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Corticotropin Stimulation Test

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161. Hyposomatotropism (Overview)

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

162. Hypopituitarism (Overview)

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

163. Glucocorticoid Therapy and Cushing Syndrome (Overview)

. Yanovski JA, Cutler GB Jr, Chrousos GP, Nieman LK. Corticotropin-releasing hormone stimulation following low-dose dexamethasone administration. A new test to distinguish Cushing's syndrome from pseudo-Cushing's states. JAMA . 1993 May 5. 269(17):2232-8. . Media Gallery Diagnosis of Cushing syndrome. Etiology of Cushing syndrome. Physical findings in Cushing syndrome. of 3 Tables ] Table 1. Glucocorticoid Equivalencies [ ] Type Drug Dose Relative Glucocorticoid Potency Relative Mineralocorticoid Potency (...) and industry to maximize their beneficial effects while minimizing their adverse effects. Thus, many synthetic compounds with glucocorticoid activity have been manufactured and tested. Alterations of the basic steroid nucleus and its side groups give rise to the pharmacologic differences between these chemicals. Such changes may affect the bioavailability of these steroid compounds, including their GI absorption; parenteral distribution; plasma half-life; their metabolism in the liver, fat, or target

2014 eMedicine Pediatrics

164. Adrenal Hypoplasia (Overview)

stimulation. J Clin Endocrinol Metab . 1991 Sep. 73(3):674-86. . Heckmann M, Hartmann MF, Kampschulte B, et al. Cortisol production rates in preterm infants 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 adrenocorticotropin and cortisol secretion. J Clin Endocrinol Metab . 1984 Dec. 59(6):1103-8. . Peter M, Partsch CJ, Dorr HG, Sippell WG. Prenatal diagnosis of congenital adrenal hypoplasia. Horm Res . 1996 Jul. 46(1):41-5. . Media Gallery of 0 Tables Contributor Information and Disclosures Author Thomas A Wilson, MD Professor of Clinical Pediatrics, Chief

2014 eMedicine Pediatrics

165. 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

166. Adrenal Glands (Overview)

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

167. Congenital Adrenal Hyperplasia (Overview)

, 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

168. Conduct Disorder (Overview)

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

169. Glucocorticoid Therapy and Cushing Syndrome (Treatment)

hormone stimulation following low-dose dexamethasone administration. A new test to distinguish Cushing's syndrome from pseudo-Cushing's states. JAMA . 1993 May 5. 269(17):2232-8. . Media Gallery Diagnosis of Cushing syndrome. Etiology of Cushing syndrome. Physical findings in Cushing syndrome. of 3 Tables ] Table 1. Glucocorticoid Equivalencies [ ] Type Drug Dose Relative Glucocorticoid Potency Relative Mineralocorticoid Potency Plasma Half-Life (mg) Biologic Half-Life (h) Short-acting Cortisol 20 1.0 (...) available mineralocorticoid in most countries. Fludrocortisone has some glucocorticoid activity. Medication is also required when the patient has Cushing syndrome due to ectopic corticotropin (ACTH) and the primary source cannot be found or when surgery has not cured the hypercortisolism. In this situation, the aim of treatment is to suppress glucocorticoid production and, in the case of malignancy, to reduce tumor growth. When possible, minimize the dose and duration of glucocorticoid treatment

2014 eMedicine Pediatrics

170. Maternal Chorioamnionitis (Follow-up)

of the sepsis calculator in a population of well-appearing neonates (≥34 weeks' gestation) exposed to the clinical maternal diagnosis of chorioamnionitis would have substantially reduced the proportion of neonates undergoing laboratory tests and receiving antimicrobial agents. [ , , , ] Term neonates undergoing an evaluation to exclude sepsis who consistently appear well can probably go home with their mothers within 48 hours after birth. Septic-appearing neonates usually receive antibiotic therapy via (...) . [ ] When the mother is allergic to penicillin, she is given clindamycin if her GBS isolate is documented to be susceptible to clindamycin. Approximately 30% of GBS isolates in the United States were clindamycin resistant in 2010, and the proportion varies by country. If, however, clindamycin susceptibility testing has not been performed, vancomycin should be administered instead. [ ] Obstetric management influencing neonatal outcome When acute chorioamnionitis is evident, delivery must be expedited

2014 eMedicine Pediatrics

171. Hypothermia, Circulatory Arrest and Cardiopulmonary Bypass (Follow-up)

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

172. Glucocorticoid Therapy and Cushing Syndrome (Follow-up)

. Philadelphia, Pa: WB Saunders; 1998. 55-95. Yanovski JA, Cutler GB Jr, Chrousos GP, Nieman LK. Corticotropin-releasing hormone stimulation following low-dose dexamethasone administration. A new test to distinguish Cushing's syndrome from pseudo-Cushing's states. JAMA . 1993 May 5. 269(17):2232-8. . Media Gallery Diagnosis of Cushing syndrome. Etiology of Cushing syndrome. Physical findings in Cushing syndrome. of 3 Tables ] Table 1. Glucocorticoid Equivalencies [ ] Type Drug Dose Relative Glucocorticoid (...) Cortrosyn stimulation testing at 6-month intervals to determine when HPA axis recovery occurs. Once a 30-minute cortisol exceeds 18 mcg/dL, hydrocortisone can be weaned and stopped. Patients who have had bilateral adrenalectomy require similar follow-up care, with the exception of the Cortrosyn testing. Plasma renin activity (PRA) should be measured to ensure adequacy of Florinef (fludrocortisone acetate) replacement. These patients may also require saline tablets in warm humid weather. If Florinef

2014 eMedicine Pediatrics

173. Anxiety Disorders (Diagnosis)

response to psychologic or pharmacologic interventions. Previous Next: Pathophysiology In the central nervous system (CNS), the major mediators of the symptoms of anxiety disorders appear to be norepinephrine, serotonin, dopamine, and gamma-aminobutyric acid (GABA). Other neurotransmitters and peptides, such as corticotropin-releasing factor, may be involved. Peripherally, the autonomic nervous system, especially the sympathetic nervous system, mediates many of the symptoms. [ ] Positron emission (...) , 22q, 4q31-q34, and probably 9q31 may be associated with the heritability of panic disorder phenotype. [ ] The cognitive theory regarding panic is that patients with panic disorder have a heightened sensitivity to internal autonomic cues (eg, tachycardia). Triggers of panic can include the following: Injury (eg, accidents, surgery) Illness Interpersonal conflict or loss Use of cannabis (can be associated with panic attacks, perhaps because of breath-holding) [ ] Use of stimulants, such as caffeine

2014 eMedicine.com

174. Fibromyalgia (Diagnosis)

-stimulating hormone level 25-hydroxy vitamin D level Vitamin B12 level Iron studies, including iron level, total iron binding capacity, percent saturation, and serum ferritin level Magnesium level Erythrocyte sedimentation rate Antipolymer antibody assay: May provide conclusive evidence for a subgroup of people with fibromyalgia; about 50% of fibromyalgia patients have antipolymer antibodies Patient self-report forms, clinical psychometric testing Self-report forms, for assessing patients’ pain, fatigue (...) be explained if platelet ATP levels are also low. ATP is necessary to move and then hold serotonin in platelets. More investigation into ATP and the link to serotonin is needed. Dysfunction of the hypothalamic-pituitary-adrenal axis Studies of the neuroendocrine aspects of fibromyalgia have found dysfunction of the HPA axis. [ ] The HPA axis is a critical component of the stress-adaptation response. The sequence of HPA action is that corticotropin-releasing hormone (CRH) from the hypothalamus stimulates

2014 eMedicine.com

175. Conn Syndrome (Diagnosis)

was described by Lifton’s group in 2011. [ ] Workup Screening (first-tier) tests for primary aldosteronism include the following: Serum potassium and bicarbonate levels Sodium and magnesium levels Plasma aldosterone/plasma renin activity ratio Confirmatory (second-tier) tests include the following: Serum aldosterone level 24-hour urinary aldosterone excretion test Salt-loading test Tests for determining the primary aldosteronism subtype (third-tier tests) include the following: Postural stimulation test (...) Furosemide (Lasix) stimulation test Diurnal rhythm of aldosterone The initial radiologic investigation in the workup of primary aldosteronism is high-resolution, thin-sliced (2-2.5 mm) adrenal computed tomography (CT) scanning with contrast. Other tests include the following: NP-59 iodo-methyl-norcholesterol scintigraphy: Although fairly difficult to set up and not routinely available, this test can be useful in select cases for distinguishing between adenomas and hyperplasia Adrenal venous sampling

2014 eMedicine.com

176. Alpha2-Plasmin Inhibitor Deficiency (Diagnosis)

. In addition, other noncoagulation proteins, such as complement, growth hormone, corticotropin, and glucagon, are substrates for plasmin. Therefore, the reasons for the bleeding disorder that develops due to the actions of excess unfettered and unneutralized plasmin are easily comprehended. Alpha 2-plasmin inhibitor (alpha 2-PI, a2-PI) belongs to the serpin family of inhibitors, is synthesized by the liver, and is present in plasma as a single-chain protein in approximately half the concentration (...) United States Very few cases of inherited alpha 2-plasmin inhibitor deficiency (alpha 2-PI deficiency, a2-PI deficiency) have been reported; therefore, data do not exist to determine the true frequency. In the next several years, as widespread high-throughput genomic testing becomes commonplace, the frequency of genetic defects will be known, and the frequency of these rare disorders can then be determined. The frequency of acquired alpha 2-plasmin inhibitor deficiency (alpha 2-PI deficiency, a2-PI

2014 eMedicine.com

177. 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

178. Carney Syndrome (Diagnosis)

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

179. Carney Complex (Diagnosis)

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

180. Hypopituitarism (Diagnosis)

, and therefore, hyperpigmentation does not take place. Patients with secondary adrenal insufficiency usually are eukalemic. This differs from primary adrenal insufficiency, in which patients develop hyponatremia and hyperkalemia. Aldosterone secretion is not affected, as it does not depend on corticotropin but instead on the renin-angiotensin axis. Thyroid-stimulating hormone deficiency Secondary due to decreased TSH (also known as thyrotropin) exhibits symptoms identical to those of primary thyroid disease (...) , hypopituitarism is difficult to diagnosis in the acutely decompensated or the stable patient. Laboratory and radiographic tests are necessary to confirm the diagnosis. A variety of diagnostic laboratory tests can be used, but significant controversy exists regarding which tests are ideal. Because many specific endocrine tests are not rapidly available in the emergency department (ED) setting, immediate confirmation of hypopituitarism may not be practical. Clinical suspicion by history and clinical examination

2014 eMedicine Emergency Medicine

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