cosyntropin and Acute-Disease

Adrenal insufficiency can result in significant patient morbidity and mortality, but due to the range of symptoms and variable clinical course and etiologies, it can be a challenging condition to diagnose and manage.. This narrative review will discuss the evaluation of an adult patient at risk for a new diagnosis of adrenal insufficiency and the management of a patient with known or suspected adrenal insufficiency.. A new presentation of adrenal insufficiency can range from nonspecific, minor symptoms including fatigue, to a life-threatening adrenal crisis with hemodynamic instability. Due to the variety of signs and symptoms, the diagnosis is often missed. Those with known adrenal insufficiency are at risk for adrenal crisis, which may occur due to a variety of triggers. Initial evaluation includes assessment for the underlying etiology or concomitant condition, laboratory analysis, and imaging, when clinically indicated. Although not necessary for evaluation in the emergency department setting, the diagnosis is confirmed by specific testing such as the cosyntropin stimulation test. The mainstay of treatment in adrenal crisis is hydrocortisone, intravenous fluid, glucose repletion, and treatment of the underlying acute trigger.. Emergency clinicians must be prepared to recognize, evaluate, and manage those with known or suspected adrenal insufficiency or adrenal crisis.

Topics: Acute Disease; Adrenal Insufficiency; Adult; Cosyntropin; Emergency Service, Hospital; Glucose; Humans; Hydrocortisone

Relative adrenal insufficiency is an increasingly documented phenomenon in acute illness. Recognizing and treating such adrenal insufficiency has the potential to improve outcome. A post-cosyntropin cortisol value greater than 20 microg/dl has been recognized as consistent with normal adrenal function. While the cosyntropin test remains a superb test of primary adrenal failure, its utilityin the diagnosis of secondary adrenal failure is less clearly defined. In the setting of acute illness, a number of other criteria such as increment from basal serum cortisol have been used; however, the criteria for establishing adrenal insufficiency remains less clearly defined. We report a 44-year-old Caucasian female who presented with hypoglycemia and hypotension. The patient had a basal cortisol of 1.6 ug/dl and a peak serum cortisol of 23.3 ug/dl after 250 ug of cosyntropin. Despite this apparent normal response to cosyntropin, the patient responded to glucocorticoids with an improvement in her clinical status. Pituitary MRI revealed a 7-mm pituitary cyst. Pending the availability of free cortisol levels, it is prudent not to disregard low basal cortisol levels, even in the presence of a normal cosyntropin response. We recommend that clinicians managing acutely ill patients have a low threshold for initiating glucocorticoid replacement in the presence of hypoglycemia and shock regardless of the peak cortisol values.

Topics: Acute Disease; Adrenal Cortex Function Tests; Adrenal Insufficiency; Adult; Cosyntropin; Female; Hormones; Humans; Hydrocortisone

Topics: Acute Disease; Adrenal Cortex; Adrenal Insufficiency; Adrenalectomy; Chronic Disease; Cosyntropin; Delayed-Action Preparations; Hormones; Humans; Hydrocortisone; Prognosis

Topics: Acute Disease; Adrenal Cortex Hormones; Adrenal Insufficiency; Cosyntropin; Critical Illness; Glucocorticoids; Humans; Hydrocortisone; Hypothalamo-Hypophyseal System; Pituitary-Adrenal System; Shock, Septic

Mometasone furoate nasal spray (MFNS) 400 microg, twice daily, as adjunctive treatment with oral antibiotic significantly improved symptoms of recurrent rhinosinusitis.. To evaluate the effectiveness and safety of MFNS 200 microg, twice daily, and 400 microg, twice daily, compared with placebo as adjunctive treatment with oral antibiotic for acute rhinosinusitis.. In this multicenter, double-blind, placebo-controlled study, 967 outpatients with computed tomographic scan-confirmed moderate to severe rhinosinusitis received amoxicillin/clavulanate potassium (Augmentin, GlaxoSmithKline, Research Triangle Park, NC) 875 mg, twice daily, for 21 days with adjunctive twice daily MFNS 200 microg, MFNS 400 microg, or placebo nasal spray. Patients recorded scores of six rhinosinusitis symptoms and any adverse events twice daily. Pre- and postcosyntropin-stimulation plasma cortisol levels were measured in a subset of patients at selected study sites.. Treatment with MFNS 200 microg or 400 microg, twice daily, produced significantly greater improvements in total symptoms score (primary efficacy variable) day 1 to day 15 average (50% and 51%, respectively) than placebo (44%, P < or = 0.017). Both doses of MFNS produced significant total symptoms score improvement over placebo by day 4, and maintained efficacy over the entire 21-day study. Relief of individual symptoms showed a similar pattern. Both doses of MFNS were well tolerated, and adverse events were similar to that of placebo. Cosyntropin stimulation showed no evidence of hypothalamic-pituitary-adrenal axis suppression.. As adjunctive therapy to oral antibiotic treatment, MFNS at doses of 200 microg or 400 microg, twice daily, was well tolerated and significantly more effective in reducing the symptoms of rhinosinusitis than antibiotic therapy alone.

Topics: Acute Disease; Administration, Intranasal; Adolescent; Adult; Aerosols; Aged; Anti-Inflammatory Agents; Child; Cosyntropin; Dose-Response Relationship, Drug; Double-Blind Method; Drug Therapy, Combination; Female; Humans; Hydrocortisone; Male; Middle Aged; Mometasone Furoate; Pregnadienediols; Sinusitis; Treatment Outcome

Topics: Acute Disease; Adrenal Insufficiency; Cosyntropin; Humans; Hydrocortisone

This study investigated the significance of baseline cortisol levels and adrenal response to corticotropin in shocked patients after acute myocardial infarction (AMI).. A short corticotropin stimulation test was performed in 35 patients with cardiogenic shock after AMI by intravenously injecting of 250 μg of tetracosactrin (Synacthen). Blood samples were obtained at baseline (T0) before and at 30 (T30) and 60 (T60) minutes after the test to determine plasma total cortisol (TC) and free cortisol concentrations. The main outcome measure was in-hospital mortality and its association with T0 TC and maximum response to corticotropin (maximum difference [Δ max] in cortisol levels between T0 and the highest value between T30 and T60).. The in-hospital mortality was 37%, and the median time to death was 4 days (interquartile range, 3-9 days). There was some evidence of an increased mortality in patients with T0 TC concentrations greater than 34 μg/dL (P=.07). Maximum difference by itself was not an independent predictor of death. Patients with a T0 TC 34 μg/dL or less and Δ max greater than 9 μg/dL appeared to have the most favorable survival (91%) when compared with the other 2 groups: T0 34 μg/dL or less and Δ max 9 μg/dL or less or T0 34 μg/dL or higher and Δ max greater than 9 μg/dL (75%; P=.8) and T0 greater than 34 μg/dL and Δ max 9 μg/dL or less (60%; P=.02). Corticosteroid therapy was associated with an increased mortality (P=.03). There was a strong correlation between plasma TC and free cortisol (r=0.85).. A high baseline plasma TC was associated with a trend toward increased mortality in patients with cardiogenic shock post-AMI. Patients with lower baseline TC, but with an inducible adrenal response, appeared to have a survival benefit. A prognostic system based on basal TC and Δ max similar to that described in septic shock appears feasible in this cohort. Corticosteroid therapy was associated with adverse outcomes. These findings require further validation in larger studies.

Topics: Acute Disease; Adrenal Insufficiency; Aged; Biomarkers; Cosyntropin; Female; Hormones; Hospital Mortality; Humans; Hydrocortisone; Injections, Intravenous; Male; Middle Aged; Myocardial Infarction; Pilot Projects; Prognosis; Prospective Studies; Shock, Cardiogenic; Shock, Septic; Time Factors

Acute adrenal insufficiency in the trauma patient is underrecognized and the impact poorly understood. Our hypothesis was that the identification and treatment of acute adrenal insufficiency reduces mortality in trauma patients. Institutional Review Board approval for the retrospective review of a prospective database from a Level 1 trauma center for 2002 to 2004 was obtained. The study population included patients receiving a cosyntropin stimulation test (250 microg) and/or random cortisol level based on our practice management guideline and an intensive care unit stay longer than 24 hours. Demographic, acuity, and outcome data were collected. The nonresponders had baseline cortisol levels less than 20 microg/dL or poststimulation rise less than 9 microg/dL. Independent t tests and chi2 statistics were used. One hundred thirty-seven patients had cosyntropin stimulation tests performed. Eighty-two (60%) patients were nonresponders of which 66 were treated with hydrocortisone and 16 went untreated as a result of the discretion of the attending physician. The 55 (40%) responders showed no statistical differences in outcome variables whether or not they received hydrocortisone. The untreated adrenal-insufficient patients had significantly higher mortality, longer hospital length of stay, intensive care unit days, and ventilator-free days. Conclusions were: (1) treatment of acute adrenal insufficiency reduces mortality by almost 50 per cent in the trauma patient; and (2) acute adrenal insufficiency recognized by low random cortisol levels or nonresponse to a stimulation tests should be considered for treatment.

Topics: Acute Disease; Adrenal Insufficiency; Adult; Cosyntropin; Drug Therapy, Combination; Glucocorticoids; Hormones; Humans; Hydrocortisone; Length of Stay; Middle Aged; Prevalence; Prospective Studies; Survival Rate; Trauma Centers; Trauma Severity Indices; Treatment Outcome; United States; Wounds and Injuries

In order to identify whether low-dose (1 microg) tetracosactide (Synacthen) testing may be preferable to high-dose (250 microg) testing in the diagnosis of adrenal insufficiency in traumatic brain injury (TBI), as suggested by studies in other forms of critical illness.. We retrospectively reviewed the results of modified tetracosactide tests (involving administration of both low-dose and high-dose tetracosactide) conducted for clinical indications in patients in a neurocritical care unit within 10 days of TBI. Sixty-three modified tests were included and cortisol concentrations before and after administration of tetracosactide were extracted from the hospital records. Data were also extracted regarding hemodynamic response to empirical corticosteroid therapy, based on rapid weaning from vasoactive drugs.. Cortisol increments at 30 and 60 min following tetracosactide correlated well in the low-dose test (r(2) = 0.875, P < 0.0001). The mean cortisol concentration was 581 nmol/l at 30 min and 556 nmol/l at 60 min in the low-dose test. Cortisol increments following low-dose and high-dose testing correlated well overall (r(2) = 0.839, P < 0.0001), but results were discordant in 27 of 63 cases (43%) when the same diagnostic threshold was used. ROC curve analysis showed that both tests performed poorly in identifying hemodynamic steroid responsiveness (AUC 0.553 and 0.502, respectively).. In the low-dose tetracosactide test, it is sufficient to determine cortisol concentrations at baseline and at 30 min. Low-dose and high-dose tests give discordant results in a significant proportion of cases when using the same diagnostic threshold. Neither test can be used to guide the initiation of corticosteroid therapy in acute TBI.

Topics: Acute Disease; Adrenal Cortex Hormones; Adrenal Insufficiency; Adrenocorticotropic Hormone; Adult; Aged; Brain Injuries; Cosyntropin; Delayed-Action Preparations; Dose-Response Relationship, Drug; Female; Hemodynamics; Humans; Hydrocortisone; Kinetics; Male; Middle Aged; Predictive Value of Tests; Retrospective Studies; ROC Curve; Sensitivity and Specificity; Young Adult

The hypothalamic-pituitary-adrenal axis is an important part of the body's natural response to acute illness. Adrenal insufficiency has the potential to lead to hemodynamic instability and electrolyte imbalances, limit the body's ability to respond to stress, and worsen overall clinical outcome. In this case series, we describe 16 patients evaluated for acute adrenal insufficiency after aneurysmal subarachnoid hemorrhage.. Over a 2-year period, the medical records of 16 patients admitted to the adult neurosurgery service for aneurysmal subarachnoid hemorrhage who were nonresponsive to vasopressor therapy and received cosyntropin for the evaluation of adrenal insufficiency within 14 days of their event were reviewed.. The median baseline cortisol in this population was 22.5 microg/dL, with a poststimulation cortisol level of 31 microg/dL. Of the population surveyed, a total of 11 patients met the preestablished criteria for adrenal insufficiency, 3 with baseline cortisol levels of less than 15 microg/dL and 11 with poststimulation concentration changes of less than 9 microg/dL. Baseline serum cortisol concentrations were significantly correlated with hospital stay (P = 0.045), intensive care unit stay (P = 0.005), and ventilator days (P = 0.006).. To date, this is the only investigation evaluating the incidence of acute relative adrenal insufficiency in this population. In our cohort, 69% of the patients met the preestablished criteria for relative adrenal insufficiency. The impact of low-dose corticosteroid therapy in this population also needs review, as it could have significant implications for the management of cerebral vasospasm.

Topics: Acute Disease; Adrenal Cortex Hormones; Adrenal Insufficiency; Adult; Aged; Aged, 80 and over; Comorbidity; Cosyntropin; Female; Hospital Mortality; Humans; Hydrocortisone; Incidence; Intracranial Pressure; Length of Stay; Male; Middle Aged; Retrospective Studies; Severity of Illness Index; Subarachnoid Hemorrhage; Treatment Outcome

Several melanocortin peptides have a prompt and sustained resuscitating effect in conditions of hemorrhagic shock. The transcription nuclear factor kappaB (NF-kappaB) triggers a potentially lethal systemic inflammatory response, with marked production of tumor necrosis factor-alpha (TNF-alpha), in hemorrhagic shock. Here we investigated whether the hemorrhagic shock reversal produced by the melanocortin ACTH-(1-24) (adrenocorticotropin) depends on the activation of the recently recognized, vagus nerve-mediated, brain "cholinergic anti-inflammatory pathway".. Anesthetized rats were stepwise bled until mean arterial pressure (MAP) stabilized at 20-25 mm Hg. The severe hypovolemia was incompatible with survival, and all saline-treated animals died within 30 min. In rats intravenously (i.v.) treated with ACTH-(1-24), neural efferent activity along vagus nerve (monitored by means of a standard system for extracellular recordings) was markedly increased, and the restoration of cardiovascular and respiratory functions was associated with blunted NF-kappaB activity and with decreased TNF-alpha mRNA liver content and TNF-alpha plasma levels. Bilateral cervical vagotomy, pretreatment with the melanocortin MC(4) receptor antagonist HS014, atropine sulfate or chlorisondamine, but not with atropine methylbromide, prevented the life-saving effect of ACTH-(1-24) and the associated effects on NF-kappaB activity and TNF-alpha levels. HS014 and atropine sulfate prevented, too, the ACTH-(1-24)-induced increase in neural efferent vagal activity, and accelerated the evolution of shock in saline-treated rats.. The present data show, for the first time, that the melanocortin ACTH-(1-24) suppresses the NF-kappaB-dependent systemic inflammatory response triggered by hemorrhage, and reverses shock condition, by brain activation (in real-time) of the "cholinergic anti-inflammatory pathway", this pathway seeming to be melanocortin-dependent.

Topics: Acute Disease; Animals; Atropine; Chlorisondamine; Cosyntropin; Electrophoretic Mobility Shift Assay; Female; I-kappa B Proteins; Liver; Male; NF-kappa B; Rats; Rats, Wistar; Receptors, Nicotinic; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Shock, Hemorrhagic; Tumor Necrosis Factor-alpha; Vagus Nerve

Cisplatin 5 mg/kg, i.p., induced an acute (day 1) and delayed (days 2 and 3) emetic response in the ferret that was used to investigate the potential anti-emetic activity of metyrapone and tetracosactrin and their potential interaction. The 11beta-hydroxylase enzymes inhibitor metyrapone 10-30 mg/kg, i.p., dose dependently potentiated the acute cisplatin-induce retching+vomiting response by up to 219% at the highest dose (P<0.001) but failed to affect significantly delayed emesis (P>0.05). The adrenocorticotropic hormone (ACTH) mimetic tetracosactrin 0.1 mg/kg, i.m., antagonised significantly the acute and delayed emetic response by 98% (P<0.01) and 75% (P<0.001), respectively. The anti-emetic action of tetracosactrin on acute but not delayed emesis was prevented by combination with metyrapone 10 mg/kg, i.p. Tetracosactrin 0.1 mg/kg, i.m., failed to modify apomorphine (0.25 mg/kg, s.c.)-induced emesis. The potential anti-emetic mechanism of action of metyrapone and tetracosactrin to modulate emesis is discussed.

Topics: Acute Disease; Animals; Antiemetics; Antineoplastic Agents; Apomorphine; Cisplatin; Cosyntropin; Ferrets; Injections, Intramuscular; Injections, Intraperitoneal; Injections, Subcutaneous; Male; Metyrapone; Steroid 11-beta-Hydroxylase; Time Factors; Vomiting

Addison's disease may present with diverse and non-specific clinical and biochemical features. Contentious issues include the appropriate criteria for the interpretation of the ACTH stimulation test and the necessary extent of investigation to identify a specific aetiology for the hypoadrenalism. The experience of Addison's disease at a South African teaching hospital was reviewed to (1) record the aetiology and spectrum of presentation, (2) examine the performance of the ACTH stimulation test and (3) determine the utility of adrenal CT scan and biopsy.. Retrospective study of patients admitted to a South African teaching hospital from 1980 to 1997 with a diagnosis of acute Addison's disease.. Fifty patients presenting with acute Addison's disease were identified by a search of hospital records. Pretreatment biochemical and haematological parameters were recorded. The cortisol response at 20 and 60 min to an intravenous injection of 250 micrograms synacthen (Cortrosyn) was analysed. In a subgroup of affected subjects, the bone mineral density (BMD) in the lumbar spine and femoral neck was measured during long-term follow-up.. Presenting features included hyperpigmentation (86%), weight loss (67%), abdominal pain (20%) and diarrhoea (16%). Thirty-nine patients (78%) were hyponatraemic, while 26 (53%) were hyperkalaemic. Nine patients (18%) were hypoglycaemic and 21% had hypercalcaemia. The mean basal cortisol was 148 nmol/l (range 10-487) and 16 patients (40%) had a normal basal cortisol. The mean cortisol 20 min after ACTH stimulation was 172 nmol/l (range 19-588). There was no significant increase in serum cortisol following ACTH stimulation (P > 0.05). Adrenal CT scans were performed in only 24 patients (48%) and were normal in 10, while abnormalities were detected in 14 patients (bilateral enlargement in 11, calcification in two and atrophic adrenals in one). Eight patients had a DEXA scan performed during follow-up--four were osteopaenic in the lumbar spine and five at the femoral neck. The probable aetiology of Addison's was idiopathic in 42%, related to active TB in 18%, old TB in 16%, autoimmune in 12% and malignancy with metastases in 6%--single cases were due to sarcoid, iron overload and adrenoleukodystrophy. Adrenal biopsy was performed in two patients and was diagnostic of malignancy in both cases. The mortality within the first month after hospitalization was 12%.. In our experience, Addison's disease is frequently idiopathic, presents with protean manifestations and should be considered in patients with unexplained hyperpigmentation or gastrointestinal complaints, particularly when associated with hyponatraemia and hyperkalaemia. A normal basal cortisol does not exclude the diagnosis which requires ACTH stimulation testing.

Topics: Abdominal Pain; Acute Disease; Addison Disease; Adolescent; Adult; Aged; Bone Density; Child; Cosyntropin; Diarrhea; Female; Follow-Up Studies; Hospitals, Teaching; Humans; Hydrocortisone; Hyperpigmentation; Male; Middle Aged; Retrospective Studies; South Africa

Adrenal function in stable asthmatics has been extensively studied. The purpose of this study was to determine the effect of asthma exacerbation on adrenal function.. We studied an observational cohort, convenience sample of patients at a university-affiliated county hospital. Adult patients with asthma who were not steroid-dependent and who presented to the emergency department because of their asthma comprised the study group. All patients were examined and pulmonary function tests were performed. Blood samples for determination of initial cortisol levels were obtained, followed by the administration of .25 mg cosyntropin intramuscularly. Standard therapy with aerosolized albuterol was then initiated. Plasma cortisol levels were measured 30 and 60 minutes later. Steroid therapy was withheld until completion of the rapid cosyntropin stimulation test.. A total of 74 patients participated; 64% (47) were women. The range of pretreatment FEV1 was from 10% predicted to 74% predicted. The range of cortisol levels on presentation was from 1.6 micrograms/dL to 35.8 micrograms/dL. Twelve patients had initial cortisol levels greater than 20 micrograms/dL, a level indicative of physiologic stress. Four patients had initial cortisol levels greater than 30 micrograms/dL. Mean plasma cortisol levels at 0, 30, and 60 minutes were 13.7 micrograms/dL (+/- 7.2 micrograms/dL), 28.7 micrograms/dL (+/- 7.4 micrograms/dL), and 33.0 micrograms/dL (+/- 8.2 micrograms/dL). We found an association between evidence of physiologic stress and severe airflow obstruction (P < .03) but no linear correlation (r = -.15).. Few patients with asthma have adrenal suppression on presentation. Asthma exacerbation does not provoke a physiologic stressor response in most asthmatic patients.

Topics: Acute Disease; Adrenal Glands; Adult; Albuterol; Asthma; Bronchodilator Agents; Cosyntropin; Emergency Service, Hospital; Female; Forced Expiratory Volume; Humans; Hydrocortisone; Male; Middle Aged; Patient Admission; Sampling Studies; Severity of Illness Index; Stress, Physiological

The adrenal glands may be involved in tuberculosis. The exact frequency and extent of adrenal involvement in tuberculosis are not well known. Although there are some studies regarding adrenal gland involvement, they are not sufficient because of inadequate endocrinological tests and radiological procedures. The aim of this study was to assess the adrenal gland in acute and chronic pulmonary tuberculosis and to compare it with the findings obtained in healthy subjects.. We studied 20 patients with acute pulmonary tuberculosis, 41 patients with chronic pulmonary tuberculosis and 20 healthy subjects. Involvement of the adrenal gland was assessed by basal cortisol level, cortisol response to Synacthen and adrenal computed tomography.. Cortisol levels were measured before, 30 and 60 minutes after Synacthen (250 micrograms i.v.) injection. Computerized tomography of the adrenals was carried out in 61 patients with tuberculosis and 20 healthy subjects.. Mean basal cortisol level and 60-minute cortisol response to Synacthen were significantly higher in acute pulmonary tuberculosis than in chronic pulmonary tuberculosis and healthy subjects. Two patients with Addison's disease were diagnosed among the chronic tuberculous patients. Both length and thickness of the right and left adrenal gland were greater in patients with acute tuberculosis.. Adrenal enlargement demonstrated by computerized tomography is common in patients with acute pulmonary tuberculosis, but our findings show that cortisol reserve is normal, in contrast to previous suggestions.

Topics: Acute Disease; Adolescent; Adrenal Glands; Adult; Aged; Chronic Disease; Cosyntropin; Female; Humans; Hydrocortisone; Male; Middle Aged; Prospective Studies; Tomography, X-Ray Computed; Tuberculosis, Pulmonary

We wished to define the cortisol response to 250 micrograms intramuscular tetracosactrin (Synacthen) in acute hospital admissions, using a modern immunoassay for cortisol.. We performed a prospective study of, as near as possible, a consecutive series of 161 admissions to a single unit.. We studied 50 patients (age range 67-98, mean 80.3 years, 31-female, 19-male) admitted as an emergency, from whom it was possible to obtain informed consent, and whom it was possible to study within 24 hours of admission.. We measured baseline, increment and peak serum cortisol following administration of 250 micrograms intramuscular tetracosactrin between 0800 and 0900 hours.. Baseline cortisol concentrations ranged from 288 to 1585 nmol/l (mean 706; median 665). Peak cortisol concentrations ranged from 602 to 2265 nmol/l (mean 1076; median 999). Baseline and peak cortisol concentrations showed a significant correlation (P less than 0.001). Increment varied from 10 to 747 nmol/l (mean 374; median 336) and did not correlate with baseline.. In acute hospital admissions, baseline serum cortisol between 0800 and 0900 hours should exceed 250 nmol/l. Peak serum cortisol after 250 micrograms intramuscular tetracosactrin should exceed 600 nmol/l. Calculation of the increment is of no value.

Topics: Acute Disease; Adrenal Cortex; Aged; Aged, 80 and over; Cosyntropin; Dehydration; Emergencies; Female; Hospitalization; Humans; Hydrocortisone; Immunoassay; Male; Patient Admission; Prospective Studies

To evaluate the effect of topical hydrocortisone therapy on cortisol secretion, the plasma cortisol response to a 2 h adrenocorticotropic hormone (ACTH) test was determined in 17 children with dermatitis. Percutaneous absorption of hydrocortisone was measured in the acute phase of dermatitis by a 4 h absorption test. Two-hour plasma cortisol in the ACTH test correlated inversely with the increment of plasma cortisol in the absorption test. The duration of topical hydrocortisone therapy had no significant influence on the adrenocortical response to ACTH. A moderately or severely subnormal 2 h plasma cortisol level was observed in three infants after 3-5 months' topical therapy with hydrocortisone.

Topics: Acute Disease; Administration, Topical; Adolescent; Child; Child, Preschool; Cosyntropin; Dermatitis; Female; Humans; Hydrocortisone; Infant; Male; Skin Absorption

Topics: Acute Disease; Adrenocorticotropic Hormone; Aged; Blood Volume; Coronary Artery Bypass; Cosyntropin; Humans; Hypotension; Male; Shock, Hemorrhagic

The release of glucocorticosteroids and aldosterone rapidly decreased after start of superfusion and reached a steady base-line within 60-90 min of superfusion. While secretion markedly varied between experiments, it was very constant in the same experiment (coefficient of variation: 7.4-2.2% for glucocorticosteroids and 5.8-3.9% for aldosterone). After repeated exposure of adrenal tissue to 1 IU/ml (1-24)ACTH, glucocorticosteroid release progressively increased; under the same conditions aldosterone secretion was not changed. Glucocorticosteroid secretion from glands of animals stressed by 1-hr confinement or of animals injected with 6 IU (1-24)ACTH was significantly higher than that of controls over the 60-min superfusion period. Aldosterone secretion was not affected significantly by these pretreatments. After reduction of temperature from 35 to 1 degrees C, steroid release ceased. Elevation of temperature from 12 to 32 degrees C resulted in a linear increase of glucocorticosteroid and aldosterone secretion. A highly significant positive correlation was found between glucocorticosteroid and aldosterone amounts secreted from adrenals superfused at temperatures between 1 and 35 degrees C (r = 0.91, n = 116, P less than 0.0001). Changes of flow rate from 0.5 to 1.5 ml/min for 5 min induced a short term (1 min) stimulation of glucocorticosteroid and aldosterone release; reduction of flow rate to 0.5 ml/min for 5 min drastically diminished secretion of steroids below control levels for 1 min.

Topics: Acute Disease; Adrenal Cortex; Adrenocorticotropic Hormone; Aldosterone; Animals; Cosyntropin; Gerbillinae; Glucocorticoids; In Vitro Techniques; Stress, Physiological; Temperature

Adrenocortical function was assessed by the intravenous short synacthen test in 22 control subjects and 68 patients admitted to hospital with acute severe asthma. The cortisol increment was subnormal in 19 of the 68 asthmatics. This included 11 of the 14 patients on continuous oral steroids, seven of the 29 patients who had had occasional courses of oral steroids, one of the seven on inhaled steroids only, and none of the 18 who had had no steroids. Adrenal suppression was greatest in those patients taking oral steroids in divided daily doses. Nineteen of 43 patients were on or had taken oral steroids in this fashion. Of those 19 patients with low cortisol increments only one half had received supplementary steroids in the 24 hours preceding admission. Based on the synacthen test, serum DHEA-SO4 values were not a good discriminant of adrenocortical function. Adrenal insufficiency may be an important cause of death in acute severe asthma in New Zealand.

Topics: Acute Disease; Adolescent; Adrenal Cortex; Adrenal Cortex Function Tests; Adrenal Cortex Hormones; Adrenal Insufficiency; Adult; Aged; Asthma; Cosyntropin; Dehydroepiandrosterone; Dehydroepiandrosterone Sulfate; Female; Humans; Hydrocortisone; Male; Middle Aged

A 37 year old black female presented with congestive cardiac failure, 2 months postpartum. She developed spontaneous hypoglycaemia and symptoms of acute adrenal crisis (hypotension, nausea, abdominal pain and tachycardia with small thready pulse), which responded to i.v. dextrose, sodium chloride and hydrocortisone. Biochemical investigations revealed low serum cortisol and plasma adrenocorticotrophic hormone (ACTH) levels. The patient initially showed an impaired cortisol response to intramuscular aqueous tetracosactrin, but an exuberant response after priming with intramuscular tetracosactrin depot. These findings, together with the normal remaining pituitary function, led us to conclude that this patient had isolated ACTH deficiency associated with congestive cardiac failure and acute adrenal crisis.

Topics: Acute Disease; Adrenal Insufficiency; Adrenocorticotropic Hormone; Adult; Cosyntropin; Female; Heart Failure; Humans; Hydrocortisone

Topics: Acute Disease; Adrenal Gland Diseases; Adrenal Insufficiency; Age Factors; Cosyntropin; Diagnosis, Differential; Hemorrhage; Hemorrhagic Disorders; Humans; Male; Middle Aged; Pulmonary Embolism; Spleen; Splenectomy; Subphrenic Abscess; Tomography, X-Ray Computed

The increase in plasma-fluorogenic-corticosteroids in response to a single injection of tetracosactrin depot was measured in eleven patients with suspected acute renal insufficiency who were treated simultaneously with prednisolone and deoxycorticosterone acetate (D.O.C.A.). Acute adrenal insufficiency was excluded in seven patients within 24 hours. There was no response in the remaining four patients, and prolonged corticotrophin stimulation tests confirmed the diagnosis of Addison's disease.

Topics: 11-Hydroxycorticosteroids; Acute Disease; Addison Disease; Adult; Aged; Cosyntropin; Desoxycorticosterone; Drug Therapy, Combination; Female; Humans; Hydrocortisone; Male; Middle Aged; Prednisolone; Stimulation, Chemical

A study of 23 patients admitted to hospital with severe acute asthma is reported in which plasma cortisol level on admission was significantly correlated with the degree of acidaemia and pulse rate. Patients who had not previously received treatment with corticosteroids responded satisfactorily to repeated daily injections of tetracosactrin depot, the rate of improvement being comparable to that observed in other patients treated with intravenous hydrocortisone hemisuccinate. A prompt and sustained rise in plasma cortisol was also seen following tetracosactrin. The total daily dose of hydrocortisone required to achieve plasma cortisol levels above 100 mug/100 ml was less when given by continuous intravenous infusion compared with intermittent injections, and a regime of 3 mg/kg body weight every six hours by infusion appeared satisfactory. Most patients reported subjective improvement by about four hours after starting treatment but objective evidence did not appear until about six hours from the start. Measurements of FEV1 and FVC proved to be the most reliable indices of the beginning of improvement although pulse rate was the first index to show maximum improvement. Previous maintenance treatment with corticosteroids in patients with asthma did not appear materially to affect the plasma half-life of intravenous hydrocortisone (4 mgm/kg body weight) when compared with healthy subjects or other patients with asthma who had not previously been treated with corticosteroids.

Topics: Acute Disease; Adolescent; Adrenocorticotropic Hormone; Adult; Asthma; Child; Child, Preschool; Cosyntropin; Female; Forced Expiratory Volume; Humans; Hydrocortisone; Male; Middle Aged; Pulse; Vital Capacity

44 patients with acute irritations of degenerative articular diseases and 66 patients with soft tissue rheumatism were treated with Synacthen Depot (tetracosactide hexacetate 1 mg/ml). During the first three days of treatment the patients received an average of 2 ampoulbs Synacthen Depot, then treatment was continued at 3-4 day intervals. In the degenerative joint disease group 86.4% and 89.4% in the group with soft tissue rheumatism became free of complaints or improved with the ACTH treatment. Most of the patients with degenerative joint diseases needed a 4 week treatment; 1/3 of the patients with soft tissue rheumatism were already free of complai

Topics: Acute Disease; Adrenocorticotropic Hormone; Adult; Aged; Arthritis, Rheumatoid; Cosyntropin; Delayed-Action Preparations; Drug Evaluation; Female; Fibromyalgia; Hip Joint; Humans; Joint Diseases; Knee Joint; Male; Middle Aged; Rheumatic Diseases; Spondylitis