2014 eMedicine Pediatrics

179. Panhypopituitarism (Overview)

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

180. Adrenal Insufficiency (Overview)

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 and high dose corticotropin stimulation tests in patients with pituitary disease. J Clin Endocrinol Metab . 1998 May. 83(5):1558-62. . . Dickstein G. Commentary to the article: Comparison of low and high dose

2014 eMedicine Pediatrics

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