Rapid Adrenocorticotropic Hormone Test Research Articles

Frequency of Adrenal Insufficiency in Patients With Hypoglycemia in an Emergency Department: A Cross-sectional Study.

ContextIn most patients presenting with hypoglycemia in emergency departments, the etiology of hypoglycemia is identified. However, it cannot be determined in approximately 10% of cases.ObjectiveWe aimed to identify the causes of unknown hypoglycemia, especially adrenal insufficiency.MethodsIn this cross-sectional study, we evaluated the etiology of hypoglycemia among patients in our emergency department with hypoglycemia (plasma glucose level < 70 mg/dL (3.9 mmol/L)] between April 1, 2016 and March 31, 2021 using a rapid adrenocorticotropic hormone (ACTH) test.ResultsThere were 528 cases with hypoglycemia included [52.1% male; median age 62 years (range 19-92)]. The majority [389 (73.7%)] of patients were using antidiabetes drugs. Additionally, 33 (6.3%) consumed alcohol; 17 (3.2%) had malnutrition; 13 (2.5%), liver dysfunction; 12 (2.3%), severe infectious disease; 11 (2.1%), malignancy; 9 (1.7%), heart failure; 4 (0.8%), insulin autoimmune syndrome; 3 (0.6%), insulinoma; 2 (0.4%) were using hypoglycemia-relevant drugs; and 1 (0.2%) suffered from non-islet cell tumor. Rapid ACTH tests revealed adrenal insufficiency in 32 (6.1%). In those patients, serum sodium levels were lower (132 vs 139 mEq/L, P < 0.01), eosinophil counts were higher (14 vs 8%, P < 0.01), and systolic blood pressure was lower (120 vs 128 mmHg, P < 0.05) at baseline than in patients with the other etiologies.ConclusionThe frequency of adrenal insufficiency as a cause of hypoglycemia was much higher than what we anticipated. When protracted hypoglycemia of unknown etiology is recognized, we recommend that the patient is checked for adrenal function using a rapid ACTH test.

Association between adrenal function and dialysis vintage in hemodialysis patients.

Adrenal insufficiency in hemodialysis patients is commonly encountered in clinical practice. However, its association with end-stage renal disease is unclear. We investigated the relationship between adrenal function and relevant clinical parameters, focusing on dialysis vintage. Altogether, 100 maintenance hemodialysis patients were enrolled (age: 69.8 ± 11.8years, dialysis vintage: 9.4 ± 9.2years). Basal serum cortisol levels were measured and their associations with relevant clinical parameters were investigated. Subsequently, hormone stimulation tests were performed to assess adrenal function. Basal serum cortisol significantly decreased with an increase in dialysis vintage (< 10years, 11.9 ± 3.7μg/dL; 10-19years, 10.9 ± 2.9μg/dL; ≥ 20years, 9.7 ± 3.8μg/dL). Basal cortisol was negatively correlated with dry weight, β2-microglobulin, creatinine, and lymphocyte count and positively correlated with brachial-ankle pulse wave velocity. Significant negative correlations were observed between basal cortisol and dialysis vintage after adjusting for confounding variables in the multivariate analysis. Standard adrenocorticotropic hormone (ACTH) and corticotropin-releasing hormone (CRH) stimulation tests were performed in 17 patients. Seven patients were diagnosed with adrenal insufficiency and all of them had a long dialysis vintage (≥ 10years). According to the rapid ACTH test, cortisol responses were significantly decreased in patients with long dialysis vintage compared to those with short dialysis vintage (< 10years). Similar findings were observed in ten patients without adrenal insufficiency. The CRH loading test showed similar tendencies, although the differences were not statistically significant. Adrenal function decreased with an increase in dialysis vintage. Long-term dialysis patients might be susceptible to adrenal insufficiency.

Primary aldosteronism in patients with acute stroke: prevalence and diagnosis during initial hospitalization.

BackgroundHypertension is the prime risk factor for stroke, and primary aldosteronism (PA) is the most common cause of secondary hypertension. The prevalence of PA in stroke patients has never been reported. The aim of this study was to elucidate the prevalence of PA.MethodsA total of 427 consecutive patients with acute stroke were prospectively enrolled for this study. The screening tests were performed at the initial visit and a week after admission by measuring plasma aldosterone concentration and plasma renin activity. The rapid adrenocorticotropic hormone (ACTH) test was performed as the confirmatory test when both screening tests were positive. The primary endpoint was a final diagnosis of PA.ResultsThe sensitivity of the dual screening system for the diagnosis of PA was 88.2 %, and PA was finally diagnosed in 4.0 % of acute stroke patients and in 4.9 % of stroke patients with a history of hypertension. Patients with PA were less likely to be male and have diabetes, and they had higher blood pressure at the initial visit, lower potassium concentration, and more intracerebral hemorrhage. The rapid ACTH test was performed safely even in acute stroke patients.ConclusionsThe prevalence of PA is not low among acute stroke patients. Efficient screening of PA should be performed particularly for patients with risk factors.Trial registrationUMIN-CTR; UMIN000011021. Trial registration date: June 23, 2013 (retrospectively registered).

Relationship between Cortisol Increment and Basal Cortisol: Implications for the Low-Dose Short Adrenocorticotropic Hormone Stimulation Test

We analyzed the low-dose (1 microg) rapid adrenocorticotropic hormone test (LDST) in 17 patients with a normal hypothalamic-pituitary-adrenal axis to determine reference intervals for the LDST on the basis of poststimulation cortisol increments. We analyzed test results for 17 patients (14 females and 3 males; age range, 18-46 years) who had received a 2-mL aliquot of low-dose (1 microg) adrenocorticotropic hormone prepared from one 250-microg vial of Synacthen diluted in 500 mL of sterile normal saline solution. Sampling took place at 0, 20, 30, and 60 min post stimulation. The cortisol increment was plotted against basal cortisol. We observed a marked interdependence of the basal cortisol concentration with the increase in cortisol concentration. The relationship was inverse and linear with the best fit observed at 30 min post stimulation. The lower 95% prediction limit for basal cortisol at the zero increment was 400 nmol/L with a mean concentration of 600 nmol/L. We propose that a peak cortisol concentration <400 nmol/L is a sufficient single criterion for abnormal adrenal function as assessed by the LDST. Concentrations of 400-600 nmol/L are in the gray area, and those >600 nmol/L confirm normal adrenal function. Repeat analyses with larger sample sizes are warranted to confirm these observations.

Cytomegalovirus (CMV) retinitis and CMV antigenemia as a clue to impaired adrenocortical function in patients with AIDS.

To elucidate the relationship between the activity of CMV disease and adrenocortical function in patients with AIDS. CMV retinitis and CMV antigenemia assay (CMV-Ag: numbers of polymorphonuclear leukocytes positive for CMV pp65 antigen per 1.5 x 10(5) cells) are the least invasive and easily accessible examinations to assess the CMV disease activity. All HIV-infected patients with CD4+ lymphocyte counts < 50 x 10(6)/l who were admitted to the Research Hospital of the Institute of the Medical Science (University of Tokyo) between May 1995 to April 1996 were included in this study. Fundoscopic examination on CMV retinitis and CMV-Ag were chosen as methods to assess CMV activity because of their simplicity. Adrenocortical function was evaluated by basal plasma adrenocorticotropin, plasma cortisol, plasma aldosterone, plasma renin activity, and responses of plasma cortisol and plasma aldosterone to 250 micrograms intravenous cosyntropin [rapid adrenocorticotropin test (RAT)]. Thirty patients were enrolled in this study with a maximum CD4+ lymphocyte count of 32 x 10(6)/l. Eleven out of 30 patients showed impaired RAT response (37%). Fourteen out of 30 patients had CMV retinitis. A significant correlation was found between the presence of CMV retinitis and subnormal cortisol response (P < 0.005). Sixteen out of the 30 patients were CMV-Ag-positive. A significant correlation was found between CMV-Ag positivity and subnormal cortisol response to RAT (P < 0.005). CMV-Ag levels in the patients with subnormal cortisol response to RAT were significantly higher than those with normal response (P < 0.001). Importantly, five patients with subnormal cortisol response but not overt adrenal insufficiency at the time of RAT developed overt disease shortly afterwards. Autopsy was performed in six patients with subnormal cortisol response and showed multiple inclusion bodies indicative of CMV adrenitis. The adrenal gland is most frequently affected by CMV in AIDS patients. Our result suggests that CMV retinitis or CMV-Ag positivity independently serve as an indication of possible adrenal dysfunction.

Hyperkalaemia in acute leukaemia: a sign of adrenocortical insufficiency.

To evaluate adrenal cortical reserve function in hyperkalaemic patients with acute leukaemia (AL). In hyperkalaemic AL patients, after basal blood collection for cortisol, rapid adrenocorticotropic hormone (ACTH) stimulation test was performed with human a1-24-ACTH 0.25 mg, intravenously. Sixty minutes following injection, additional plasma was obtained for cortisol. Normal response was a peak cortisol level greater than 15 micrograms dL-1 with an increment greater than 5 micrograms dL-1. Hacettepe University Hospital, Ankara, Turkey. Newly diagnosed AL patients with plasma K+ values exceeding 4.5 mmol L-1, who had never received antileukaemia therapy were eligible for entry into the trial. Thirteen patients fulfilled these criteria. Twenty AL patients with normal serum K+ levels were studied as controls. In six patients with hyperkalaemia, adrenal cortical response to rapid ACTH test was inadequate. One patient died during induction chemotherapy due to sepsis. Five of the remaining patients entered remission. Repeat ACTH tests during remission revealed normalization of the adrenocortical function in these patients. However, in only one patient with normal serum K+ level, adrenocortical reserve was decreased. We suggest that in any AL patient with hyperkalaemia, adrenal reserve function should be evaluated with rapid ACTH stimulation test. In states of resistant hypotension and hyperkalaemia, steroids may be life saving.

The potential for serious consequences from misinterpretation of normal responses to the rapid adrenocorticotropin test

The potential for serious consequences from misinterpretation of normal responses to the rapid adrenocorticotropin test

The potential for serious consequences from misinterpretation of normal responses to the rapid adrenocorticotropin test

The potential for serious consequences from misinterpretation of normal responses to the rapid adrenocorticotropin test

The potential for serious consequences from misinterpreting normal responses to the rapid adrenocorticotropin test

The potential for serious consequences from misinterpreting normal responses to the rapid adrenocorticotropin test

The potential for serious consequences from misinterpreting normal responses to the rapid adrenocorticotropin test.

Despite unequivocal published evidence that patients with subnormal hypothalamic-pituitary-adrenal (HPA) function may respond normally to ACTH, such normal results are still considered reliable indications of unimpaired HPA function. This view was tested in four patients with clinical features suggesting corticotropin deficiency, in whom cosyntropin (0.25 mg, i.v.) raised serum cortisol above 560 nmol/L (20 micrograms/dL) at 1 h. All four patients had subnormal responses to metyrapone and excellent persistent improvement during subsequent glucocorticoid therapy. Serum cortisol concentrations 1 h after cosyntropin treatment in these patients closely resembled cortisol concentrations 1 h after uncomplicated cholecystectomy in six other patients. However, the rapid ACTH test in the patients with hypopituitarism failed to indicate whether more prolonged stimulation by ACTH or their endogenous stress would stimulate the normal continuing rise in serum cortisol, which reached 1358 +/- 170 nmol/L (+/- SE) 5 h after the incision in the cholecystectomized patients. As the three hypocorticotropic patients who were recognizably stressed had unstressed serum cortisol levels despite persistent adrenocortical reserve (shown by their ACTH responses) and recovered during glucocorticoid therapy, the ACTH test, if interpreted to indicate normal HPA function, would probably have had disastrous consequences. We conclude that a normal response to the rapid ACTH test can be dangerously misleading, particularly in incomplete ACTH deficiency states.

Adrenocortical insufficiency in Rhodesian sleeping sickness is not attributable to suramin

Suramin, a polysulphonated naphthylurea used in the treatment of human African trypanosomiasis (HAT), is known to cause adrenocortical insufficiency in doses exceeding the quantity used for treatment of HAT. We have previously reported that Trypanosoma brucei rhodesiense infection causes a combined central and peripheral adrenal insufficiency. To evaluate whether suramin therapy acts as an additional adrenotoxic factor, we assessed adrenocortical function in 72 patients suffering from HAT at different times during treatment with either suramin or melarsoprol by a rapid adrenocorticotropic hormone test. We found a significantly diminished peak cortisol response to stimulation in the acutely ill patients ( P = 0·001), indicating impaired adrenocortical function, as well as a high incidence of partial adrenocortical insufficiency (27%). During and after trypanocidal therapy the incidence of partial adrenal insufficiency gradually declined (to 25% and 18% respectively). Stimulated peak cortisol levels did not differ significantly between patients receiving suramin and those given melarsoprol. No correlation was found between serum suramin concentration and the cortisol response to stimulation ( r = 0·09, P = 0·47). Thus we conclude that suramin in trypanocidal doses neither causes nor worsens the adrenocortical dysfunction observed in Rhodesian HAT.

Rapid Adrenocorticotropic Hormone Test in Practice. Retrospective Review

Retrospective analysis of the rapid adrenocorticotropic hormone (ACTH) test in a large adult population shows a marked interdependence of the basal cortisol concentration, peak cortisol concentration, and increase in cortisol concentration. Repetition of the rapid ACTH test in the same patient does not improve diagnostic accuracy. A significant number of falsely abnormal rapid ACTH test results were observed (in comparison to continuous ACTH infusion as a reference test). This supports the use of the rapid ACTH test as a screening test, but not as a diagnostic test for adrenocortical failure. It is proposed that a peak cortisol level greater than or equal to 20 micrograms/dl (550 nmol/liter) is a sufficient single criterion for normal adrenal function as assessed by the rapid ACTH test.

Rapid adrenocorticotropic hormone test in practice. Retrospective review

Retrospective analysis of the rapid adrenocorticotropic hormone (ACTH) test in a large adult population shows a marked interdependence of the basal cortisol concentration, peak cortisol concentration, and increase in cortisol concentration. Repetition of the rapid ACTH test in the same patient does not improve diagnostic accuracy. A significant number of falsely abnormal rapid ACTH test results were observed (in comparison to continuous ACTH infusion as a reference test). This supports the use of the rapid ACTH test as a screening test, but not as a diagnostic test for adrenocortical failure. It is proposed that a peak cortisol level greater than or equal to 20 μg/dl (550 nmol/liter) is a sufficient single criterion for normal adrenal function as assessed by the rapid ACTH test.