Post-Dural Puncture Headache
Adrenal Cortex Function Tests
On the meaning of low-dose ACTH(1-24) tests to assess functionality of the hypothalamic-pituitary-adrenal axis. (1/142)To analyse further the ACTH(1-24) low-dose test, which is of clinical interest, we have examined the dose-response relationship between plasma ACTH(1-24) and cortisol concentrations after i.v. administration of increasing doses (1, 5 or 250 microg) of ACTH(1-24) as a bolus. In addition, we have measured plasma ACTH(1-39) and cortisol levels after an insulin tolerance test (ITT). Although there was a dose response relationship between plasma ACTH(1-24) immunoreactivity and the dose injected, cortisol peaks were comparable, but lower than those reached after an ITT. Under these experimental conditions, an increase in plasma ACTH as low as 13 pmol/l (i.e. the increase obtained with the 1 microg dose) induced a near maximal cortisol response. Following injection of 1 microg ACTH(1-24), peak ACTH values were short lasting, similar to physiological daily bursts. After injection of 5 microg ACTH(1-24), plasma ACTH concentrations were higher than those reached during an ITT, but clearly shorter lasting. Injection of 250 microg ACTH(1-24) induced strikingly supraphysiological levels of plasma ACTH. We conclude that neither regular nor low-dose ACTH tests can fully reproduce the ITT. Our observations strongly suggest that the low-dose ACTH(1-24) test (1 microg) can be useful to estimate the adrenal sensitivity under basal, physiological conditions. (+info)
Tests of adrenal insufficiency. (2/142)AIM: In suspected adrenal insufficiency, the ideal test for assessing the hypothalamo-pituitary-adrenal axis is controversial. Therefore, three tests were compared in patients presenting with symptoms suggestive of adrenal insufficiency. METHOD: Responses to the standard short Synacthen test (SSST), the low dose Synacthen test (LDST), and the 08:00 hour serum cortisol concentration were measured in 32 patients. A normal response to the synacthen test was defined as a peak serum cortisol of >/= 500 nmol/l and/or incremental concentration of >/= 200 nmol/l. The sensitivity and specificity of the 08:00 hour serum cortisol concentration compared with other tests was calculated. RESULTS: Three patients had neither an adequate peak nor increment after the SSST and LDST. All had a serum 08:00 hour cortisol concentration of < 200 nmol/l. Eight patients had abnormal responses by both criteria to the LDST but had normal responses to the SSST. Three reported amelioration of their symptoms on hydrocortisone replacement. Twenty one patients had a normal response to both tests (of these, 14 achieved adequate peak and increment after both tests and seven did not have an adequate peak after the LDST but had a normal increment). The lowest 08:00 hour serum cortisol concentration above which patients achieved normal responses to both the LDST and SSST was 500 nmol/l. At this cut off value (compared with the LDST), the serum 08:00 hour cortisol concentration had a sensitivity of 100% but specificity was only 33%. CONCLUSION: The LDST revealed mild degrees of adrenal insufficiency not detected by the SSST. The value of a single 08:00 hour serum cortisol concentration is limited. (+info)
Regression of cardiac abnormalities after replacement therapy in Addison's disease. (3/142)OBJECTIVE: To evaluate by echocardiography the cardiac structure and function in patients with primary adrenocortical insufficiency. DESIGN AND METHODS: Two-dimensionally guided M-mode echocardiograms and spectral Doppler studies were performed in seven consecutive patients with newly diagnosed autoimmune primary adrenal failure before and 4-8 months after an adequate regimen of steroid substitution. Echocardiographic parameters were also studied in ten healthy controls. RESULTS: In the cases with untreated Addison's disease, both left ventricular end-systolic and end-diastolic dimensions were significantly reduced in comparison with those in controls (P<0.01). Four patients had echocardiographic signs of mitral valve prolapse (MVP) at the anterior leaflet, with no evidence of mitral regurgitation by Doppler echocardiography. Systolic clicks characteristic of MVP were present on auscultation in two of these cases. Left ventricular chamber size normalized, i.e. significantly increased (P<0.01), and both echocardiographic and physical signs of MVP resolved after steroid substitution in all patients. All other echocardiographic indices were normal before and after treatment. CONCLUSIONS: Patients with untreated Addison's disease have cardiac abnormalities which regress after steroid substitution. A valvular-ventricular disproportion due to the hypovolemic state could explain these findings. (+info)
Adrenocortical response profiles to corticotrophin-releasing hormone and adrenocorticotrophin challenge in the chronically catheterized adult guinea-pig. (4/142)The guinea-pig has been used extensively to investigate adrenal steroidogenesis. However, very little is known about adrenocortical responses to corticotrophin-releasing hormone (CRH) and adrenocorticotrophin (ACTH) in this species, in vivo. In the present study, we have developed a stress-free sampling system, in the chronically catheterized adult guinea-pig, that has allowed us to investigate basal and activated adrenocortical activity. Indwelling carotid artery and jugular vein catheters were surgically implanted into female guinea-pigs (n = 5). Each animal was treated with vehicle, human CRH (0.2 or 2 microg kg-1) and ACTH1-24 (0.2 or 2 microg kg-1), and serial plasma samples removed for analysis of ACTH and cortisol concentrations by radioimmunoassay. There was no effect of serial sampling on pituitary-adrenocortical activity, indicating that the animals remain in an unstressed state. Basal plasma ACTH and cortisol concentrations were 703.9 +/- 24.5 pg ml-1 and 117.9 +/- 5.2 ng ml-1, respectively. Both CRH and ACTH significantly increased adrenocortical activity in a dose-dependent manner. ACTH (2 microg kg-1) was the most potent activator leading to plasma cortisol concentrations of 647 +/- 116 ng ml-1. In conclusion, we have shown that basal plasma cortisol concentrations in the guinea-pig are low compared to those obtained in previous studies by cardiac puncture or following decapitation. However, plasma ACTH concentrations are high compared to other species. We have also shown that human CRH and ACTH1-24 act as potent activators of the guinea-pig pituitary-adrenocortical axis, leading to response profiles consistent with mild cortisol resistance. (+info)
Effect of adrenocorticotrophic hormone on sodium appetite in mice. (5/142)A main vector of the effects of stress is secretion of corticotrophin releasing factor (CRF), adrenocorticotrophin (ACTH), and adrenal steroids. Systemic administration of ACTH (2.8 microgram/day sc) for 7 days in BALB/c mice caused a very large increase of voluntary intake of 0.3 M NaCl equivalent to turnover of total body sodium content each day. Intracerebroventricular infusion of ACTH (20 ng/day) had no effect. Intracerebroventricular infusion of ovine CRF (10 ng/h for 7 days) caused an increase of sodium intake. The large sodium appetite-stimulating effect of systemic ACTH was not influenced by concurrent systemic infusion of captopril (2 mg/day). Induction of stress by immobilization of mice on a running wheel caused an increase in Na appetite associated with a 50% decrease of thymus weight, indicative of corticosteroid effects. The present data suggest that stress and the hormone cascade initiated by stress evoke a large sodium appetite in mice, which may be an important survival mechanism in environmental conditions causing stress. (+info)
Evidence that melanocortin 4 receptor mediates hemorrhagic shock reversal caused by melanocortin peptides. (6/142)Melanocortin peptides are known to be extremely potent in causing the sustained reversal of different shock conditions, both in experimental animals and humans; the mechanism of action includes an essential brain loop. Three melanocortin receptor subtypes are expressed in brain tissue: MC(3), MC(4,) and MC(5) receptors. In a volume-controlled model of hemorrhagic shock in anesthetized rats, invariably causing the death of control animals within 30 min after saline injection, the i.v. bolus administration of the adrenocorticotropin fragment 1-24 (agonist at MC(4) and MC(5) receptors) at a dose of 160 microg/kg i.v. (54 nmol/kg) produced an almost complete and sustained restoration of cardiovascular and respiratory functions. An equimolar dose of gamma(1)-melanocyte stimulating hormone (selective agonist at MC(3) receptors) was completely ineffective. The selective antagonist at MC(4) receptors, HS014, although having no influence on cardiovascular and respiratory functions per se, dose-dependently prevented the antishock activity of adrenocorticotropin fragment 1-24, with the effect being complete either at the i.v. dose of 200 microg/kg or at the i.c.v. dose of 5 microg/rat (17-20 microg/kg). We concluded that the effect of melanocortin peptides in hemorrhagic shock is mediated by the MC(4) receptors in the brain. (+info)
Effect of leptin on ACTH-stimulated secretion of cortisol in rhesus macaques and on human adrenal carcinoma cells. (7/142)OBJECTIVE: Because glucocorticoids stimulate leptin release and, at least in vitro, leptin inhibits cortisol secretion, a feedback system between glucocorticoids and leptin has been proposed. However, in humans and non-human primates there are no in vivo studies to support any role for leptin in the control of the hypothalamic-pituitary-adrenal axis. In this study, we investigated the effect of leptin on (i) ACTH-stimulated secretion of cortisol in six male rhesus monkeys and (ii) basal and forskolin (FSK)-stimulated cortisol secretion by the human adrenal carcinoma cell H295R in vitro. DESIGN AND METHODS: In vivo studies: after suppression of endogenous ACTH with either dexamethasone (n=6) or a corticotropin-releasing factor (CRF) antagonist (d-Phe CRF(12-41)) (n=3), 1 microg bolus of human ACTH(1-24) was administered to stimulate adrenal cortisol release. Blood samples were collected every 15 min for 3 h. Leptin (1 mg) was infused over 4 h, starting 1 h before ACTH bolus. IN VITRO STUDIES: NCI-H295R cells were incubated for 6, 12, 24 and 48 h in the absence or presence of 20 micromol/l FSK in combination with leptin (100 ng/ml medium). Cortisol levels in serum and medium were measured by solid phase radioimmunoassay. RESULTS: Acute leptin infusion to rhesus monkeys did not change basal cortisol levels, peak cortisol levels after ACTH(1-24) or the area under the curve when compared with studies in which leptin was not given. FSK increased cortisol levels in medium at 24 and 48 h, but leptin did not change cortisol release in either control or FSK-stimulated cells. CONCLUSIONS: Short-term leptin infusion affected neither the cortisol response to ACTH in non-human primates in vivo nor cortisol release (basal or FSK stimulated) by H295R cells, in vitro. These data suggest that leptin may not be an acute regulator of primate adrenal cortisol secretion. (+info)
Isolated corticotropin deficiency in chronic alcoholism. (8/142)Three patients who chronically abused alcohol were found to be hyponatraemic with normal plasma potassium. The first had been admitted with confusion and weight loss, the second with hypotension and sepsis, and the third with confusion and hypoglycaemia-induced seizures. All three patients had a subnormal cortisol response in the short synacthen test; however, the plasma cortisol after three days of tetracosactrin administration was greater than 550 nmol/L. Baseline corticotropin levels were less than 10 pg/mL in all three. No structural lesions of the hypothalamo-pituitary tract were found and there was no evidence of other endocrinopathies. Glucocorticoid replacement therapy led to the resolution of hyponatraemia and hypoglycaemia, where present, and to clinical improvement. The two surviving patients remained hypocortisolaemic in the long term, without recurrence of hyponatraemia or hypoglycaemia. The features of isolated corticotropin deficiency are easily confused with other effects of chronic alcohol abuse. In alcoholic patients with unexplained hyponatraemia, hypoglycaemia or haemodynamic instability, a short tetracosactrin test is advisable. (+info)
Primary adrenal insufficiency, also known as Addison's disease, is a rare condition where the adrenal glands are damaged or destroyed, leading to a decrease in cortisol and aldosterone production. This can be caused by autoimmune disorders, genetic defects, or viral infections.
Secondary adrenal insufficiency is more common and occurs when the pituitary gland, located at the base of the brain, does not produce enough adrenocorticotropic hormone (ACTH), which stimulates the adrenal glands to produce cortisol and aldosterone. This can be caused by a variety of factors, including hypothyroidism, hyperthyroidism, and pituitary tumors.
Adrenal insufficiency can cause a range of symptoms, including fatigue, weight loss, muscle weakness, and low blood pressure. Treatment typically involves hormone replacement therapy with cortisol and aldosterone supplements, as well as addressing any underlying causes of the condition.
In summary, adrenal insufficiency is a condition where the adrenal glands do not produce enough cortisol and aldosterone hormones, leading to a range of symptoms and potential complications. It can be classified into primary and secondary types, and treatment involves hormone replacement therapy and addressing any underlying causes.
Post-dural puncture headaches are usually characterized by a severe, throbbing pain that is often worse when standing up or bending forward. They can also be accompanied by nausea, vomiting, and sensitivity to light and sound. In some cases, the headache may be accompanied by a feeling of stiffness in the neck or back.
The symptoms of a post-dural puncture headache typically begin within 24 hours of the procedure and can last for several days. Treatment for this type of headache usually involves medication, such as pain relievers or anti-inflammatory drugs, and fluid replacement to help restore the balance of CSF in the body. In severe cases, a blood patch may be necessary to seal the puncture site and prevent further leakage of CSF.
There are two main types of Addison's disease: primary and secondary. Primary Addison's disease is caused by an autoimmune disorder that destroys the adrenal glands, while secondary Addison's disease is caused by a problem with the pituitary gland, which regulates the adrenal glands.
Symptoms of Addison's disease can include fatigue, weakness, weight loss, dehydration, and changes in skin color. Treatment involves replacing the missing hormones with medication and managing symptoms. If left untreated, Addison's disease can be life-threatening.
Specialists who may be involved in treating Addison's disease include endocrinologists, primary care physicians, and surgeons. Treatment options can include medication, hydration therapy, and in some cases, surgery to remove the affected adrenal gland(s).
It is important for individuals with Addison's disease to work closely with their healthcare team to manage their condition and avoid complications. With proper treatment and self-management, most people with Addison's disease can lead active and fulfilling lives.
Adrenocorticotropic hormone (medication)
ACTH stimulation test
Cerebrospinal fluid leak
Congenital adrenal hyperplasia due to 21-hydroxylase deficiency
List of MeSH codes (D06)
List of MeSH codes (D12.644)
Cosyntropin Injection0.25 mg/mL
MedlinePlus - Search Results for: Cosyntropin
COSYNTROPIN/TU - Search Results - PubMed
DailyMed - COSYNTROPIN injection, powder, for solution
ACTH stimulation test: MedlinePlus Medical Encyclopedia
Use of Intravenous Cosyntropin in the Treatment of Postdural Puncture Headache | Anesthesiology | American Society of...
Dr. Raghava Bhaskaran, MD - Family Medicine Specialist in Dublin, GA | Healthgrades
Cushing Syndrome: Signs, Causes, and Treatment
No items found - Books - NCBI
Multiple courses of betamethasone to enhance fetal lung maturation do not suppress neonatal adrenal response - PubMed
Publications - Theo Heller, M.D. - NIDDK
Diuril (chlorothiazide) dosing, indications, interactions, adverse effects, and more
MESH TREE NUMBER CHANGES - 2008 MeSH
DailyMed - HYDROCORTISONE BUTYRATE lotion
Managing Immunotherapy Side Effects in MBC
Efficacy and safety of triamcinolone acetonide aqueous nasal spray in children aged 2 to 5 years with perennial allergic...
RACGP - The short Synacthen test and laboratory assay inter-ference
Topical Steroid Use in Psoriasis Patient Leads to Severe Adrenal Insufficiency - MPR
Hypogonadism: Practice Essentials, Background, Pathophysiology
NIH Clinical Center Search the Studies: Study Number, Study Title
Hyperkalemia | AAFP
Ovarian Leydig Cell Hyperplasia: An Unusual Case of Virilization in a Postmenopausal Woman
National Ambulatory Medical Care Survey, 1994
Publikasjoner - Helse Bergen
- Cosyntropin is α 1-24 corticotropin, a synthetic subunit of ACTH. (nih.gov)
- Cosyntropin for injection exhibits the full corticosteroidogenic activity of natural ACTH. (nih.gov)
- The pharmacologic profile of cosyntropin for injection is similar to that of purified natural ACTH. (nih.gov)
- It has been established that 0.25 mg of cosyntropin will stimulate the adrenal cortex maximally and to the same extent as 25 units of natural ACTH. (nih.gov)
- The extra-adrenal effects which natural ACTH and cosyntropin for injection have in common include increased melanotropic activity, increased growth hormone secretion and an adipokinetic effect. (nih.gov)
- This property of cosyntropin for injection assumes added importance in view of the known antigenicity of natural ACTH. (nih.gov)
- Successful treatment was obtained by administering intravenous cosyntropin, a synthetic form of adrenocorticotropic hormone (ACTH). (silverchair.com)
- Patients are given an injection of a drug called "ACTH" or "cosyntropin," which is a version of a hormone normally produced by the pituitary gland. (nih.gov)
- La ACTH (1-24), un segmento similar en todas las especies, posee la actividad biológica, que estimula la producción CORTICOESTEROIDES en la CORTEZA SUPRARRENAL. (bvsalud.org)
- Safety measures included reports of adverse events, morning serum cortisol levels before and after cosyntropin infusion, and growth as measured using office stadiometry. (nih.gov)
- There was no significant change from baseline in serum cortisol levels after cosyntropin infusion at study end. (nih.gov)
- Cosyntropin for injection is a sterile lyophilized powder in vials containing 0.25 mg of cosyntropin and 10 mg of mannitol to be reconstituted with 1 mL of 0.9% Sodium Chloride Injection, USP. (nih.gov)
- This dose of cosyntropin for injection will produce maximal secretion of 17-OH corticosteroids, 17-ketosteroids and/or 17-ketogenic steroids. (nih.gov)
- Cosyntropin for injection is intended for use as a diagnostic agent in the screening of patients presumed to have adrenocortical insufficiency. (nih.gov)
- When presumptive adrenal insufficiency is diagnosed by a subnormal cosyntropin test, further studies are indicated to determine if it is primary or secondary. (nih.gov)
- There isn't any proof, however, that the response to pharmacological doses of cosyntropin has any physiological relevance to immunological function (537, 538). (suzumgerecleri.com)
- Fellows review advanced imaging studies such as nuclear imaging and pituitary MRIs and study the interpretation of dynamic testing such as cosyntropin stimulation and insulin tolerance testing. (wvu.edu)