cosyntropin has been researched along with Hypotension* in 9 studies
1 review(s) available for cosyntropin and Hypotension
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Adrenocortical insufficiency.
Adrenocortical insufficiency causes difficulty in diagnosis and morbidity out of proportion to its rarity, because of the non-specific, multi-system nature of the clinical features. Most of these are due to cortisol deficiency. Prominent features are well-known ones such as weight loss and asthenia, and hypoglycaemia. Less prominent in recent accounts are those due to failure of cellular sodium export and to vasopressin excess, which are frequent and clinically significant. For this reason, the clinical features of isolated ACTH deficiency, isolated glucocorticoid deficiency and Addison's disease overlap greatly. In addition, cortisol deficiency has secondary endocrine effects, e.g. glucocorticoid-reversible hypothyroidism, hyperprolactinaemia and hypercalcaemia. Further overlap between the various steroid insufficiency syndromes occurs because of the association of various organ-specific autoimmune endocrinopathies with Addison's disease. Over 80% of Addison's disease is of the autoimmune type, though almost any systemic destructive process can cause similar steroid insufficiency. Demonstration of adrenal insufficiency requires various combinations of tetracosactrin adrenal stimulation tests, and hypoglycaemia or equivalent tests, if the cause is ACTH deficiency but the correct test can only be chosen to suit a firm clinical diagnosis. The treatment of adrenocortical insufficiency is described. Topics: Addison Disease; Adrenal Insufficiency; Adrenocorticotropic Hormone; Aldosterone; Androstenedione; Animals; Autoimmune Diseases; Blood Volume; Body Water; Calcium; Catecholamines; Cosyntropin; Dehydroepiandrosterone; Dehydroepiandrosterone Sulfate; Delayed-Action Preparations; Disease Models, Animal; Glomerular Filtration Rate; Glucocorticoids; Humans; Hypoglycemia; Hyponatremia; Hypotension; Hypothalamo-Hypophyseal System; Kidney; Posture; Prolactin; Regional Blood Flow; Skin Pigmentation; Thyroid Gland; Tomography, X-Ray Computed; Water-Electrolyte Balance | 1985 |
1 trial(s) available for cosyntropin and Hypotension
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The rapid low-dose (1 microgram) cosyntropin test in the immediate postoperative period: results in elderly subjects after major abdominal surgery.
Recently the rapid low-dose (1 microgram) cosyntropin test has been found to be superior to the standard (250 micrograms) rapid cosyntropin test for evaluating the hypothalamic-pituitary-adrenal axis. Because the 1-microgram test has not been studied in postoperative patients, we evaluated the test after major abdominal surgery.. We performed rapid 1-microgram cosyntropin tests in 20 patients aged 65 years or older immediately and 24 hours after uncomplicated elective abdominal surgery (group A) and in 10 patients who were suspected of having adrenal insufficiency after abdominal surgery (group B). Subsequently, 250 micrograms of cosyntropin was infused over 8 hours on 2 successive days in group B patients.. Ninety-five percent of group A patients had normal rapid 1-microgram cosyntropin test results immediately after surgery and 90% had normal test results 24 hours postoperatively. Six group B patients had abnormal rapid 1-microgram cosyntropin test results. Additional testing indicated primary adrenal insufficiency in 2 patients and central adrenal insufficiency in 1 patient; another patient probably had primary adrenal insufficiency and 2 patients appeared to be euadrenal. Four group B patients had normal rapid 1-microgram cosyntropin test results. After additional testing, 3 of these patients appeared to have normal adrenal function; 1 probably had primary adrenal insufficiency.. The rapid 1-microgram cosyntropin test accurately evaluated adrenal gland function in selected patients after uncomplicated surgery. The test, however, was difficult to interpret in unselected seriously ill postoperative patients. Therefore we recommend that postoperative patients with unexplained hypotension or other features suggestive of adrenal insufficiency who have random plasma cortisol levels less than 20 micrograms/dL be treated with glucocorticoids and the hypothalamic-pituitary-adrenal axis be studied by standard tests after recovery. Topics: Abdominal Neoplasms; Adrenal Insufficiency; Adrenocorticotropic Hormone; Aged; Aged, 80 and over; Aortic Aneurysm, Abdominal; Carcinoma; Colectomy; Colonic Neoplasms; Cosyntropin; Female; Humans; Hydrocortisone; Hypotension; Hypothalamo-Hypophyseal System; Male; Postoperative Complications | 1999 |
7 other study(ies) available for cosyntropin and Hypotension
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The use of an early ACTH test to identify hypoadrenalism-related hypotension in low birth weight infants.
To investigate if in preterm newborns, an early adrenocorticotropin hormone (ACTH) test can identify possible transient adrenal insufficiency (TAI), using significant hypotension as a clinical marker.. We studied 40 premature newborns born 24 to 29 weeks gestational age (GA) before 8 h of life. Serum cortisol levels were obtained before and 40 min after administration of 1.0 mcg kg(-1) cosyntropin. Inotropes were used to treat hypotension based on clinical assessment following no response to fluid boluses. Functional echocardiogram was used to support the clinical diagnosis of hypotension. The accuracy of the ACTH test was evaluated using receiver operating characteristic (ROC) curve.. Study patients had mean GA of 26.6 weeks and birth weight of 876 g. In all, 30% required inotropes. The area under the ROC curve for the ACTH test was 87%. Using a cutoff of an increase in cortisol below 12% from baseline had 75% sensitivity and 93% specificity for detecting hypotension. This cutoff was associated with bronchopulmonary dysplasia (8/12 vs 7/28, 95% CI: 0.1 to 0.72), but not with other morbidities or death.. An early ACTH test using the above cutoff has high specificity for detecting hypotension, and thus, can serve as a marker for potential TAI in preterm newborns. Future studies should focus on identifying those newborns for which steroid supplementation would be most beneficial. Topics: Adrenal Insufficiency; Adrenocorticotropic Hormone; Biomarkers; Bronchopulmonary Dysplasia; Cosyntropin; Early Diagnosis; Echocardiography; Female; Humans; Hydrocortisone; Hypotension; Infant, Low Birth Weight; Infant, Newborn; Infant, Premature; Infant, Premature, Diseases; Male; Pregnancy; Prospective Studies; ROC Curve; Sensitivity and Specificity | 2012 |
The challenge of defining relative adrenal insufficiency.
Topics: Adrenal Insufficiency; Adrenocorticotropic Hormone; Cosyntropin; Female; Humans; Hydrocortisone; Hypotension; Infant, Premature, Diseases; Male; Pregnancy | 2012 |
Adrenal insufficiency in acute spinal cord injury.
A 21-year-old man with a C6 American Spinal Injury Association A spinal cord injury (SCI) developed symptomatic hypotension resistant to vasopressors and volume replacement 2 weeks after injury and was diagnosed with adrenal insufficiency by cosyntropin test. Adrenal insufficiency has been documented in chronic SCI; this case shows documented adrenal insufficiency in acute SCI.. Case report.. Secondary adrenal insufficiency complicated the medical and rehabilitative course of this patient with SCI. During 2 infectious episodes, this patient's dosage of hydrocortisone had to be doubled to control symptomatic hypotension, lethargy, diffuse weakness, and anorexia.. The nonspecific symptomatology of adrenal insufficiency can be easily overlooked in patients with SCI. Low basal cortisol levels may be an important clue to this disorder. Low-dose adrenocorticotropic hormone stimulation may be more sensitive than high doses for detecting subclinical adrenal insufficiency. A high index of clinical suspicion is needed for the correct diagnosis of acute and chronic adrenal insufficiency. Topics: Adrenal Insufficiency; Adult; Cervical Vertebrae; Cosyntropin; Dose-Response Relationship, Drug; Humans; Hydrocortisone; Hypotension; Male; Neurologic Examination; Spinal Cord Injuries; Spinal Fractures | 2006 |
Further evidence that melanocortins prevent myocardial reperfusion injury by activating melanocortin MC3 receptors.
In rats subjected to myocardial ischemia/reperfusion, melanocortin peptides, including gamma(1)-melanocyte-stimulating hormone (gamma(1)-MSH), are able to exert a protective effect by stimulating brain melanocortin MC(3) receptors. A non-melanocortin receptor belonging to a group of receptors for Phe-Met-Arg-Phe-NH(2) (FMRFamide)-like peptides may be involved in some of the cardiovascular effects of the gamma-MSHs. FMRFamide-like peptides and gamma(1)-/gamma(2)-MSH share, among other things, the C-terminal Arg-Phe sequence, which seems to be essential for cardiovascular effects in normal animals. So we aimed to further investigate which receptor and which structure are involved in the protective effects of melanocortins in anesthetized rats subjected to myocardial ischemia by ligature of the left anterior descending coronary artery (5 min), followed by reperfusion. In saline-treated rats, reperfusion induced, within a few seconds, a high incidence of ventricular tachycardia and ventricular fibrillation, and a high percentage of death within the 5 min of observation period. Reperfusion was associated with a massive increase in free radical blood levels and with an abrupt and marked fall in systemic arterial pressure. The i.v. treatment (162 nmol/kg) during the ischemic period with the adrenocorticotropin fragment 1-24 [ACTH-(1-24): the reference protective melanocortin which binds all melanocortin receptors], as well as with both the melanocortin MC(3) receptor agonists gamma(2)-MSH and [D-Trp(8)]gamma(2)-MSH, reduced the incidence of ventricular tachycardia, ventricular fibrillation and death, the increase in free radical blood levels and the fall in arterial pressure. On the contrary, gamma(2)-MSH-(6-12) (a fragment unable to bind melanocortin receptors) was ineffective. Such protective effect was prevented by the melanocortin MC(3)/MC(4) receptor antagonist SHU 9119. In normal (i.e., not subjected to myocardial ischemia/reperfusion) rats, the same i.v. dose (162 nmol/kg) of gamma(2)-MSH, [D-Trp(8)]gamma(2)-MSH and gamma(2)-MSH-(6-12) provoked a prompt and transient increase in arterial pressure; on the other hand, ACTH-(1-24), which lacks the C-terminal Arg-Phe sequence, decreased arterial pressure, but only at higher doses. Heart rate of normal rats was not affected by any of the assayed peptides. The present data confirm and extend our previous findings that melanocortins prevent myocardial reperfusion injury by activating melanocortin MC(3) receptors Topics: alpha-MSH; Animals; Coronary Disease; Cosyntropin; Female; FMRFamide; gamma-MSH; Hypotension; Injections, Intravenous; Lidocaine; Male; Melanocyte-Stimulating Hormones; Myocardial Reperfusion Injury; Rats; Rats, Wistar; Receptor, Melanocortin, Type 3; Signal Transduction; Tachycardia, Ventricular; Time Factors; Ventricular Fibrillation | 2003 |
Adrenal insufficiency in high-risk surgical ICU patients.
To examine the incidence and response to treatment of adrenal insufficiency (AI) in high-risk postoperative patients.. Prospective observational case series.. Large urban tertiary-care surgical ICU (SICU).. Adults > 55 years of age who required vasopressor therapy after adequate volume resuscitation in the immediate postoperative period.. Each patient underwent a cosyntropin (ACTH) stimulation test; at the discretion of the clinical team, some patients were empirically given hydrocortisone (100 mg IV q8h for three doses) before serum cortisol values became available.. Adrenal dysfunction (AD), defined as serum cortisol < 20 microg/dL at all time points, with Delta cortisol (60 min post-ACTH minus baseline) of < or = 9 microg/dL; functional hypoadrenalism (FH), defined as serum cortisol < 30 microg/dL at all time points or Delta cortisol (60 min post-ACTH minus baseline) < or = 9 microg/dL; and AI, as the presence of either AD or FH.. One hundred four patients were enrolled with a mean age (SD) of 65.2 +/- 16.9 years. AI (AD plus FH) was found in 34 of 104 patients (32.7%): AD was found in 9 patients (8.7%), FH in 25 patients (24%), and normal adrenal function in 70 patients (67.3%). The absolute eosinophil count was significantly higher in the combined AD and FH groups compared with the group with normal adrenal function (p < 0.05). Forty-six of 104 patients (44.2%) received hydrocortisone; 29 (63%) could be weaned from treatment with vasopressors within 24 h. This beneficial effect of hydrocortisone reached statistical significance in the FH group when compared with untreated patients (p < 0.031); a similar trend was seen in the AD group (p = 0.083). Mortality was also lower in the hydrocortisone-treated AI patients (5 of 23 [21%] vs 5 of 11 [45%] in those not receiving hydrocortisone; p < 0.01).. There is a high incidence of AI among SICU patients > 55 years of age with postoperative hypotension requiring vasopressors. There is also a significant association between hydrocortisone replacement therapy, resolution of vasopressor requirements, and improved survival. Topics: Adrenal Insufficiency; Aged; Cosyntropin; Critical Illness; Female; Humans; Hydrocortisone; Hypotension; Incidence; Intensive Care Units; Male; Middle Aged; Postoperative Complications; Prospective Studies; Risk Factors; Vasoconstrictor Agents | 2001 |
Transient corticotropin deficiency in critical illness.
We describe three critically ill patients who displayed indirect evidence of transient corticotropin deficiency. All these patients were elderly, were poorly nourished, and had unexplained hypotension intraoperatively or immediately postoperatively. During the hypotensive episodes, they had inappropriately low plasma cortisol levels (10, 12, and 6 micrograms/dl) and responded dramatically to the administration of glucocorticoids. A normal response to infusion of synthetic corticotropin excluded primary adrenal insufficiency. Two patients tested had low thyroxine levels without increased thyrotropin concentrations and depressed levels of gonadotropins. In all three patients, the dose of glucocorticoids was successfully tapered and then discontinued. After recovery, serum thyroxine levels increased, gonadotropins reverted to normal concentrations, and the administration of metyrapone to two patients demonstrated normal hypothalamic-pituitary-adrenal function. Cortisol levels of less than 15 micrograms/dl in critically ill patients suggest the presence of adrenal insufficiency. The infusion of synthetic corticotropin may not exclude adrenal insufficiency attributable to corticotropin deficiency. If direct tests of corticotropin reserve are impractical, treatment with glucocorticoids is warranted. Topics: Adrenocorticotropic Hormone; Aged; Cosyntropin; Critical Illness; Dexamethasone; Female; Humans; Hydrocortisone; Hypotension; Male; Middle Aged | 1993 |
ACTH-(1-24) restores blood pressure in acute hypovolaemia and haemorrhagic shock in humans.
Topics: Acute Disease; Adrenocorticotropic Hormone; Aged; Blood Volume; Coronary Artery Bypass; Cosyntropin; Humans; Hypotension; Male; Shock, Hemorrhagic | 1987 |